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Mobile phone use has increased rapidly. The central nervous system has been shown to be adversely affected by its electromagnetic field (EMF) resulting in headache and sleep disturbances. How the cells make up the CNS and are affected by EMF is unclear. However, because of their central role in inflammation through diverse stimuli including radiation, this study aimed to investigate the effects of electromagnetic fields induced by mobile phones on mast cells in rat dura mater. A total of 18 adult, female, SpragueDawley rats were divided into two groups. The choice of female rats for his study was based on recent surveys demonstrating that mobile phone use is more frequent and prolonged among females. The study group was exposed to 900 MHz electromagnetic field (1 h/day for 45 days). In the end of the study, duramater tissue was extracted and stained using Toluidine blue. Mast cells were counted and results were analysed using Student t test. Mean mast cell number was 202.33±9.82 and 456.78±35.01 in the control and study groups, respectively (p<0.05). Analysis of serum electrolyte and immunoglobulin E levels showed no statistically significant difference between the two groups (p>0.05). The study showed that mobile phone exposure increased mast cell number and degranulation in rat dura mater. Further studies are required to evaluate the clinical implications of these findings.
El uso del teléfono móvil ha aumentado rápidamente. Se ha demostrado que el sistema nervioso central (SNC) se ve afectado de manera adversa debido al campo electromagnético (CEM) que produce dolor de cabeza y trastornos del sueño. No está claro cómo se ve afectada la composición celular del SNC por el CEM. Sin embargo, debido a su función principal en la inflamación a través de diversos estímulos que incluyen la radiación, este estudio tuvo como objetivo investigar los efectos de los campos electromagnéticos inducidos por los teléfonos móviles en los mastocitos de la duramadre de ratas. Un total de 18 ratas Sprague-Dawley adultas, hembras, se dividieron en dos grupos. Se usaron ratas hembras para este estudio en base a investigaciones recientes que han demostrado que el uso de teléfonos móviles es más frecuente y prolongado en las mujeres. Los grupos de estudio fueron expuestos a un campo electromagnético de 900 MHz (1 h / día durante 45 días). Al término del estudio, fue extirpado el tejido de la duramadre y teñido con azul de toluidina. Se contaron los mastocitos y se analizaron los resultados utilizando la prueba t de Student. La cantidad media de células cebadas fue de 202,33 ± 9.82 y 456,78 ± 35,01 en los grupos control y estudio, respectivamente (p <0,05). El análisis del electrolito sérico y los niveles de inmunoglobulina E no mostraron diferencias estadísticamente significativas entre los dos grupos (p> 0,05). El estudio mostró que la exposición a teléfonos móviles aumentó el número de mastocitos y la desgranulación en la duramadre de las ratas. Se requieren estudios adicionales para evaluar las implicaciones clínicas de estos hallazgos.
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Animales , Ratas , Teléfono Celular , Duramadre/efectos de la radiación , Campos Electromagnéticos/efectos adversos , Mastocitos/efectos de la radiación , Ratas Sprague-DawleyRESUMEN
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+100mg whortleberry extract, cisplatin+200mg 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.
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Antocianinas/uso terapéutico , Antineoplásicos/toxicidad , Cisplatino/toxicidad , Cóclea/efectos de los fármacos , Audición/efectos de los fármacos , Sustancias Protectoras/uso terapéutico , Estimulación Acústica , Animales , Antioxidantes/uso terapéutico , Cóclea/patología , Masculino , Emisiones Otoacústicas Espontáneas/efectos de los fármacos , Estrés Oxidativo/efectos de los fármacos , Extractos Vegetales , Distribución Aleatoria , Ratas Wistar , Valores de Referencia , Reproducibilidad de los Resultados , Relación Señal-Ruido , Resultado del Tratamiento , Vaccinium myrtillusRESUMEN
PURPOSE: This study investigated the antioxidant effects of whortleberry against cisplatin-induced nephrotoxicity in rats. MATERIAL AND METHODS: This study included 48 female Sprague-Dawley rats weighing 263.68 ± 8.29 g. The rats were divided into the following six groups, with eight rats in each group: control, ethanol control, whortleberry control, cisplatin control, 16 mg/kg cisplatin +100 mg/kg whortleberry, and 16 mg/kg cisplatin +200 mg/kg whortleberry groups. Biochemical analysis was performed by measuring total oxidant status and total antioxidant status, histopathological analysis was performed by calculating proximal and distal tubule areas (µm2), and immunohistochemical analysis was performed by determining anti-Caspase-3 immunostaining. Differences among the groups were examined using one-way analysis of variance, and p < .05 was considered statistically significant. RESULTS: Cisplatin treatment decreased the total antioxidant status and increased the total oxidant status and Caspase-3 level. Moreover, it resulted in the dilatation, vacuolization and loss of tubular epithelial cells; and glomerular degeneration and edema in the kidney tissues (p < .05). Treatment with 100 and 200 mg whortleberries increased the total antioxidant status; decreased the total oxidant status and Caspase-3 level and ameliorated distal and proximal tubule degeneration, glomerular degeneration and edema in the kidney tissues (p < .05). CONCLUSIONS: Our results indicate that the antioxidant effects of the whortleberry decrease cisplatin-associated nephrotoxicity.
