Pollution characteristics, source analysis, and risk assessment of metal and metalloid in PM2.5 of Shijiazhuang city / 中华预防医学杂志

In 2020, the mass concentration of PM2.5 in Shijiazhuang urban area was(80.30±71.43)μg/m3. The Spearman correlation analysis between metals and metalloids showed that Sb with Cd, Pb, Ni, Se, Cd with Pb, Ni, Se, Pb with Ni, Se, Ni with Se, and Se with Tl were positively correlated, with a coefficient greater than 0.5. The main sources of metals and metalloids of PM2.5 were traffic emissions, fuel combustion, metal smelting and dust. The HQ values of Pb, Hg and Mn for each population were less than 1, with lower non-carcinogenic risk. The R values of carcinogenic risk of Ni and Cd in each population were less than 1×10-6, which could be acceptable risk level for the population. The R values of carcinogenic risk of As and Cr in different populations were between 1×10-6 and 1×10-4, with potential carcinogenic risk, particularly higher in adult males.

Mecanismo carcinogénico asociado a la exposición al Bisfenol A / Carcinogenic mechanism associated of Bisphenol A exposure

Resumen Introducción: El Bisfenol A (BPA) es un producto químico al que los seres humanos están expuestos ampliamente por la vía oral, inhalación y transdérmica. Justificación: Dada la importancia de la patología oncológica que puede estar asociada a exposición a este químico, resulta imprescindible comprender mejor sus posibles mecanismos de acción asociados a carcinogénesis. Objetivo General: Investigar el mecanismo carcinogénico asociado a la exposición a BPA. Resultados: Aunque la mayoría de las investigaciones se han orientado hacia el efecto disruptor endocrino, con la limitante que los estudios in vivo son realizados en animales, existen estudios recientes que muestran su posible efecto carcinogénico en tejidos humanos. Sin embargo, se requiere más investigación sobre el papel del BPA de dosis baja (como ocurre en condiciones ambientales normales) y su efecto en la regulación de los cambios globales de expresión génica y las alteraciones epigenéticas en las células, que permitan establecer vínculos con carcinogénesis; esta revisión demuestra que los estudios realizados hasta la fecha señalan varios factores que pueden estar involucrados, como efectos mutagénicos que incluyen cambios en la transcripción génica y enzimáticos que promueven la proliferación celular limitando la apoptosis y favorecen la angiogénesis y migración de células tumorales. Conclusión: Si bien en la actualidad se reconoce que la célula cancerígena adquiere características patológicas que le ayudan a sobrevivir en el organismo, estas características obedecen a mecanismos moleculares genéticos y epigéneticos, muchos de los cuales han sido descritos para el caso de la exposición humana al BPA.

Abstract Introduction: Bisphenol A (BPA) is a chemical to which humans are extensively exposed orally, inhaled and transdermally. Justification: Given the importance of the oncological pathology that may be associated with exposure to this chemical, it is essential to better understand its possible mechanisms of action associated with carcinogenesis. Objective: To investigate the carcinogenic mechanism associated with BPA exposure. Results: Although the majority of investigations have been oriented towards the endocrine disrupting effect, with the limitation that in vivo studies are carried out in animals, recent studies have shown that they can be carcinogenic in human tissues. However, more research is required on the role of low-dose BPA (as occurs under normal environmental conditions) and its effect on the regulation of global changes in gene expression and epigenetic alterations in cells, which allow establishing links with carcinogenesis; this review shows that the studies carried out to date point to several factors that may be involved, such as mutagenic effects that include changes in gene transcription and enzymes that promote cell proliferation, limiting apoptosis and promoting angiogenesis and migration of tumor cells. Conclusion: Although it is currently recognized that the cancer cell acquires pathological characteristics that help it to survive in the organism, these characteristics are due to genetic and epigenetic molecular mechanisms, many of which have been described for the case of human exposure to BPA.

Cigarrillo electrónico: ¿otra herramienta para ayudar a dejar de fumar o una nueva estrategia para promover la adicción a la nicotina? / Electronic cigarette: another tool to help quit smoking or a new strategy to promote nicotine addiction?

