In vivo Gonadoprotective Effects of Myricetin on Cisplatin- Induced Testicular Damage via Suppression of TLR4/NF-kB Inflammation Pathway and Heat-Shock Response / Efectos Gonadoprotectores in vivo de la Miricetina sobre el Daño Testicular Inducido por Cisplatino Mediante la Supresión de la Vía de Inflamación TLR4/NF-kB y la Respuesta al Choque Térmico

SUMMARY: The aim of this study is to reveal the gonadoprotective effects of myricetin (MYC), which has many biological properties, on cisplatin (CP)-induced testicular damage in rats. For this purpose, 40 male Wistar albino rats were divided into 4 groups as Control (group given no treatment), MYC (group given 5 mg/kg/i.p myricetin for 7 days), CP (group given 7 mg/kg/i.p cisplatin at 7th day) and MYC + CP (group given 5 mg/kg/i.p myricetin for 7 days before 7 mg/kg/i.p cisplatin injection). After administrations, testicular tissues of animals were extracted and processed according to tissue processing protocol. Hematoxylin & Eosin staining were performed to evaluate the histopathological changes and Johnsen'sTesticular Biopsy Score (JTBS) was applied and mean seminiferous tubule diameters (MSTD) were measured to compare experimental groups in terms of histopathological changes. Moreover, TLR4, NF-kB, HSP70 and HSP90 expression levels were detected by immunohistochemical staining and the density of immunoreactivity were measured to determine the difference in the expression levels of these factors among groups. Additionally, testicular apoptosis was detected via TUNEL assay. JTBS and MSTD data were significantly lower in CP group compared to other groups and MYC administrations significantly protects testicular tissue against CP-induced damage. Moreover, TLR4, NF-kB, HSP70 and HSP90 expressions and apoptotic cells significantly increased in the CP group (p<0.05). However, MYC administrations exerted a strong gonadoprotective effect on testicular tissue in terms of these parameters in MYC+CP group (p<0.05). According to our results, we suggested that MYC can be considered as a protective agent against cisplatin-induced testicular damage.

El objetivo de este estudio es revelar los efectos gonadoprotectores de la miricetina (MYC), que tiene muchas propiedades biológicas, sobre el daño testicular inducido por cisplatino (CP) en ratas. Para este propósito, se dividieron 40 ratas albinas Wistar macho en 4 grupos: Control (grupo que no recibió tratamiento), MYC (grupo que recibió 5 mg/kg/i.p de miricetina durante 7 días), CP (grupo que recibió 7 mg/kg/i.p de cisplatino al séptimo día) y MYC + CP (grupo que recibió 5 mg/ kg/i.p de miricetina durante 7 días antes de la inyección de 7 mg/ kg/i.p de cisplatino). Después de las administraciones, se extrajeron y procesaron tejidos testiculares de animales según el protocolo de procesamiento de tejidos. Se realizó tinción con hematoxilina y eosina para evaluar los cambios histopatológicos y se aplicó la puntuación de biopsia testicular de Johnsen (JTBS) y se midieron los diámetros medios de los túbulos seminíferos (MSTD) para comparar los grupos experimentales en términos de cambios histopatológicos. Además, los niveles de expresión de TLR4, NF-kB, HSP70 y HSP90 se detectaron mediante tinción inmunohistoquímica y se midió la densidad de inmunorreactividad para determinar la diferencia en los niveles de expresión de estos factores entre los grupos. Además, se detectó apoptosis testicular mediante el ensayo TUNEL. Los datos de JTBS y MSTD fueron significativamente más bajos en el grupo CP en comparación con otros grupos y las administraciones de MYC protegen significativamente el tejido testicular contra el daño inducido por CP. Además, las expresiones de TLR4, NF-kB, HSP70 y HSP90 y las células apoptóticas aumentaron significativamente en el grupo CP (p<0,05). Sin embargo, las administraciones de MYC ejercieron un fuerte efecto gonadoprotector sobre el tejido testicular en términos de estos parámetros en el grupo MYC+CP (p<0,05). Según nuestros resultados, sugerimos que MYC puede considerarse como un agente protector contra el daño testicular inducido por cisplatino.

Effect of kefir on increased apoptosis in liver and kidney in cisplatin toxicity / Efecto del kéfir sobre el aumento de la apoptosis en el hígado y los riñones en la toxicidad del cisplatino

SUMMARY: Cisplatin is a chemotherapeutic agent inducing liver and kidney damage. In this study, we intended to investigate the impact of kefir beverage, an essential probiotic and functional food, on liver and kidney damage induced by cisplatin. Wistar albino rats were divided into four groups: Control, Cisplatin (single dose of 7 mg/kg, intraperitoneal), Kefir (2 ml/d, 7 d, oral gavage), and Cisplatin+Kefir (CK). At the end of day 7, animals were euthanized. Blood, kidney, and liver tissue samples were collected. For both tissues, biochemically ALT, AST, Urea, Creatine; histomorphologically, hematoxylin-eosin, Masson's Trichrome, and immunohistochemical staining of caspase-3, a marker of apoptosis, were performed. Serum urea and creatinine levels of the Cisplatin group were significantly higher than the Control group (p<0.05). In the CK group, kefir consumption decreased urea and creatinin levels approached to Control and Kefir groups. Cisplatin resulted in higher ALT and AST activities, indicating hepatocellular damage, compared to the Control group (p<0.05). Kefir consumption decreased ALT activities approached to both the Control and Kefir group. Histomorphological observations were in agreement biochemical results. In liver and kidney tissues, structural damage was observed with an increase in collagen fibers in the Cisplatin group, and Caspase-3 activity was immunohistochemically higher than in the other groups. In the CK group, collagen fiber increase, structural damage, and Caspase-3 activities were less than in the Cisplatin group. Kefir consumption alleviated liver and kidney damage. However, more research is required to understand such effect of kefir better.