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Lesión Renal Aguda/inducido químicamente , Lesión Renal Aguda/prevención & control , Cisplatino/toxicidad , Extractos Vegetales/farmacología , Vaccinium myrtillus/química , Lesión Renal Aguda/patología , Animales , Antineoplásicos/toxicidad , Antioxidantes/metabolismo , Femenino , Riñón/patología , Estrés Oxidativo/efectos de los fármacos , Ratas , Ratas Sprague-DawleyRESUMEN
BACKGROUND: Methotrexate (MTX), a folate antagonist, is commonly used in the treatment of many different types of cancer and inflammatory diseases, including pancreatic cancer, although its side effects on the pancreas have not yet been researched. The mechanism of MTX-induced toxicity is not well known, and it has been reported in high-dose toxicity studies that the pancreas is sensitive to toxic effects. OBJECTIVES: The aim of our study was to determine whether adalimumab (ADA) has a preventive effect on MTX-induced pancreas toxicity in rats. MATERIAL AND METHODS: The rats were equally and randomly divided into 3 groups (Group 1 comprised the healthy controls, Group 2 was the MTX group, and Group 3 was the MTX + ADA group). The rats in Groups 2 and 3 received an intraperitoneal (ip.) single-dose injection of MTX (20 mg/kg). A single dose of 5 mg/kg ADA (REMICADE®) was administered ip. to Group 3. All the rats were sacrificed under anesthesia 5 days after receiving the MTX injection. RESULTS: Significantly higher mean edema, necrotic cell, and inflammatory scores were recorded in Groups 2 and 3 compared to those recorded in Group 1. Significantly decreased edema, number of necrotic cells, and inflammatory scores were noted in Group 3 than in Group 2. A decrease in islets of Langerhans cell insulin and somatostatin-positive interneurons was demonstrated after the administration of MTX. An increase in insulin and somatostatin-positive cells in islets of Langerhans, as well as a remodeling of the structure of the pancreas, was shown following treatment with ADA. CONCLUSIONS: Adalimumab was demonstrated to have a protective effect against MTX-induced pancreatic injury in this study.
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Adalimumab/farmacología , Antiinflamatorios/farmacología , Antineoplásicos/toxicidad , Metotrexato/toxicidad , Páncreas/efectos de los fármacos , Animales , Efectos Colaterales y Reacciones Adversas Relacionados con Medicamentos/prevención & control , Masculino , Distribución Aleatoria , Ratas , Ratas Sprague-Dawley , Factor de Necrosis Tumoral alfa/antagonistas & inhibidoresRESUMEN
BACKGROUND: Topiramate (TPM) decreases cytokine release and generation of reactive oxygen species (ROS). Cytokine and endothelin-1 (ET-1) secretion and ROS formation play an important role in ischemia-reperfusion (I/R) injury. We aimed to evaluate whether TPM prevents damage occurring in lung tissue during I/R. MATERIALS AND METHODS: A total of 27 Wistar albino rats were divided into three groups of nine. To the I/R group, two hours of ischemia via infrarenal abdominal aorta cross-ligation and then two hours of reperfusion process were applied. TPM (100 mg/kg/day) orally for seven days was administered in the TPM treatment group. After the last dose of TPM treatment, respectively, two hours of ischemia and two hours of reperfusion were applied in this group. RESULTS: Tumor necrosis factor-alpha (TNF-α) (p < 0.05), malondialdehyde (MDA) (p < 0.05), myeloperoxidase (MPO) (p < 0.05) and ET-1 (p < 0.05) levels of TPM treatment group's lung tissue were significantly lower than for the I/R group. Caspase-3 and histopathological damage were rather lower than that of the I/R group. CONCLUSIONS: During I/R, lung damage occurs due to excessive TNF-α and ET-1 release and ROS generation. TPM could well reduce development of lung damage by decreasing cytokine and ET-1 release and levels of ROS produced.