Los autores de este artículo describen las principales características del cigarrillo electrónico y sus componentes, anali-zan la controversia sobre su potencial uso como terapia de sustitución del tabaco y describen las experiencias regulato-rias de Argentina y de otros países. (AU)

The authors of this article describe the main features of electronic cigarettes and its components, analyze the controversy about its potential use as tobacco substitution therapy, and summarize the regulatory experiences in Argentina and other countries. (AU)

Properties of catechol 1, 2 dioxygenase in the cell free extract and immobilized extract of Mycobacterium fortuitum

Polycyclic aromatic hydrocarbons (PAH) are carcinogenic compounds which contaminate water and soil, and the enzymes can be used for bioremediation of these environments. This study aimed to evaluate some environmental conditions that affect the production and activity of the catechol 1,2-dioxygenase (C12O) by Mycobacterium fortuitum in the cell free and immobilized extract in sodium alginate. The bacterium was grown in mineral medium and LB broth containing 250 mg L-1 of anthracene (PAH). The optimum conditions of pH (4.0-9.0), temperature (5-70 ºC), reaction time (10-90 min) and the effect of ions in the enzyme activity were determined. The Mycobacterium cultivated in LB shown higher growth and the C12O activity was two-fold higher to that in the mineral medium. To both extracts the highest enzyme activity was at pH 8.0, however, the immobilized extract promoted the increase in the C12O activity in a pH range between 4.0 and 8.5. The immobilized extract increased the enzymatic activity time and showed the highest C12O activity at 45 ºC, 20 ºC higher than the greatest temperature in the cell free extract. The enzyme activity in both extracts was stimulated by Fe3+, Hg2+ and Mn2+ and inhibited by NH4+ and Cu2+, but the immobilization protected the enzyme against the deleterious effects of K+ and Mg2+ in tested concentrations. The catechol 1,2-dioxygenase of Mycobacterium fortuitum in the immobilized extract has greater stability to the variations of pH, temperature and reaction time, and show higher activity in presence of ions, comparing to the cell free extract

Quantificação de danos em DNA induzidos por acetaldeído: potencial biomarcador de poluição ambiental / Quantification of DNA damage induced by acetaldehyde: potential biomarker for environmental pollution

O acetaldeído é um comprovado agente mutagênico e carcinogênico, pode ser produzido endogenamente pela oxidação do álcool ingerido em bebidas alcoólicas e alimentos ou exogenamente, inalado como poluente, advindo da oxidação de combustíveis fósseis e etanol. O efeito do acetaldeído foi avaliado em modelos celulares e animais com o propósito de avaliarmos o aumento do estresse oxidativo, por lipoperoxidação, fragmentação do DNA, e a formação de adutos DNA, tais como 8-oxo-7,8-dihidro-2-desoxiguanosina, além de, 1,N2-eteno-2-desoxiguanosina e 1,N2-propano-2-desoxiguanosina que foram analisados por HPLC acoplado a espectrometria de massa com a utilização de metodologia ultra-sensível e reprodutiva. O tratamento de fibroblastos pulmonares humanos normais (IMR-90) com diversas concentrações de acetaldeído (58 µM a 711 µM) resultou em aumentos de morte celular, lipoperoxidação, fragmentação do DNA, cálcio intracelular e adutos de DNA. O efeito protetor do licopeno (20 µM) foi comprovado minimizando todos os efeitos deletérios promovidos pelo acetaldeído. O tratamento dos ratos Wistar por 8 e 30 dias com 150 mg/kg e 60 mg/kg via intra-peritoneal ou gavage, evidenciaram os efeitos tóxicos provocados pelo acetaldeído, como aumento significativo de lipoperoxidação, adutos e fragmentação de DNA no fígado e cérebro destes animais. A detecção dos adutos de DNA se mostrou uma ferramenta importante para a detecção dos efeitos provocados por exposição ao aldeído. No tratamento de animais por inalação com variadas concentrações de acetaldeído, que expôs os animais a quantidades do aldeído similares às encontradas em atmosferas poluídas, foi observado aumento de lipoperoxidação, sendo este dose dependente no fígado e pulmão. Já no cérebro, os níveis de MDA foram significativamente maiores em 10 ppb e 30 ppb em relação a 0 ppb e controle, e diminuíram significativamente em 90 ppb. Em relação aos níveis de fragmentação do DNA, observamos no pulmão aumento foi dose dependente...