RESUMEN: El cisplatino es un agente quimioterapéutico que induce daño hepático y renal. En este estudio, intentamos investigar el efecto del kéfir, un alimento funcional y probiótico esencial, en el daño hepático y renal inducido por el cisplatino. Se dividieron ratas albinas Wistar en cuatro grupos: control, cisplatino (dosis única de 7 mg/kg, intraperitoneal), kéfir (2 ml/día, 7 días, sonda oral) y cisplatino + kéfir (CK). Al final del día 7, los animales fueron sacrificados. Se recolectaron muestras de sangre, riñón y tejido hepático. Se determinó ALT, AST, Urea y Creatina; Para el análisis histomorfológico, se realizaron tinciones con hematoxilina-eosina, tricrómico de Masson y para inmunohistoquímica, caspasa-3, un marcador de apoptosis. Los niveles séricos de urea y creatinina del grupo de cisplatino fueron significativamente más altos que los del grupo de control (p<0,05). En el grupo CK, el consumo de kéfir disminuyó los niveles de urea y creatinina acercándose a los grupos Control y Kéfir. El cisplatino resultó en actividades más altas de ALT y AST, lo que indica daño hepatocelular, en comparación con el grupo Control (p<0.05). El consumo de kéfir disminuyó las actividades de ALT tanto en el grupo Control como en el de Kéfir. Las observaciones histomorfológicas coincidieron con los resultados bioquímicos. En tejidos hepáticos y renales se observó daño estructural con aumento de fibras colágenas en el grupo de Cisplatino, y la actividad de Caspasa-3 fue inmunohistoquímicamente mayor que en los otros grupos. En el grupo de CK, el aumento de las fibras colágenas, el daño estructural y las actividades de Caspasa-3 fueron menores que en el grupo Cisplatino. El consumo de kéfir mejoró el daño hepático y renal. Sin embargo, se requiere más investigación para comprender mejor el efecto del kéfir.

Importancia de la cardiooncología. Cómo detectar la insuficiencia cardiaca subclínica / Importance of cardio-oncology. How to detect suclinical heart failure

Resumen Hoy una de las principales causas de mortalidad es el cáncer. La supervivencia en pacientes con cáncer ha incrementado de 1970 (25%) a la actualidad (80%). A raíz de la introducción de las antraciclinas como tratamiento de cáncer desde 1960-1970, más del 60% de los pacientes son tratados con estos agentes; sin embargo, la exposición de quimioterápicos conlleva las enfermedades cardiovasculares como la principal causa de mortalidad en enfermos supervivientes de cáncer en el s. XXI. Hay múltiples factores que incrementan la sensibilidad de cardiotoxicidad inducida por antracíclicos. En 1970 el estándar de oro para la detección de disfunción ventricular era la biopsia endomiocárdica, en forma posterior la detección y manejo de la cardiotoxicidad fue guiada por los síntomas, en 1981 la detección de cardiotoxicidad fue reportada con la determinación de la fracción de expulsión del ventrículo izquierdo (FEVI) por ecocardiografía 2D. En la actualidad el ecocardiograma 3D para FEVI y volúmenes sistólico y diastólico han presentado una alta correlación de los valores obtenidos por resonancia magnética para la evaluación de la función cardiaca. Hoy en día la ecocardiografía strain, strain-rate y speckle tracking se utilizan para determinar la función miocárdica regional y global. Para una valoración integral estos resultados se pueden complementar con biomarcadores cardiacos (troponinas y propéptido natriurético tipo B) y cambios electrocardiográficos. De esta forma se puede detectar insuficiencia cardiaca subclínica y dar un tratamiento oportuno.

Abstract Today one of the main causes of mortality is cancer. Survival in cancer patients has increased from 1970 (25%) to the present (80%). Following the introduction of anthracyclines as a cancer treatment since 1960-70, more than 60% of patients are treated with these agents, although chemotherapeutic exposure leads to cardiovascular diseases as the main cause of mortality in surviving patients. of cancer in the 21st Century. There are multiple factors that increase the sensitivity of anthracyclic-induced cardiotoxicity. In 1970 the gold standard for the detection of ventricular dysfunction was endomyocardial biopsy, subsequently the detection and management of cardiotoxicity was guided by symptoms, in 1981 the detection of cardiotoxicity was reported with the determination of the ejection fraction of the left ventricle (LVEF), by 2D echocardiography. Currently, the 3D echocardiogram for LVEF and systolic and diastolic volumes have presented a high correlation of the values obtained by magnetic resonance imaging for the evaluation of cardiac function. Today strain, strain-rate and speckle tracking echocardiography are used to determine regional and global myocardial function. For a comprehensive assessment, these results can be complemented with cardiac biomarkers (troponins) and electrocardiographic changes. In this way, subclinical heart failure can be detected and timely treatment can be given.

The ameliorative effects of caffeic acid phenethyl ester in cisplatin-induced nephrotoxicity: assessment of the oxidative stress an inflammation / Los efectos de mejora del éster fenetílico del ácido cafeico en la nefrotoxicidad inducida por cisplatino: evaluación del estrés oxidativo y la inflamación

SUMMARY: The aim of this study is to determine the potential therapeutic effects of CAPE in CP-induced nephrotoxicity in rats. Cisplatin (CP) is an antineoplastic chemotherapeutic used for treatment of many cancer types but its applications may induce nephrotoxicity. Caffeic acid phenethyl ester (CAPE) is an active component of propolis and it has several important physiological activities. Rats were divided into four groups: Control, CAPE (10 µmol/kg/i.p), CP (7 mg/kg/i.p), and CP+CAPE (7 mg/kg/i.p, CP and 10 µmol/kg/i.p, CAPE). After administrations, animals were sacrificed, and kidney tissues were extracted. Histopathological changes were evaluated and TNF-α and IL-6 immunostaining were performed. Moreover, tissue SOD, CAT and MDA levels were measured by ELISA assay to assessment of oxidative stress and lipid peroxidation. CP group showed histopathological deterioration compared to the Control group and CAPE treatment attenuated this damage. When compared with Control and CAPE group, an increase in TNF-α and IL-6 immunoreactivities and tissue MDA levels were observed in the CP group while a decrease in tissue SOD and CAT levels were detected. Furthermore, an improvement was observed in the CP+CAPE compared to the CP group. We suggest that CAPE can be used as a therapeutic agent to attenuate the toxic effects of cisplatin, thanks to its antioxidant and anti-inflammatory properties.