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Lesión Pulmonar/tratamiento farmacológico , Daño por Reperfusión/tratamiento farmacológico , Topiramato/farmacología , Animales , Aorta Abdominal , Biomarcadores/sangre , Caspasa 3/sangre , Ligadura , Masculino , Malondialdehído/sangre , Peroxidasa/sangre , Ratas , Ratas Wistar , Factor de Necrosis Tumoral alfa/sangreRESUMEN
OBJECTIVE: Sciatic nerve neuropathy can be observed following intramuscular gluteal injections. The histopathological examination of sciatic nerve damage following intramuscular injection in the gluteal region for acute pain treatment is not feasible in humans due to the inability to dissect and examine the nerve tissue. To overcome this issue, we used a rat model for demonstrating damage to the sciatic nerve tissue after the application of commonly used drug injections. METHODS: We investigated possible damage following the intramuscular injection of diclofenac, lornoxicam, morphine, and pethidine in a rat model based on histopathological characteristics such as myelin degeneration, axon degeneration, epineurium degeneration, fibrosis, epineurium thickening, perineurium thickening, lymphocyte infiltration, vacuolization, and edema. RESULTS: All the analgesic drugs used in our study induced histopathological changes in the sciatic nerve. Anti-S100 positivity, showing nerve damage, was found to be the lowest in the group treated with diclofenac. Neurotoxic effects of diclofenac on the sciatic nerve were greater than those of the other drugs used in the study. Lornoxicam induced the least histopathological changes in the nerve. CONCLUSION: Diclofenac induced severe nerve damage not only after direct injection in the sciatic nerve but also after injection in the area around the nerve. Thus, we recommend restricting the use of intramuscular gluteal injections of diclofenac. Intramuscular use of morphine and pethidine should also be overviewed.
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We explored the effects of topical curcumin on the healing of nasal mucosal wounds. A total of 32 Sprague-Dawley Albino rats were randomized in equal numbers into four groups, and unilateral nasal wounds were created using an interdental brush. Group 1 (the sham-control group) contained untreated rats with traumatized right-side nasal cavities; Group 2 and 3 rats were similarly traumatized and treated with topical curcumin (5 and 10 mg/mL) dissolved in dimethyl sulfoxide daily for 7 days after trauma; Group 4 rats were treated with topical dimethyl sulfoxide only. All rats were decapitated on day 15 and the healing sites evaluated by blinded observers in terms of the presence of cellular hyperplasia, goblet cell hypertrophy and degeneration, leucocytic infiltration, ciliary loss and degeneration, edema, and vascular dilation. On histopathological evaluation, all of cellular hyperplasia, leukocytic infiltration, and edema were significantly reduced in Group 3 compared with Group 1 (p = 0.001, p = 0.004, and p = 0.008, resp.). Thus, curcumin reduced the inflammatory response and significantly accelerated wound healing.
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INTRODUCTION: The use of mobile phones has become widespread in recent years. Although beneficial from the communication viewpoint, the electromagnetic fields generated by mobile phones may cause unwanted biological changes in the human body. OBJECTIVE: In this study, we aimed to evaluate the effects of 2100MHz Global System for Mobile communication (GSM-like) electromagnetic field, generated by an electromagnetic fields generator, on the auditory system of rats by using electrophysiological, histopathologic and immunohistochemical methods. METHODS: Fourteen adult Wistar albino rats were included in the study. The rats were divided randomly into two groups of seven rats each. The study group was exposed continuously for 30days to a 2100MHz electromagnetic fields with a signal level (power) of 5.4dBm (3.47mW) to simulate the talk mode on a mobile phone. The control group was not exposed to the aforementioned electromagnetic fields. After 30days, the Auditory Brainstem Responses of both groups were recorded and the rats were sacrificed. The cochlear nuclei were evaluated by histopathologic and immunohistochemical methods. RESULTS: The Auditory Brainstem Responses records of the two groups did not differ significantly. The histopathologic analysis showed increased degeneration signs in the study group (p=0.007). In addition, immunohistochemical analysis revealed increased apoptotic index in the study group compared to that in the control group (p=0.002). CONCLUSION: The results support that long-term exposure to a GSM-like 2100MHz electromagnetic fields causes an increase in neuronal degeneration and apoptosis in the auditory system.