Acetaldehyde is a known mutagen and carcinogen that can be produced endogenously by ethanol oxidation or directly inhaled as an air pollutant produced by fuel oxidation. The toxicity of acetaldehyde was evaluated in vitro and in vivo models, by means of oxidative stress parameters such as lipid peroxidation (measured as malonaldialdehyde -MDA), DNA fragmentation and DNA adducts such as 8-oxo-7,8-dihydro-2-desoxiguanosine, 1,N2-eteno-2-desoxiguanosine and 1,N2-propano-2-desoxiguanosine, this adducts were analyzed by an ultra-sensible and reproducible HPLC coupled to mass spectrometry assay. Treatment of human normal fibroblast (IMR-90) with a wide range of concentrations (58 µM to 711 µM) resulted in an increase in citotoxicity, lipid peroxidation, DNA fragmentation, intracellular calcium release and DNA adducts. Furthermore, lycopene (20 µM) presented a protective effect against the cellular deleterious properties of acetaldehyde. Treatment of Wistar rats for 8 and 30 days with 150 mg/kg and 60 mg/kg intra-peritonially or by gavage resulted in increased toxicity, measured by lipid peroxidation and DNA damage in liver and brain. The detection of DNA adducts was shown an important tool for the identification of deleterious effects induced by exposure to the aldehyde. Animals treated by inhalation, of amounts commonly found in polluted air samples, presented increased levels of lipid peroxidation in a dose dependent manner in liver and lungs. Nevertheless, in the brain of those animals the higher concentration was devoid of toxic effect measured as MDA levels. Lung tissue presented increased levels of DNA fragmentation. Furthermore, increased levels of 1,N2-εdGuo and 1,N2-propanodGuo was also observed in lungs of all animals. In DNA from livers, 1,N2-propanodGuo presented increased levels. Formation of 8-oxo-7,8-dihydro-2-desoxiguanosine, 1,N2-eteno-2-desoxiguanosine and 1,N2-propano-2-desoxiguanosine in urine samples of people living in the city of São Paulo…

Aspectos inmunológicos en la depresión / Immunological aspects in the depression

Existe evidencia que el sistema inmune puede modular tanto los neurotransmisores a nivel central como la respuesta endocrina, interrelación que explicaría los síntomas de la depresión. Se analizaron una serie de investigaciones que relacionaban la depresión y función inmune predominando hallazgos heterogéneos. Se ha descrito un patrón de citoquinas similar al del cáncer, como posible perfil depresivo carcinógeno de las citoquinas. Por otro lado, existe una hiperfunción del eje hipotálamo, hipófisis suprarrenal con alteración de la retroalimentación negativa. A pesar de estos avances, existe controversia acerca de la relación causal entre el estado pro inflamatorio y las alteraciones conductuales de la depresión, necesitándose esclarecer si los cambios inmunológicos son directamente responsables de la alteración de los neurotransmisores a nivel central. Se reportó cómo diversos antidepresivos modifican la hiperactividad del eje y modifican la inmunidad humoral y celular, abriendo la posibilidad de modular la respuesta inmune a través de estos fármacos.

There is evidence that immune system modulates neurotransmitters at central level as well as the endocrine response, interrelation that would explain the depression symptoms. A series of investigations that related the depression and immune function was analyzed, predominating heterogeneous findings. A pattern of cytokines has been described as similar as the one of cancer, suggesting a depressive carcinogenic cytokines profile. On the other hand, a hyperfuntion of the hypothalamus, hypofisis adrenal axis, with alteration of the negative feedback exists in these patients. Despite of these advances, controversy about the causal relationship between the pro inflammatory state and the behavior alterations of depression exists, being needed to clarify if the immunological changes are directly responsible for the neurotransmitters alteration at central level. It was reported how diverse antidepressants modify the hyperactivity of axis and modify the humoral and cellular immunity, opening the possibility of modulating the immune response through these drugs.