RESUMEN: El objetivo de este estudio fue determinar los posibles efectos terapéuticos de éster fenetílico del ácido cafeico (EFAC) en la nefrotoxicidad inducida por cisplatino (CP) en ratas. El CP es un quimioterapéutico antineoplásico utilizado para el tratamiento de muchos tipos de cáncer, sin embargo sus aplicaciones pueden inducir nefrotoxicidad. El EFAC es un componente activo del propóleo y tiene varias actividades fisiológicas importantes. Para el estudio las ratas se dividieron en cuatro grupos: Control, EFAC (10 µmol / kg / ip), CP (7 mg / kg / ip) y CP + EFAC (7 mg / kg / ip, CP y 10 µmol / kg / ip, EFAC). Después de las administraciones, se sacrificaron los animales y se extrajeron los tejidos renales. Se evaluaron los cambios histopatológicos y se realizó inmunotinción de TNF-α e IL-6. Además, los niveles tisulares de SOD, CAT y MDA se midieron mediante un ensayo ELISA para evaluar el estrés oxidativo y la peroxidación lipídica. El grupo CP mostró deterioro histopatológico en comparación con el grupo Control y el tratamiento con EFAC atenuó este daño. En comparación con el grupo de control y EFAC, se observó un aumento en las inmunorreactividades de TNF-α e IL-6 y los niveles de MDA en el tejido en el grupo de CP, mientras que se detectó una disminución en los niveles de SOD y CAT en los tejidos. Además, se observó una mejora en el CP + EFAC en comparación con el grupo CP. Sugerimos que EFAC puede utilizarse como agente terapéutico para atenuar los efectos tóxicos del cisplatino, gracias a sus propiedades antioxidantes y antiinflamatorias.

The effects of rapamycin and 3-methyladenine on nitric oxide synthase enzymes in cisplatin-induced neurotoxicity / Efectos de la rapamicina y la 3-metiladenina sobre la enzima óxido nítrico sintasa en la neurotoxicidad inducida por cisplatino

SUMMARY: The aim of this study was to determine the relationship of autophagy-enhancing rapamycin (RAPA) and autophagy- inhibitor 3-methyladenine (3-MA) with Nitric oxide synthases (NOS) in Cisplatin (CIS)-induced neurotoxicity in rats. Rats were divided into 4 groups (n=10): Control was applied saline, CIS (a single dose of 8mg/kg intraperitoneal (i.p.) on 7th day of experiment), RAPA+CIS (2 mg/kg/i.p. RAPA per day and 8 mg/kg/i.p. CIS on 7th day), 3-MA+CIS (15 mg/kg/i.p. 3-MA per day and 8 mg/kg/i.p. CIS on 7th day). Rats were sacrificed under anesthesia. Brain tissues were evaluated histopathologically. eNOS, Inos, nNOS and MAP 2 immunostaining were performed to determine the expression levels of these proteins among groups. Superoxide dismutase (SOD), Catalase (CAT), Malondialdehyde (MDA) and Interleukin IL-6 levels in brain tissue and serum nitric oxide (NO) level were measured by ELISA assay. In histopathological evaluation, neurodegeneration was seen in the CIS group. There was an increase in eNOS, iNOS and nNOS immunostaining in CIS group. While MAP2 immunostaining of the CIS group decreased. There was a decrease in SOD and CAT levels of brain tissue in CIS group. However, there was an increase in MDA, IL-6 and NO levels of brain tissue in CIS group. We found that antioxidant capacity increase while, inflammation and nitric oxide levels decreased in the RAPA-treated group. 3-MA does not have a significant effect. We suggest that CIS-induced neurotoxicity is more effective than Rapa 3-MA and may also be linked to NOS enzymes.

RESUMEN: El objetivo de este estudio fue determinar la relación de la rapamicina potenciadora de la autofagia (RAPA) y el inhibidor de la autofagia 3-metiladenina (3-MA) con óxido nítrico sintasas (NOS) en la neurotoxicidad inducida por cisplatino (CIS) en ratas. Las ratas se dividieron en 4 grupos (n = 10): grupo control se aplicó solución salina, CIS (una dosis única de 8 mg / kg intraperitoneal (ip) el día 7 del experimento), RAPA + CIS (2 mg / kg / ipRAPA por día y 8 mg / kg / ip CIS el día 7), 3-MA + CIS (15 mg / kg / ip 3-MA por día y 8 mg / kg / ip CIS el día 7). Las ratas se sacrificaron bajo anestesia y los tejidos cerebrales fueron analizados histopatológicamente. Se realizaron inmunotinciones con eNOS, Inos, nNOS y MAP 2 para determinar los niveles de expre- sión de estas proteínas entre los grupos. Se midieron los niveles de superóxido dismutasa (SOD), catalasa (CAT), malondialdehído (MDA) e interleucina IL-6 en el tejido cerebral y el nivel de óxido nítrico (NO) en suero mediante ensayo ELISA. En la evaluación histopatológica, se observó neurodegeneración en el grupo CIS. Hubo un aumento en la inmunotinción de eNOS, iNOS y nNOS en el grupo CIS. Mientras que la inmunotinción de MAP2 del grupo CIS disminuyó. Hubo una disminución en los niveles de SOD y CAT del tejido cerebral en el grupo CIS, sin embargo, hubo un aumento en los niveles de MDA, IL-6 y NO en el tejido cerebral en el grupo CIS. Observamos que la capacidad antioxidante aumentó, mientras que la inflamación y los niveles de óxido nítrico disminuyeron en el grupo tratado con RAPA. 3-MA no tiene un efecto significativo. Sugerimos que la neurotoxicidad inducida por CIS es más eficaz que Rapa 3-MA y también puede estar relacio- nada con las enzimas NOS.

Otoprotection Mechanisms Against Oxidative Stress Caused by Cisplatin

Abstract Introduction Cisplatin damages the auditory system and is related to the generation of free radicals. Glutathione peroxidase is an endogenous free radicals remover. Objective To investigate the mechanisms involved in otoprotection by N-acetylcys- teine through the expression of glutathione peroxidase in outer hair cells from rats treated with cisplatin. Methods Male Wistar rats were intraperitoneally injected with cisplatin (8 mg/Kg) and/or received oral administration by gavage of N-acetylcysteine (300 mg/Kg) for 3 consecutive days. On the 4th day, the animals were euthanized and beheaded. The tympanic bullae were removed and prepared for scanning electron microscopy and Results Among the groups exposed to ototoxic doses of cisplatin, there was an increase in glutathione peroxidase immunostaining in two groups, the one exposed to cisplatin alone, and the group exposed to both cisplatin and N-acetylcysteine. Conclusion The expression of glutathione peroxidase in the outer hair cells of rats exposed to cisplatin showed the synthesis of this enzyme under cellular toxicity conditions.