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Teléfono Celular , Núcleo Coclear/efectos de la radiación , Campos Electromagnéticos/efectos adversos , Audición/efectos de la radiación , Exposición a la Radiación/efectos adversos , Ondas de Radio/efectos adversos , Animales , Apoptosis/efectos de la radiación , Núcleo Coclear/patología , Potenciales Evocados Auditivos del Tronco Encefálico/efectos de la radiación , Inmunohistoquímica , Masculino , Degeneración Nerviosa/etiología , Ratas Wistar , Valores de Referencia , Factores de Riesgo , Factores de TiempoRESUMEN
OBJECTIVES: We investigated the histopathological effects of metamizole sodium (MS) on the sciatic nerve. MATERIALS AND METHODS: This study was performed using 48 adult male Wistar albino rats. Ten groups were constituted with 6 rats in each group. MS injection into the sciatic nerve (group 1), MS injection into the muscle [group 3 (50 mg/kg, 0.4 ml) and group 5 (50 mg/kg, 0.8 ml)], MS injection into the muscle cavity in the vicinity of the sciatic nerve [group 2 (50 mg/kg, 0.4 ml) and group 4 (50 mg/kg, 0.8 ml)], normal saline injection into the muscle in the vicinity of the sciatic nerve [group 6A (0.4 ml) and 6B (0.8 ml)], subjected to injury by drilling the entire layer of nerve without injecting any drug, normal saline injection in the sciatic nerve, and control group. Nerve and muscle samples were taken 7 days after administrations. Tissue sections were stained using a hematoxylin and eosin-Luxol® fast blue stain, assessed by a histologist. RESULTS: The levels of axonal degeneration of the rats in groups 1, 2, 3, 4, 5, 6A, and 8 were found to be significantly higher compared to the levels of the rats in the control group (P<0.05). Myelin degeneration of the rats in all groups was found to be significantly higher compared to myelin degeneration of the rats in the control group (P<0.05). CONCLUSION: It was observed that MS could lead to injury in the sciatic nerve with a toxic effect due to diffusion.
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BACKGROUND: Cisplatin (Cis) is one of the most commonly used antineoplastic drugs. It is used as chemotherapy for many solid organ malignancies such as brain, neck, male and female urogenital, vesical and pulmonary cancers. Infliximab blocks tumor necrosis factor alpha (TNF-α). Several studies have reported that infliximab ameliorates cell damage by reducing cytokine levels. AIMS: We aimed to investigate whether infliximab has a preventive effect against cisplatin-induced hepatotoxicity and whether it has a synergistic effect when combined with Cis. STUDY DESIGN: Animal experimentation. METHODS: Male Wistar albino rats were divided in three groups as follows: Cis group, infliximab + Cis (CIN) group and the control group. Each group comprised 10 animals. Animals in the Cis group received an intraperitoneal single-dose injection of Cis (7 mg/kg). In the CIN group, a single dose of infliximab (7 mg/kg) was administered 72 h prior to the Cis injection. After 72 h, a single dose of Cis (7 mg/kg) was administered. All rats were sacrificed five days after Cis injection. RESULTS: TNF-α levels in the Cis group were significantly higher (345.5±40.0 pg/mg protein) than those of the control (278.7±62.1 pg/mg protein, p=0.003) and CIN groups (239.0±64.2 pg/mg protein, p=0.013). The Cis group was found to have high carbonic anhydrase (CA)-II and low carbamoyl phosphate synthetase-1 (CPS-1) levels. Aspartate transaminase (AST) and alanine transaminase (ALT) levels were lower in the CIN group as compared to the Cis group. Total histological damage was greater in the Cis group as compared to the control and CIN groups. CONCLUSION: Cis may lead to liver damage by increasing cytokine levels. It may increase oxidative stress-induced tissue damage by increasing carbonic anhydrase II (CA-II) enzyme levels and decreasing CPS-1 enzyme levels. Infliximab decreases Cis-induced hepatic damage by blocking TNF-α and it may also protect against liver damage by regulating CPS-1 and CA-II enzyme levels.
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BACKGROUND: Adalimumab (ADA) is a potent inhibitor of tumor necrosis factor (TNF-α). ADA treatment suppresses proinflammatory cytokines, leading to a decrease or inhibition of the inflammatory process. OBJECTIVES: The aim of this study was to investigate the possible protective effects of ADA on oxidative stress and cellular damage on rat kidney tissue after ischemia/reperfusion (I/R). MATERIAL AND METHODS: A total of 30 male Wistar albino rats were divided into three groups: control, I/R, and I/R plus ADA (I/R + ADA); each group comprised 10 animals. The control group underwent laparotomy without I/R injury. After undergoing laparotomy, I/R groups underwent two hours of infrarenal abdominal aortic cross ligation, which was followed by two hours of reperfusion. ADA (50 mg/kg) was administered as a single dose, intraperitoneally, to the I/R + ADA group, 5 days before I/R. RESULTS: The I/R group's TNF-α (1150.9 ± 145.6 pg/mg protein), IL-1ß (287.0 ± 32.4 pg/mg protein) and IL-6 (1085.6 ± 56.7 pg/mg protein) levels were significantly higher than those of the control (916.1 ± 88.7 pg/mg protein, p = 0.003; 187.5 ± 37.2 pg/mg protein, p < 0.001; 881.4 ± 57.1 pg/mg protein, p < 0.001, respectively) and I/R + ADA groups (864.2 ± 169.4 pg/mg protein, p = 0.003; 241.4 ± 33.4 pg/mg protein, p = 0.010; 987.7 ± 66.5 pg/mg protein, p = 0.004, respectively). To date, a few histopathological changes have been reported regarding renal I/R injury in rats due to ADA treatment whereas I/R caused severe histopathological injury to kidney tissue. CONCLUSIONS: ADA treatment significantly attenuated the severity of kidney I/R injury, inhibiting I/R-induced oxidative stress and renal damage. Because of its anti-inflammatory and antioxidant effects, ADA pretreatment may have protective effects on experimental kidney injury.