Estudos sobre a toxicologia da ε - caprolactama: [revisão] / Studies on the toxicology of ε - caprolactam: [review]

A ε-caprolactama (CAP) é um monômero precursor de polímeros denominados nylon 6. Esses polímeros destinam-se à produção de tapetes, vestuário e materiais plásticos tais como equipamentos, sistemas e componentes automotivos, conectores, além de embalagens plásticas. Resíduos de CAP podem migrar de embalagens plásticas de nylon 6 para os alimentos. Diante disso, foi de interesse realizar uma revisão dos efeitos relativos à exposição à CAP e o seu impacto sobre a saúde humana. Estudos epidemiológicos indicam a possibilidade da CAP causar inflamações oculares e cutâneas, além de irritações no sistema respiratório. Pode ocorrer ainda hipotensão, taquicardia, palpitações, rinorréia, ressecamento nasal, efeitos geniturinários e sobre a reprodução como distúrbios nas funções menstrual e ovariana, e complicações no parto; além de problemas neurológicos e hematológicos. Estudos com animais são consistentes com tais relatos. Os estudos de genotoxicidade in vitro e in vivo por via oral e intraperitoneal mostram em sua grande maioria, resultados negativos, bem como ausência de efeitos carcinogênicos em ratos e camundongos e sobre o desenvolvimento e reprodução em ratos e coelhos.

ε -Caprolactam (CAP) is a precursor monomer of nylon 6 polymers. Nylon 6 is used in the manufacture of carpets, clothes and plastic materials, such as equipment, systems and automotive components, connectors and plastic packaging. CAP residues can migrate from nylon 6 plastic packaging to foods. Given this fact, this review was realized concerning the effects of CAP exposure and its impact on human health. Epidemiological studies indicate that CAP could cause ocular, cutaneous and respiratory irritations, as well as hypotension, tachycardia, palpitations, rhinorrhea, nose dryness, neurological and blood problems, and genitourinary and reproductive effects, such as alterations in ovarian-menstrual functions and pregnancy/birth complications. Animal studies are consistent with such reports; however, the majority of in vitro and in vivo genotoxicity studies by oral and intraperitoneal routes show negative results, including the absence of carcinogenicity in rats and mice and developmental and reproductive effects in rats and rabbits.

Reversal of hepatotoxin-induced pre-fibrogenic events by Emblica officinalis--a histological study.

Efficacy of a herbal product of E. officinalis (fruit) (EO) has been evaluated against carbon tetrachloride (CCl4) and thioacetamide (TAA) induced changes in rat liver. Chronic treatment of CCl4 and TAA revealed abnormal histopathology indicative of pre-fibrogenic events. EO reversed such alterations with significant regenerative changes suggestive of its preventive role in prefibrogenesis of liver.

Avaliação da influência da nulidade dos genótipos GSTT1 e GSTM1 na carcinogênese em cabeça e pescoço / Evaluation of the influence of GSTT1 and GSTM1 null genotypes in head and neck carcinogenesis

OBJETIVO: Avaliar a influência dos genótipos nulos dos genes GSTT1 e GSTM1 na carcinogênese em cabeça e pescoço. MÉTODOS: Foram avaliadas as freqüências dos genótipos nulos GSTT1 e GSTM1 pela técnica de reação em cadeia de polimerase (PCR) multiplex em 45 pacientes com carcinoma espinocelular de cabeça e pescoço e 45 indivíduos sem história de doença neoplásica. Ambos os grupos foram compostos por indivíduos fumantes pareados por sexo, idade e etnia. RESULTADOS: O genótipo GSTT1 nulo foi encontrado em 24,4 por cento dos pacientes e em 17,8 por cento dos indivíduos controle (P = 0,606), enquanto 44,4 por cento dos pacientes e 48,9 por cento dos indivíduos controle revelou genótipo GSTM1 nulo (P = 0,832). Não foi observada correlação entre os genótipos nulos GSTT1 e GSTM1 e os sítios primários de tumor. CONCLUSÃO: Em nosso estudo não foi possível estabelecer a influência da nulidade dos genótipos GSTT1 e GSTM1 na carcinogênese em cabeça e pescoço.