Cascos fríos para la prevención de alopecia inducida por quimioterápicos / Cold caps for the prevention of chemotherapy-induced alopecia

Uno de los efectos adversos que generan mayor impacto psicosocial en los pacientes que se someten a quimioterapia es la pérdida de cabello. El uso de los cascos fríos podría representar una alternativa para prevenir la alopecia. Estos dispositivos producen vasoconstricción en los vasos sanguíneos del cuero cabelludo provocando que los quimioterápicos lleguen en menores concentraciones a los folículos pilosos, y por consiguiente, evitando que los citotóxicos alcancen el metabolismo de las células foliculares. Se propone que este proceso permita prevenir la alopecia, aunque existe una preocupación que es la posibilidad de metástasis en cuero cabelludo si la quimioterapia no llega a este tejido. Partiendo de la consulta de una paciente con diagnóstico reciente de cáncer de mama, surge el interrogante si en pacientes en tratamiento con quimioterapia el uso de cascos fríos en comparación con su no utilización, disminuye la caída del cabello y si aumenta el riesgo de metástasis en cuero cabelludo. Luego de realizar una búsqueda, se analizaron los resultados de tres artículos pertinentes. Se concluye que el uso de cascos fríos en pacientes que reciben quimioterapia representaría una opción válida para prevenir la alopecia sin indicios de problemas de seguridad y se realiza una reseña acerca de la disponibilidad de los cascos fríos en Argentina. (AU)

One of the adverse effects that generate greater psychosocial impact in patients undergoing chemotherapy is hair loss. The use of cold caps could represent an alternative to prevent alopecia. These devices produce vasoconstriction in the blood vessels of the scalp, causing chemotherapeutic agents to reach the hair follicles in lower concentrations, and there forepreventing toxins from being metabolized by the follicular cells. Thus, alopecia could be prevented but, there is a concern that is the possibility of metastasis to the scalp if the therapy does not reach this tissue. Based on a consultation of a patient recently diagnosed with breast cancer, the question arises whether in patients undergoing chemotherapy the useof cold caps compared to their non-use reduces hair loss and whether it in creases the risk of metastasis to the scalp. After performing a search, the results of three relevant articles were analyzed. It is concluded that the use of cold helmets in patients receiving chemotherapy would represent a valid option to prevent alopecia without indications of safety problems. Finally, a review is made about the availability of scalp-cooling devices in Argentina.

Amifostine protects from the peripheral sensory neuropathy induced by oxaliplatin in mice

Sensory neuropathy is a dose-limiting side effect of oxaliplatin-based cancer treatment. This study investigated the antinociceptive effect of amifostine and its potential neuroprotective mechanisms on the oxaliplatin-related peripheral sensory neuropathy in mice. Oxaliplatin (1 mg/kg) was injected intravenously in Swiss albino male mice twice a week (total of nine injections), while amifostine (1, 5, 25, 50, and 100 mg/kg) was administered subcutaneously 30 min before oxaliplatin. Mechanical and thermal nociceptive tests were performed once a week for 49 days. Additionally, c-Fos, nitrotyrosine, and activating transcription factor 3 (ATF3) immunoexpressions were assessed in the dorsal root ganglia. In all doses, amifostine prevented the development of mechanical hyperalgesia and thermal allodynia induced by oxaliplatin (P<0.05). Amifostine at the dose of 25 mg/kg provided the best protection (P<0.05). Moreover, amifostine protected against neuronal hyperactivation, nitrosative stress, and neuronal damage in the dorsal root ganglia, detected by the reduced expression of c-Fos, nitrotyrosine, and ATF3 (P<0.05 vs the oxaliplatin-treated group). In conclusion, amifostine reduced the nociception induced by oxaliplatin in mice, suggesting the possible use of amifostine for the management of oxaliplatin-induced peripheral sensory neuropathy.

The effectiveness of eugenol against cisplatin-induced ototoxicity / A eficácia do eugenol contra a ototoxicidade induzida pela cisplatina

Abstract Introduction: Ototoxicity refers to cellular damage or function impairment developing in the inner ear in association with any therapeutic agent or chemical substance, and still represents the principal side-effect restricting the use of cisplatin. Objective: The aim of this study was to perform a biochemical, functional and histopathological investigation of the potential protective effect of eugenol against cisplatin-induced ototoxicity. Methods: The study was performed with 24 female Sprague Dawley rats. Distortion product otoacoustic emissions tests were performed on all animals, which were randomized into four equal groups. A single intraperitoneal dose of 15 mg/kg cisplatin was administered to cisplatin group, while the eugenol group received 100 mg/kg eugenol intraperitoneal for five consecutive days. 100 mg/kg eugenol was administered to cisplatin + eugenol group for 5 days. On the third day, these rats were received a single dose of 15 mg/kg cisplatin. The control group was given 8 mL/kg/day intraperitoneal saline solution for five days. The distortion product otoacoustic emissions test was repeated 24 h after the final drug administration. All animals were sacrificed, and the cochleas were subsequently used for biochemical and histopathological examinations. Results: Cisplatin caused oxidative stress in the cochlea, impaired the cochlear structure and significantly reduced signal noise ratio levels. Administration of eugenol together with cisplatin reversed these effects and provided functional, biochemical and histopathological protection. Conclusion: The study findings represent the first indication in the literature that eugenol may protect against ototoxicity by raising levels of antioxidant enzymes and lowering those of oxidant parameters.

Resumo Introdução: A ototoxicidade refere-se ao dano celular ou comprometimento da função da orelha interna associado a qualquer agente terapêutico ou substância química e ainda representa o principal efeito colateral que restringe o uso da cisplatina. Objetivo: O objetivo deste estudo foi realizar uma investigação bioquímica, funcional e histopatológica do potencial efeito protetor do eugenol contra a ototoxicidade induzida pela cisplatina. Método: O estudo foi realizado com 24 ratos fêmeas Sprague Dawley. Testes de emissões otoacústicas por produto de distorção foram realizados em todos os animais, os quais foram randomizados em quatro grupos iguais. Uma única dose intraperitoneal de 15 mg/kg de cisplatina foi administrada ao grupo cisplatina, enquanto o grupo eugenol recebeu 100 mg/kg de eugenol intraperitoneal por cinco dias consecutivos. Foram administrados 100 mg/kg de eugenol ao grupo cisplatina + eugenol durante 5 dias. No terceiro dia, estes ratos receberam uma dose única de 15 mg/kg de cisplatina. O grupo controle recebeu 8 mL/kg/dia de solução salina intraperitoneal por cinco dias. O teste de emissões otoacústicas por produto de distorção foi repetido 24 horas após a administração final do medicamento. Todos os animais foram sacrificados e as cócleas foram posteriormente utilizadas para exames bioquímicos e histopatológicos. Resultados: A cisplatina causou estresse oxidativo na cóclea, prejudicou a estrutura coclear e reduziu significativamente os níveis da relação sinal/ruído. A administração de eugenol juntamente com a cisplatina reverteu esses efeitos e forneceu proteção funcional, bioquímica e histopatológica. Conclusão: Os achados do estudo representam a primeira indicação na literatura de que o eugenol pode proteger contra a ototoxicidade, eleva os níveis de enzimas antioxidantes e diminui os níveis dos parâmetros oxidantes.