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Lesión Renal Aguda/prevención & control , Adalimumab/farmacología , Antiinflamatorios/farmacología , Antioxidantes/farmacología , Aorta Abdominal/cirugía , Riñón/efectos de los fármacos , Daño por Reperfusión/prevención & control , Lesión Renal Aguda/etiología , Lesión Renal Aguda/metabolismo , Lesión Renal Aguda/patología , Animales , Apoptosis/efectos de los fármacos , Anhidrasa Carbónica II/metabolismo , Constricción , Citoprotección , Modelos Animales de Enfermedad , Mediadores de Inflamación/metabolismo , Interleucina-6/metabolismo , Riñón/metabolismo , Masculino , Estrés Oxidativo/efectos de los fármacos , Ratas Wistar , Daño por Reperfusión/etiología , Daño por Reperfusión/metabolismo , Daño por Reperfusión/patología , Factor de Necrosis Tumoral alfa/antagonistas & inhibidores , Factor de Necrosis Tumoral alfa/metabolismoRESUMEN
OBJECTIVES: Carbon tetrachloride (CCl4) causes pulmonary toxicity. Infliximab (Ib) is a potent inhibitor of tumor necrosis factor-alpha (TNF-α). We aimed to investigate whether Ib has a protective effect on CCl4 induced lung injury. MATERIALS AND METHODS: Rats were divided into control, CCl4, and CCl4+Ib groups. A single dose of 2 ml/kg CCI4 was administered to CCI4 group and a single dose of 7 mg/kg Ib was given to CCl4+Ib group 24 hr before applying CCI4. RESULTS: TNF-α, malondialdehyde (MDA), nitric oxide (NO) and caspase-3 levels of the CCl4 group were markedly higher than both the control and CCl4+Ib groups. The CCI4+Ib group had lower histopathological injury than the CCl4 group. CONCLUSION: Ib as a strong TNF-α blocker decreases the production of proinflammatory cytokines, MDA, and oxidative stress leading to a protective effect against CCl4 induced lung tissue injury.
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PURPOSE: To investigate the effects of preoperative rectal ozone insufflation on surgical wound healing over the proinflammatory cytokines and histopathological changes. METHODS: Twenty one rabbits were divided into 3 groups. Sham, surgical wound, and ozone applied (6 sessions, every other day 70 µg/mL in 12 mL O2-O3 mixture rectally) surgical wound groups were created. TNF-alpha and IL-6 levels from all rabbits were studied at the basal, 24th hour, and 72nd hour. The histopathological examination was done by removing the surgical scar tissue at the end of 72nd hour. RESULTS: TNF-alfa and IL-6 levels were significantly lower compared to the control group, in the rabbits treated with ozone. The increase in angiogenesis, the decrease in the number of inflammatory cells, epidermal and dermal regeneration, better collagen deposition, and increased keratinisation in stratum corneum were observed in the histopathological examination. It was determined that the wound healing noticeably accelerated in the ozone group. CONCLUSION: Preoperative rectal ozone insufflation had a positive effect on surgical wound healing in acute period.
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Interleucina-6/metabolismo , Ozono/farmacología , Herida Quirúrgica/tratamiento farmacológico , Factor de Necrosis Tumoral alfa/metabolismo , Cicatrización de Heridas/efectos de los fármacos , Animales , Antiinflamatorios/uso terapéutico , Tejido de Granulación/patología , Insuflación/métodos , Ozono/administración & dosificación , Cuidados Preoperatorios/métodos , Conejos , Herida Quirúrgica/patología , Resultado del TratamientoRESUMEN
The aim of this study was to investigate the possible protective effects of infliximab on expression of laminin, anti-TNF, and NFκB in the rat hepatic cells after ischemia/reperfusion (I/R). A total of 30 male Wistar albino rats were divided into three groups: Control (C), sham I/R (ISC), and I/R+ infliximab (ISC inf); each group comprised 10 animals. C group animals underwent laparotomy without I/R injury. In ISC groups after undergoing laparotomy, 1 hour of superior mesenteric artery ligation was done, which was followed by 1 hour of reperfusion. In the ISC inf group, 3 days before I/R, infliximab (3 mg/kg) was administered intravenously. All animals were killed at the end of reperfusion and hepatic tissue samples were obtained for histopathological and histochemical investigations in all groups. Laminin, anti-TNF, and NFκB immunoreactivity were performed for all groups. ISC caused severe histopathological injury including mucosal erosions, inflammatory cell infiltration, necrosis, hemorrhage, and villous congestion. Infliximab treatment significantly attenuated the severity of intestinal I/R injury and it is shown by laminin, anti-TNF, and NFκB immunoreactivity. Because of its anti-inflammatory and antioxidant effects, infliximab pretreatment may have protective effects on hepatic cells in the experimental intestinal I/R model of rats.