Pericyte loss and detachment in experimental cisplatin-induced neuropathy / Pérdida y desprendimiento de pericitos en la neuropatía experimental inducida por cisplatino

Cisplatin is an antineoplastic agent with neuropathy as one of its major side effect. However, effective treatment is lacking. Increasing evidence suggests that cisplatin might damage nerve capillaries leading to impaired functions of blood-nerve barrier (BNB) and neuropathy. This study was aimed to examine the effects of cisplatin on pericytes. Rats were either treated with intraperitoneal injection of cisplatin 2 mg/kg twice a week for five continuous weeks. Cisplatin-treated rats showed reduced body weight, thermal hypoalgesia and slow sciatic motor nerve conduction velocity, indicating neuropathy. The density of pericytes in the distal sciatic nerves determined by immunohistochemistry to desmin was significantly reduced in the cisplatin compared with that of the control groups. Electron microscopic analysis demonstrated the detachment of pericytes from endothelial cells including the disruption of shared basement membrane in the sciatic nerves from cisplatin-treated rats. These data indicate the pericyte loss and detachment caused by cisplatin. Future studies of the BNB components and functions after cisplatin treatment are needed and will be essential for the development of effective treatments against cisplatin-induced neuropathy.

El cisplatino es un agente antineoplásico y presenta como uno de sus principales efectos secundarios, la neuropatía. Sin embargo, falta un tratamiento eficaz. La creciente evidencia sugiere que el cisplatino podría dañar los capilares nerviosos, lo que puede provocar una alteración de las funciones de la barrera hematoencefálica (BHE) y neuropatía. Este estudio tuvo como objetivo examinar los efectos del cisplatino en los pericitos. Las ratas se trataron con inyección intraperitoneal de cisplatino (2 mg/kg) dos veces por semana durante 5 semanas seguidas. Las ratas tratadas con cisplatino mostraron una reducción del peso corporal, hipoalgesia térmica y una velocidad de conducción del nervio ciático lenta, lo que indicaría neuropatía. La densidad de los pericitos en los nervios ciáticos distales determinada por inmunohistoquímica para desmina se redujo significativamente en el grupo cisplatino en comparación con la de los grupos controles. El análisis al microscopio electrónico demostró el desprendimiento de pericitos de las células endoteliales, incluida la ruptura de la membrana basal compartida en los nervios ciáticos de ratas tratadas con cisplatino. Estos datos indican la pérdida de pericitos y el desprendimiento causado por el cisplatino. Se necesitan estudios futuros de los componentes y funciones del BHE después del tratamiento con cisplatino y serán esenciales para el desarrollo de tratamientos efectivos contra la neuropatía inducida por el cisplatino.

The protective effects of whortleberry extract against cisplatin-induced ototoxicity in rats / Efeitos protetores do extrato de uva-do-monte contra a ototoxicidade induzida por cisplatina em ratos

Abstract Introduction: Cisplatin is one of the main chemotherapeutic agents used for the treatment of many types of cancer. However, ototoxicity, one of the most serious side effects of cisplatin, restricts its usage. Objective: We aimed to investigate the protective effects of whortleberry extract against cisplatin-induced ototoxicity by evaluating hearing and histopathological cochlear damage and by measuring the biochemical parameters affected byoxidative stress. Methods: Forty-eight male rats were included in the study after performing Distortion Product Otoacoustic Emission test to confirm that their hearing levels were normal. The rats were randomly divided into six groups: the control group, the sham group, and, which received only whortleberry extract, only cisplatin, cisplatin + 100 mg whortleberry extract, cisplatin + 200 mg whortleberry extract, respectively. Audiologic investigation was performed by performing the Distortion Product Otoacoustic Emission test at the beginning and at the eighth day of the study. Cardiac blood samples were collected for biochemical analysis, and the rats were sacrificed to obtain cochlear histopathological specimens on the eighth day. Results: The results revealed that whortleberry protects hearing against cisplatin-induced ototoxicity independent of the dose. However, high doses of whortleberry extract are needed to prevent histopathological degeneration and oxidative stress. Conclusion: The results obtained in this study show that whortleberry extract has a protective effect against cisplatin-induced ototoxicity.

Resumo Introdução: A cisplatina é um dos principais agentes quimioterápicos utilizados para o tratamento de muitos tipos de câncer. No entanto, a ototoxicidade, um dos efeitos colaterais mais graves da cisplatina, restringe seu uso. Objetivo: Nosso objetivo foi investigar os efeitos protetores do extrato de uva-do-monte contra a ototoxicidade induzida por cisplatina, avaliar o dano auditivo e histopatológico coclear e medir os parâmetros bioquímicos afetados pelo estresse oxidativo. Método: Foram incluídos no estudo 48 ratos machos após teste de emissão otoacústica evocada por produto de distorção para confirmar que seus níveis de audição eram normais. Os ratos foram divididos aleatoriamente em seis grupos: o grupo controle, o grupo simulado, o que recebeu apenas extrato de uva-do-monte, o que recebeu apenas cisplatina, o que recebeu cisplatina + 100 mg de extrato de uva-do-monte e o que recebeu cisplatina + 200 mg de extrato de uva-do-monte, respectivamente. A investigação audiológica foi feita através do teste de emissão otoacústica de produto de distorção no início e no oitavo dia do estudo. As amostras de sangue cardíaco foram coletadas para análise bioquímica e os ratos foram sacrificados para obtenção de espécimes histopatológicos cocleares no oitavo dia. Resultados: Os resultados revelaram que o extrato de uva-do-monte protege a audição contra a ototoxicidade induzida por cisplatina, independentemente da dose. No entanto, são necessárias doses elevadas do extrato para evitar a degeneração histopatológica e o estresse oxidativo. Conclusão: Os resultados obtidos neste estudo mostram que o extrato de uva-do-monte tem um efeito protetor contra a ototoxicidade induzida por cisplatina.

Therapeutic effect of thymoquinone against methotrexate- induced damage on sperm parameters in mice / Efecto terapéutico de la tiroyoquinona contra el daño inducido por metotrexato en los parámetros espermáticos en ratones

Methotrexate drug is commonly used to treat cancer; it is known to cause reproductive damage. Thymoquinone, as a natural component of herbs has many healthy benefits shown in researches. The present study aimed to investigate probable therapeutic effects of Thymoquinone against Methotrexate-induced damage on sperm parameters in mice. In this experimental study, 30 male mice (25-30 g) were divided into five groups of six in each group. The mice were received normal saline (control group), Methotrexate (20 mg/kg), Methotrexate (20 mg/kg) + Thymoquinone (2, 10 and 20 mg/kg) by intraperitoneal injection. On the day after the last injection, the sperm parameters including motility, viability and count of sperms were assessed. Data analysis was performed using one-way ANOVA followed by Tukey test. Methotrexate alone showed a significant reduction in sperm parameters compared to the control group (P=0.00). In groups treated with Methotrexate and Thymoquinone, sperm parameters (motility ,viability, count sperm) did not show any significant differences with control group (P=0.00). Thymoquinone, as a potent antioxidant, could compensate for the toxicity induced by Methotrexate. These medical trends may be useful for diminishing the side effects of Methotrexate on the male reproductive system.

El metotrexato es un fármaco utilizado comúnmente para tratar el cáncer pero además causa daño en los órganos reproductivos. Durante las investigaciones se ha demostrado que la timoquinona, un componente natural de las hierbas, tiene numerosos beneficios. El objetivo del estudio fue investigar el probable efecto terapéutico de la timoquinona contra el daño inducido por metotrexato, en los parámetros espermáticos en ratones. En este estudio experimental, se dividieron 30 ratones machos (25-30 g) en cinco grupos de seis en cada uno. Los ratones recibieron solución salina normal (grupo control), metotrexato (20 mg / kg), metotrexato (20 mg / kg) + timoquinona (2, 10 y 20 mg / kg) por inyección intraperitoneal. El día después de la última inyección, se evaluaron los parámetros espermáticos, incluida la motilidad, la viabilidad y el recuento de espermatozoides. El análisis de los datos se realizó utilizando test de ANOVA seguido de la prueba de Tukey. Durante el uso exclusivo de metotrexato se observó una reducción significativa en los parámetros espermáticos en comparación con el grupo control (P = 0.00). En los grupos tratados con metotrexato y timoquinona, los parámetros espermáticos (motilidad, viabilidad, conteo de espermatozoides) no mostraron diferencias significativas con el grupo control (P = 0.00). Como potente antioxidante, la timoquinona podría compensar la toxicidad inducida por metotrexato. Estas tendencias médicas pueden ser útiles para disminuir los efectos secundarios de metotrexato en el sistema reproductivo masculino.

Protective effects of Tribulus terrestris hydroalcoholic extract against cisplatin-induced germ cell apoptosis in male mice / Efectos protectores del extracto hidroalcohólico Tribulus terrestris contra la apoptosis de células germinales inducida por cisplatino en ratones machos

SUMMARY: Toxic effects of anti-cancer and other drugs on the normal tissues could be reduced by the herbal plants and their fractions. This study investigated the protective effect of Tribulus terrestris (TT) on Cisplatin- induced cytotoxicity germ cell apoptosis in male mice. In this experimental study, thirty male Balb/c mice were divided randomly into 5 groups (n=6). A single dose of Cisplatin (5.5 mg/kg) and differ-ent concentrations of Tribulus terrestris were administrated for 14 consecutive days. Reverse transcription polymerase chain reaction (RT-PCR) of apoptosis-re-lated genes was performed with RNA extracted from testes of the mice. Statistical analysis was done using one-way ANOVA. In the Cisplatin group, there was a significant increase in mRNA expression of p53 (P=0.008), bax (P=0.004) and the ratio of bax/Bcl-2 (P=0.000), whereas there was an decrease in the expression of Bcl-2 (P=0.003), as compared to control group. In Cis+TT groups, the data showed that different concentrations of TT could improve the harmful effects caused by the Cisplatin. The best protective effects were achieved in Cis+TT (300 mg/kg). Tribulus terrestris protects testicular germ cell against Cisplatin induced apoptosis by affecting related genes regulation.

RESUMEN: Los efectos tóxicos en los tejidos normales, de los medicamentos contra el cáncer al igual que otras medicamentos podrían mejorar con el uso de plantas medicinales y hierbas. Este estudio investigó el efecto protector de Tribulus terrestris (TT) sobre la apoptosis de células germinales por citotoxicidad inducida por cisplatino en ratones machos. En este estudio se dividieron treinta ratones Balb/c macho aleatoriamente en 5 grupos (n = 6). Se administró una sola dosis de cisplatino (5,5 mg / kg) y diferentes concentraciones de Tribulus terrestris durante 14 días consecutivos. La reacción en cadena de la polimerasa de transcripción reversa de los genes relacionados con la apoptosis, se realizó con ARN extraído de los testículos de los ratones. El análisis estadístico se realizó usando ANOVA de una vía. En el grupo cisplatino, hubo un aumento significativo en la expresión de mRNA de p53 (P = 0,008), bax (P = 0,004) y la relación de bax / Bcl-2 (P = 0.000), mientras que hubo una disminución en la expresión de Bcl-2 (P = 0,003), en comparación con el grupo control. En los grupos Cis + TT, los datos mostraron que las diferentes concentraciones de TT podrían mejorar los efectos nocivos causados por el cisplatino. Los mejores efectos protectores se lograron en Cis + TT (300 mg / kg). Tribulus terrestris protege las células germinales testiculares contra la apoptosis inducida por cisplatino al afectar la regulación de los genes relacionados.

Study of the protective effect of dexamethasone on cisplatin-induced ototoxicity in rats

Abstract Purpose: To evaluate the ability of dexamethasone to protect against cisplatin (CDDP)-induced ototoxicity. Methods: Male Wistar rats were divided into the following three groups: 1) Control (C): 6 animals received intraperitoneal (IP) saline solution, 8 ml/kg/day for four days; 2) C + CDDP: 11 animals received 8 ml/kg/day of IP saline and, 90 min after saline administration, 8 mg/kg/day of IP CDDP for four days; and 3) DEXA15 + CDDP: 11 animals received IP dexamethasone 15 mg/kg/day and, 90 min after dexamethasone administration, received 8 mg/kg/day of IP CDDP for four days. Results: It was found that dexamethasone did not protect against weight loss in CDDP-exposed animals. The mortality rate was comparable with that previously reported in the literature. The auditory threshold of animals in the DEXA15 + CDDP group was not significantly altered after exposure to CDDP. The stria vascularis of animals in the DEXA15 + CDDP group was partially preserved after CDDP exposure. Conclusions: Dexamethasone at the dose of 15 mg/kg/day partially protected against CDDP-induced ototoxicity, based on functional evaluation by brainstem evoked response audiontry (BERA) and morphological evaluation by optical microscopy. However, dexamethasone did not protect against systemic toxicity.