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PURPOSE: To investigated the effects of exposure to an 1800 MHz electromagnetic field (EMF) on bone development during the prenatal period in rats. METHODS: Pregnant rats in the experimental group were exposed to radiation for six, 12, and 24 hours daily for 20 days. No radiation was given to the pregnant rats in the control group. We distributed the newborn rats into four groups according to prenatal EMF exposure as follows: Group 1 was not exposed to EMF; groups 2, 3, and 4 were exposed to EMF for six, 12, and 24 hours a day, respectively. The rats were evaluated at the end of the 60th day following birth. RESULTS: Increasing the duration of EMF exposure during the prenatal period resulted in a significant reduction of resting cartilage levels and a significant increase in the number of apoptotic chondrocytes and myocytes. There was also a reduction in calcineurin activities in both bone and muscle tissues. We observed that the development of the femur, tibia, and ulna were negatively affected, especially with a daily EMF exposure of 24 hours. CONCLUSION: Bone and muscle tissue development was negatively affected due to prenatal exposure to 1800 MHz radiofrequency electromagnetic field.
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Desarrollo Óseo/efectos de la radiación , Calcineurina/metabolismo , Campos Electromagnéticos/efectos adversos , Efectos Tardíos de la Exposición Prenatal/patología , Animales , Apoptosis/efectos de la radiación , Cartílago/patología , Condrocitos/metabolismo , Condrocitos/patología , Femenino , Cabeza Femoral/patología , Humanos , Recién Nacido , Masculino , Modelos Animales , Embarazo , Músculo Cuádriceps/metabolismo , Músculo Cuádriceps/patología , Ratas Sprague-Dawley , Factores de TiempoRESUMEN
PURPOSE: To investigated the effects of exposure to an 1800 MHz electromagnetic field (EMF) on bone development during the prenatal period in rats. METHODS: Pregnant rats in the experimental group were exposed to radiation for six, 12, and 24 hours daily for 20 days. No radiation was given to the pregnant rats in the control group. We distributed the newborn rats into four groups according to prenatal EMF exposure as follows: Group 1 was not exposed to EMF; groups 2, 3, and 4 were exposed to EMF for six, 12, and 24 hours a day, respectively. The rats were evaluated at the end of the 60th day following birth. RESULTS: Increasing the duration of EMF exposure during the prenatal period resulted in a significant reduction of resting cartilage levels and a significant increase in the number of apoptotic chondrocytes and myocytes. There was also a reduction in calcineurin activities in both bone and muscle tissues. We observed that the development of the femur, tibia, and ulna were negatively affected, especially with a daily EMF exposure of 24 hours. CONCLUSION: Bone and muscle tissue development was negatively affected due to prenatal exposure to 1800 MHz radiofrequency electromagnetic field.
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Humanos , Animales , Masculino , Femenino , Recién Nacido , Efectos Tardíos de la Exposición Prenatal/patología , Desarrollo Óseo/efectos de la radiación , Calcineurina/metabolismo , Campos Electromagnéticos/efectos adversos , Factores de Tiempo , Embarazo , Cartílago/patología , Ratas Sprague-Dawley , Apoptosis/efectos de la radiación , Condrocitos/metabolismo , Condrocitos/patología , Modelos Animales , Músculo Cuádriceps/metabolismo , Músculo Cuádriceps/patología , Cabeza Femoral/patologíaRESUMEN
AIM: To evaluate the antioxidant effects of thymoquinone (TQ) and to investigate the biochemical, histopathological and immunohistochemical changes in experimental rat ovarian torsion. METHODS: A total of 48 female adult rats were used in this study and randomly divided into 7 groups: (1) sham operation; (2) bilateral 3-hour ovarian ischemia; (3) 3-hour ischemia and 3-hour reperfusion; (4) and (5) rats were administered 20 and 40 mg/kg of TQ, respectively, before 0.5 h of ischemia, and then 3 h of ovarian ischemia was applied; (6) and (7) 3-hour ovarian ischemia was applied; 2.5 h after the induction of ischemia, rats were administered the same doses of TQ; at the end of 3 h of ischemia, a 3-hour reperfusion was applied. Histologic changes under light microscopy, immunoreactivity for anticaspase-3 and serum levels of malondialdehyde, interleukin-6, catalase and glutathione peroxidase were noted and compared between the 7 groups. RESULTS: Ischemia and ischemia/reperfusion cause a deterioration of biochemical and histopathological parameters. Administration of TQ seems to reverse these alterations and alleviate the injury. Antioxidant defense mechanisms appear to be enhanced by the administration of TQ. CONCLUSION: TQ at different doses attenuates ovarian ischemia and ischemia/reperfusion injury in rats.