Medidas de biossegurança na administração de quimioterapia antineoplásica: conhecimento dos enfermeiros / Biosafety measures in chemotherapy administration: nurses' knowledge / Medidas de bioseguridad en administración de quimioterapia: conocimiento de los enfermeiros

Introdução: A exposição ocupacional às propriedades citotóxicas da quimioterapia implica em riscos à saúde desses profissionais, podendo causar alterações agudas ou crônicas oriundas do manuseio dos agentes antineoplásicos em longo prazo. Objetivo: Identificar o conhecimento de enfermeiros a respeito das medidas de biossegurança para administração de quimioterapia. Método: Estudo descritivo transversal com enfermeiros de um hospital geral. A coleta de dados ocorreu por meio de questionário autoaplicado e os dados foram analisados através de medidas de tendência central, dispersão e correlações. Resultados: Trinta enfermeiros participaram do estudo e 23 deles informaram nunca ter recebido capacitação para trabalhar com quimioterápicos. O escore médio de conhecimento dos participantes foi 27,6 de um total possível de 37 pontos. Conclusão: Os enfermeiros da instituição pesquisada apresentam conhecimento parcialmente adequado às recomendações de biossegurança. A identificação de lacunas no conhecimento pode orientar o desenvolvimento de protocolos e programas de capacitação, aspecto fundamental atualmente, haja vista o elevado número de pacientes com câncer internados em unidades de clínica médica em hospitais gerais.

Introduction: Occupational exposure to the cytotoxic properties of chemotherapy entails risks to professionals' health and may cause acute or chronic changes arising from the long-term handling of antineoplastic agents. Objective: To identify the nurses' knowledge of the biosecurity measures for administering chemotherapy. Method: Cross-sectional descriptive study with nurses at a general hospital. The data were collected through a self-applied questionnaire and the data were analyzed using measures of central tendency, dispersion, and correlation. Results: Thirty nurses were enrolled in this study and 23 reported they had never received training on working with chemotherapy drugs. The average score of the subjects was 27.6 out of a possible 37 points. Conclusion: The nurses of the institution investigated have partially adequate knowledge of biosafety recommendations. Identifying gaps in knowledge can guide the development of protocols and training programs, a fundamental aspect, given the high number of cancer patients admitted to medical units in general hospitals.

Introducción: La exposición ocupacional a las propiedades citotóxicas de la quimioterapia implica riesgos para la salud de estos profesionales, puede causar cambios agudos o crónicos derivados de la manipulación de agentes antineoplásicos a largo plazo. Objetivo: Identificar los conocimientos de los enfermeros acerca de las medidas de bioseguridad para administración de la quimioterapia. Método: Estudio descriptivo transversal, con enfermeros de un hospital general. Los datos fueron recolectados a través cuestionario autoadministrado y se analizaron los datos utilizando medidas de tendencia central, dispersión y correlación. Resultados: Treinta enfermeros participaron en el estudio, 23 de ellos informaron que nunca recibieron capacitación para trabajar con agentes quimioterapéuticos. La puntuación media de los participantes fue de 27,6 de un máximo de 37 puntos. Conclusión: Los enfermeros de la institución investigada tienen conocimiento parcialmente adecuado a las recomendaciones de bioseguridad. La identificación de lagunas en el conocimiento puede guiar el desarrollo de protocolos y programas de formación, un aspecto fundamental en la actualidad visto teniendo en cuenta elevado número de pacientes con cáncer ingresados en unidades médicas en los hospitales generales.

Effects of thymoquinone against cisplatin-induced cardiac injury in rats

PURPOSE: T o investigate the possible protective effect of thymoquinone (TQ) in cisplatin (CP) induced myocardial injury. METHODS: A total of 28 adult male Wistar-Albino rats were randomly and equally divided into four groups as follows: Group 1 (control), Group 2 (CP at 15 mg/kg dose), Group 3 (TQ 40 mg/kg/day for two days prior to CP injection and on third day, CP at 15 mg/kg dose was intraperitoneally administered and TQ treatment continued until fifth day) and Group 4 (TQ at 40mg/kg/day dose for five days). RESULTS: There was a significant increment in CP group in terms of congestion, edema and pycnotic nuclei in myocardial fibers, comparing with other groups. TQ group exhibited significant increase in expression of antiapoptotic protein Bcl-2, comparing with CP group (p<0.05). In only CP administered group, expression of antiapoptotic protein Bcl-2 was lowest comparing with other groups. CONCLUSION: Established data indicate that cisplatin is cardiotoxic and thymoquinone may be useful in treating CP-induced cardiac injury.

Silencing of ABCG2 by MicroRNA-3163 Inhibits Multidrug Resistance in Retinoblastoma Cancer Stem Cells

To investigate the function and regulation mechanism of ATP-binding cassette, subfamily G, member 2 (ABCG2) in retinoblastoma cancer stem cells (RCSCs), a long-term culture of RCSCs from WERI-Rb1 cell line was successfully established based on the high expression level of ABCG2 on the surface of RCSCs. To further explore the molecular mechanism of ABCG2 on RCSCs, a microRNA that specifically targets ABCG2 was predicted. Subsequently, miR-3163 was selected and confirmed as the ABCG2-regulating microRNA. Overexpression of miR-3163 led to a significant decrease in ABCG2 expression. Additionally, ABCG2 loss-of-function induced anti-proliferation and apoptosis-promoting functions in RCSCs, and multidrug resistance to cisplatin, carboplatin, vincristine, doxorubicin, and etoposide was greatly improved in these cells. Our data suggest that miR-3163 has a significant impact on ABCG2 expression and can influence proliferation, apoptosis, and drug resistance in RCSCs. This work may provide new therapeutic targets for retinoblastoma.

Selenium protects cerebral cells by cisplatin induced neurotoxicity

PURPOSE: To evaluate the central nervous system toxicity of cisplatin and neuroprotective effect of selenium. METHODS: Twenty-one male Wistar albino rats were divided into three groups: control (C), cisplatin (CS), cisplatin and selenium (CSE, n=7 in each group). Cisplatin (12 mg/kg/day, i.p.) was administered to CS and CSE groups for three days. Furthermore, CSE group received 3mg/kg/day (twice-a-day as 1.5 mg/kg) selenium via oral gavage five days before cisplatin injection and continued for 11 consecutive days. The same volumes of saline were administered to C group intraperitoneally and orally at same time. RESULTS: Heterochromatic and vacuolated neurons and dilated capillary vessels in the brain were observed in the histochemical examinations of cisplatin treated group. Rats that were given a dose of 3mg/kg/day selenium decreased the cisplatin induced histopathological changes in the brain, indicating a protective effect. In addition, cytoplasmic staining of the cell for bcl-2, both cytoplasmic and nuclear staining for bax were determined to be positive in the all groups. Bax positive cells were increased in the CS group compared to C group, in contrast to decreased bcl-2 positivity. CONCLUSION: Selenium limited apototic activity and histological changes due to the cisplatin related central neurotoxicity. .

Protective effect of Tribulus terrestris hydroalcoholic extract against cisplatin­induced apoptosis on testis in mice / Efecto protector del extracto hidroalcohólico de Tribulus terrestris contra la apoptosis inducida por cisplatino sobre los testículos en ratones

Cisplatin is an anti-cancer drug used in chemotherapy. One of the limiting side effects of cisplatin is decreasing genital gland function, azoospermia and oligospermia. Tribulus terrestris (TT) has been used as an aphrodisiac. The present study amid to investigate protective effect of TT hydroalcoholic extract against cisplatin-induced apoptosis on testis in mice. Male adult mice (n=30) were divided into control and 4 experimental groups (n=6). Control group received saline, first experimental group received cisplatin (5.5 mg/kg) and other three experimental group received cisplatin (5.5 mg/kg) and different doses of hydroalcoholic extact of TT (100, 300 and 500 mg/kg/i.p) respectively. Day after the last injection, histopathology and histomorphic analysis and also TUNEL assay on mice testis were performed. Weights of body and testis, seminiferous tubules diameter and apoptotic index were assessed. Data analysis was performed using one-way ANOVA followed by Tukeys' test. The results showed that cisplatin lead to a reduction in the weight of body and testes, and significantly increased apoptotic index compared to the control group (P<0.001), while in treated groups with TT, the weights of body and testis and seminiferous tubules diameter were significantly higher compared with cisplatin group (P<0.001), but apoptotic index did not show significant differences. The study demonstrates that extract of TT could protective effect of on cisplatin-induced apoptosis of testis and seminiferous tubules diameter that may be related to the presence of antioxidant components acting via a multitude of central and peripheral mechanisms.

El cisplatino es un medicamento anticancerígeno utilizado en tratamientos de quimioterapia. Uno de los efectos secundarios que limitan el uso del cisplatino es la disminución en la función de la glándula genital, provocando azoospermia y oligospermia. El Tribulus terrestris (TT) se ha utilizado como un afrodisíaco. El objetivo fue investigar el efecto protector del extracto hidroalcohólico de TT contra la apoptosis inducida por el cisplatino en los testículos de ratones. Ratones machos adultos (n=30) fueron divididos en un grupo control y cuatro grupos experimentales (n=6). Al grupo control se le administró una solución salina, mientras que el primer grupo experimental recibió cisplatino (5,5 mg/kg) y los tres restantes recibieron cisplatino (5,5 mg/kg) con diferentes dosis del extracto hidroalcohólico de TT (100, 300 y 500 mg/kg/ip), respectivamente. El día posterior a la última inyección, se realizaron análisis histopatológicos y morfométricos, junto al ensayo TUNEL, de los testículos de los ratones. Se registró el peso corporal y testicular de cada ratón, así como el diámetro de los túbulos seminíferos e índice de apoptosis. Los datos fueron analizados mediante ANOVA de una vía, seguida de la prueba de Tukey. El cisplatino provocó una reducción del peso corporal y testicular, y un aumento del índice de apoptosis, que fue significativo en comparación con el grupo control (P<0,001), mientras que en los grupos tratados con TT, el peso corporal y testicular, junto al diámetro de los túbulos seminíferos fueron significativamente mayores en comparación con el grupo tratado con cisplatino (P<0,001), sin embargo, el índice de apoptosis no mostró diferencias significativas. El estudio demuestra que el extracto de TT podría poseer un efecto protector de la apoptosis inducida por cisplatino sobre los testículos, así como en el diámetro de los túbulos seminíferos, lo que podría relacionarse con la presencia de componentes antioxidantes que actúan a través de diversos mecanismos, centrales y periféricos.

Physicochemical Properties of a Methacrylate-Based Dental Adhesive Incorporated with Epigallocatechin-3-gallate

This study aimed to evaluate the influence of epigallocatechin-3-gallate (EGCG) incorporation on the physicochemical properties of a methacrylate-based dental adhesive. EGCG was added to Adper Easy One (3M-ESPE) except in control group, to obtain concentrations of 0.01% w/w and 0.1% w/w of EGCG-doped adhesives. For water sorption (WS) and solubility (SL) surveys, resin discs were assayed following ISO recommendations (n=10). The degree of conversion (DC) was analyzed by FTIR whereas flexural strength (FS) was tested by three-point bending with bar specimens (n=10). Data were subjected to one-way ANOVA and Tukey's test (p<0.05). No significant difference in the DC, WS and FS were found between the different concentrations of EGCG (p>0.05). Adhesives containing 0.1% or 0.01% of EGCC demonstrated similar values of SL (p>0.05) and higher than those found for adhesive without EGCC (p<0.05). In conclusion, the addition of EGCC to adhesive reduced the solubility without affecting the other evaluated properties.

Esse estudo teve como objetivo avaliar a influência da incorporação de epigalocatequina-3-galato (EGCG) nas propriedades físico-químicas de um sistema adesivo à base de metacrilato. O EGCG foi adicionado ao Adper Easy One (3M-ESPE), exceto para o grupo controle, para a obtenção das concentrações de 0,01% e 0,1% p/p. No ensaio de sorção (S) e solubilidade (SL), foram confeccionados discos de resina de acordo com as recomendações da ISO (n=10). O grau de conversão (GC) foi analisado através de FTIR, enquanto a resistência flexural (RF) foi avaliada em teste de flexão de três pontos com espécimes em forma de barra (n=10). Os dados foram submetidos à Análise de Variância a um critério e teste de Tukey (p<0,05). Não houve diferença significativa entre as concentrações de EGCG testadas no GC, SL e RF (p>0,05). Adesivos contendo EGCG a 0,1% ou 0,01% apresentaram valores similares de SL (p>0,05) e maiores do que os valores obtidos pelo adesivo não incorporado por EGCG. Conclui-se que a adição de EGCG ao adesivo reduziu a solubilidade sem afetar as outras propriedades avaliadas.