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Benzoquinonas/farmacología , Isquemia/terapia , Enfermedades del Ovario/terapia , Daño por Reperfusión/terapia , Animales , Benzoquinonas/administración & dosificación , Modelos Animales de Enfermedad , Femenino , Isquemia/prevención & control , Enfermedades del Ovario/prevención & control , Ratas , Ratas Wistar , Daño por Reperfusión/prevención & controlRESUMEN
Mobile phones are extensively used throughout the world. There is a growing concern about the possible public health hazards posed by electromagnetic radiation emitted from mobile phones. Potential health risk applies particularly to the most intensive mobile phone users-typically, young people. The aim of this study was to investigate the effects of mobile phone exposure to the testes, by assessing the histopathological and biochemical changes in the testicular germ cells of rats during pubertal development. A total of 12 male Sprague Dawley rats were used. The study group (n = 6) was exposed to a mobile phone for 1 h a day for 45 days, while the control group (n = 6) remained unexposed. The testes were processed with routine paraffin histology and sectioned. They were stained with hematoxylin-eosin, caspase 3, and Ki-67 and then photographed. No changes were observed between the groups (p > 0.05). The interstitial connective tissue and cells of the exposed group were of normal morphology. No abnormalities in the histological appearance of the seminiferous tubules, including the spermatogenic cycle stage, were observed. Our study demonstrated that mobile phones with a low specific absorption rate have no harmful effects on pubertal rat testicles.
Asunto(s)
Teléfono Celular , Radiación Electromagnética , Túbulos Seminíferos/efectos de la radiación , Maduración Sexual/efectos de la radiación , Animales , Masculino , Ratas , Ratas Sprague-Dawley , Espermatogénesis/efectos de la radiaciónRESUMEN
Introducción: El metotrexato (MTX) se emplea para tratar el cáncer, varias formas de artritis y otras patologías reumáticas, pero puede causar toxicidad pulmonar debido a la producción de radicales libres del oxígeno y varias citocinas. Infliximab (IB) es un potente inhibidor del factor de necrosis tumoral-alfa (TNF-alfa) e inhibe también la liberación de endotelina-1 (ET-1). Nos propusimos investigar si IB reduce el daño pulmonar inducido por una sobredosis de MTX. Método: Las ratas se dividieron en 3 grupos de 8 animales. Al grupo control solamente se le administró solución salina. Al grupo MTX se le administró una dosis intraperitoneal de 20 mg/kg de MTX. Al grupo de MTX + IB (MI) se le administraron 7 mg/kg de IB. Tres días después de la administración de IB se administraron 20mg/kg de MTX. Todas las ratas se sacrificaron 5días después de la administración de MTX. Resultados: Las concentraciones de TNF-alfa, ET-1, malondialdehído (MDA), mieloperoxidasa (MPO) y caspasa-3 fueron significativamente más altas en el grupo MTX que en el grupo control: TNF-alfa (p < 0,001), ET-1 (p < 0,001), MDA (p < 0,001), MPO (p < 0,001) y caspasa-3 (p < 0,001) y en el grupo MI: TNF-alfa (p < 0,009), ET-1 (p < 0,001), MDA (p < 0,047), MPO (p < 0,007) y caspasa-3 (p < 0,003). El grupo MI mostró menos daño histopatológico en el tejido pulmonar que en el grupo MTX. Conclusión: La sobredosis de MTX induce la liberación de citocinas y la formación de especies reactivas de oxígeno, además de una mayor secreción de ET-1 que provoca daño pulmonar. IB es un agente proinflamatorio potente, bloquea el TNF-alfa, puede reducir la liberación de ET-1 y el estrés oxidativo y mostrar importantes efectos protectores del tejido pulmonar frente al daño causado por una sobredosis de MTX
Introduction: Methotrexate (MTX) is used to treat cancers, several forms of arthritis and other rheumatic conditions, although MTX may cause pulmonary toxicity related to the production of free oxygen radicals, various cytokines. Infliximab (IB) with its potent effect on tumor necrosis factor-alpha (TNF-alfa) inhibition also inhibits the release of endothelin-1 (ET-1). We aimed to investigate whether IB reduces pulmonary damage induced by an overdose of MTX. Method: The rats were divided into 3 groups of 8 animals. The control group was given only saline. One dose of 20 mg/kg MTX intraperitoneal was administered in the MTX group. IB 7 mg/kg was given to the MTX + IB (MI) group. Three days after IB was administered, 20 mg/kg MTX was given. Five days after MTX was administered, all rats were sacrificed. Results: The TNF-α, ET-1, malondialdehyde (MDA), myeloperoxidase (MPO) and caspase-3 levels in MTX group were significantly higher than in control groups of TNF- alfa (P = .001), ET-1 (P = .001), MDA (P = .001), MPO (P = .001) and caspase-3 levels (P = .001) and MI groups of TNF-alfa (P=.009), ET-1 (P = .001), MDA (P = .047), MPO (P = .007) and caspase-3 levels (P = .003). The MI group had less histopathological damage in lung tissue than the MTX group. Conclusion: Overdose of MTX leads to cytokine release and the formation of reactive oxygen species in addition to increased ET-1 secretion release that causes lung damage. IB, as a potent proinflammatory agent, TNF-alfa blocker, can decrease ET-1 release and oxidative stress, it may show significant protective effects in lung tissue against damage caused by MTX overdose
Asunto(s)
Animales , Ratas , Efectos Colaterales y Reacciones Adversas Relacionados con Medicamentos/prevención & control , Factor de Necrosis Tumoral alfa/antagonistas & inhibidores , Anticuerpos Monoclonales/farmacocinética , Metotrexato/efectos adversos , Modelos Animales de Enfermedad , Sustancias Protectoras/farmacocinética , Endotelinas , Sobredosis de Droga/complicacionesRESUMEN
OBJECTIVES: Electromagnetic radiation (ER) emitted from cell phones may exert a detrimental influence on human health and may affect the man reproductive system. We aimed to study the biological and morphological effects on the testes of 60-day-old male rats after ER exposure (900 MHz), which was applied continuously throughout embryogenesis. METHODS: A total of six pregnant Sprague Dawley rats were included in the study. Three pregnant rats (experimental group) were exposed to radiation from a cell phone set to talking mode for 24 hours a day for 20 days, and the other 3 pregnant rats (control group) were not to exposed to radiation. Newborn male rats were included from the experimental group (n=7) and the control group (n=7). At the end of 60 days, the rats' testes were excised, and testis length, width, depth, and weight were measured. Histopathological examinations were compared and serum testosterone (T) levels were assayed biochemically. RESULTS: : While serum T level (3.51±0.21 ng/ml) of ER Exposed group was significantly lower than the control group (4.04±0.47 ng/ml, p = 0.018), Caspase-3 enzyme activity (2.00±0.88) was significantly higher than the control group control (1.00±0.63, p = 0.026). Johnsen score (8.4±0.5) of ER group was fairly lower than the control group (9.4±0.5, p= 0.010). CONCLUSION: Our study demonstrated that ER exposure throughout embryogenesis may cause reductions in serum total T levels and in the size and weight of the testes of male rats, while causing modest increase in apoptosis
OBJETIVOS: La radiación electromagné- tica (RE) emitida por los teléfonos móviles puede tener una influencia deletérea sobre la salud en humanos y puede afectar al sistema reproductor masculino. Buscamos estudiar los efectos biológicos y morfológicos en los testículo de ratas macho de 60 días de edad después de la exposición continua a RE (900 MHz) aplicada continuamente durante el periodo embrionario. MÉTODOS: En el estudio se incluyeron un total de seis ratas Sprague Dawley embarazadas. Tres ratas embarazadas (Grupo experimental) fueron expuestas a la radiación de un teléfono móvil en modo conversación las 24 horas diarias durante 20 días, y las otras tres (grupo control) no fueron expuestas a radiación. Fueron incluidas las ratas macho nacidas del grupo experimental (n=7) y del grupo control (n=7). Al final de los 60 días se extirparon los testículos de las ratas y se midieron la longitud, anchura, profundidad y peso testiculares. Se compararon las valoraciones histopatológicas y se detectaron bioquímicamente los niveles de testosterona sérica. RESULTADOS: Mientras que los niveles de testosterona sérica del grupo expuesto a RE (3,51±0,21ng/ml) eran significativamente menores que los del grupo control (4,04±0,47 ng/ml, p = 0,018), la actividad de la enzima Caspasa 3 era significativamente superior a la del grupo control (1,00±0,63, p = 0,026). El score de Johnsen del grupo de RE (8,4±0,5) fue bastante más bajo que el del grupo control (9,4±0,5, p= 0,010). CONCLUSIONS: Nuestro estudio demostró que la exposición a RE durante la embriogénesis puede provocar reducción de los niveles séricos de Testosterona total y del tamaño y peso de los testículos de las ratas macho, causando a la vez un aumento modesto de la apoptosis