BACKGROUND: To evaluate the influence of GSTM1 and GSTT1 null genotypes in head and neck carcinogenesis. METHODS: The frequencies of GSTM1 and GSTT1 null genotypes were evaluated by multiplex polymerase chain reaction (PCR) in 45 patients with head and neck squamous cell carcinoma and in 45 control group individuals. Both groups were composed of smokers paired by gender, age and race. RESULTS: The GSTT1 null genotype was found in 24.4 percent of the patients and 17.7 percent of the control group (P= 0.606), while 44.4 percent of the patients and 48.8 percent of the control group were bearers of the GSTM1 null genotype (P=0.832). No associations between GSTT1 and GSTMI null genotypes and primary tumor sites were found. CONCLUSION: In our study, it was impossible to establish the influence of the GSTT1 and GSTM1 null genotypes in head and neck carcinogenesis.

Genética, biologia molecular e carcinogênese mamária / Genetics, molecular biology and mammary carcinogenesis

Neste artigo são apresentados conceitos atuais sobre a carcinogênese mamária, enfocando aspectos de genética e de biologia molecular. Sabe-se que a carcinogênese pode ser subdividida em três fases: iniciação, promoção e progressão. A iniciação decorre de lesão genética em uma única célula-tronco, quase sempre localizada em lóbulo indiferenciado (tipo I). A alteração genética fundamental é a inativação de genes supressores (esporádica ou hereditária) ou a ativação de proto-oncogenes. A promoção é basicamente hormonal, destacando-se o papel dos esteróides sexuais, que atuam mediante interação com proteínas receptoras intranucleares. Na fase de progressão, ocorre a invasão da membrana basal e do estroma e embolização linfática, após perda no processo de adesão entre as células em conseqüência de ação de enzimas proteolíticas.

Current concepts on mammary carcinogenesis focusing genetics and molecular biology are presented. The carcinogenic process can be divided in 3 phases: initiation, promotion and progression. Initiation occurs in only one stem cell located in undifferentiated lobules (type I) and is caused by a genetic damage. The main genetic alteration is suppressor gene inactivation (sporadic or hereditary) or proto-oncogene activation. Promotion is basically due to steroid hormones action which interacts with intra-nuclear receptor proteins. After loosing adhesion malignant cells produce proteolytic enzymes, invade basal membrane and stroma and can embolyze through lymphatic channels.

Arsenic burden survey among refuse incinerator workers.

BACKGROUND: Incinerator workers are not considered to have arsenic overexposure although they have the risk of overexposure to other heavy metals. AIM: To examine the relationship between arsenic burden and risk of occupational exposure in employees working at a municipal refuse incinerator by determining the concentrations of arsenic in the blood and urine. SETTINGS AND DESIGN: The workers were divided into three groups based on their probability of contact with combustion-generated residues, namely Group 1: indirect contact, Group 2: direct contact and Group 3: no contact. Healthy age- and sex-matched residents living in the vicinity were enrolled as the control group. MATERIALS AND METHODS: Heavy metal concentrations were measured by atomic absorption spectrophotometer. Downstream rivers and drinking water of the residents were examined for environmental arsenic pollution. A questionnaire survey concerning the contact history of arsenic was simultaneously conducted. STATISTICAL ANALYSIS: Non-parametric tests, cross-tabulation and multinomial logistic regression. RESULTS: This study recruited 122 incinerator workers. The urine and blood arsenic concentrations as well as incidences of overexposure were significantly higher in the workers than in control subjects. The workers who had indirect or no contact with combustion-generated residues had significantly higher blood arsenic level. Arsenic contact history could not explain the difference. Airborne and waterborne arsenic pollution were not detected. CONCLUSION: Incinerator workers run the risk of being exposed to arsenic pollution, especially those who have incomplete protection in the workplace even though they only have indirect or no contact with combustion-generated pollutants.

Mecanismos geneticos da iniciacao da carcinogenese mamaria / Genetic mechanisms of breast carcinogenesis initiation

O evento desencadeador da carcinogenese mamaria e o processo de iniciacao genetica, que se traduz pela desregulacao dos...

Aplicaciones de la citogenética en bioquímica clínica: marcadores biológicos tempranos en la exposición laboral inadecuada a óxido de etileno / Laboral ethylene oxide exposure: early biochemical and cytogenetic biomarkers applications

El óxido de etileno (OE), compuesto de amplio uso en la esterilización de materiales médico-quirúrgicos, es un agente alquilante con actividad mutagénica en distintos sistemas experimentales y probable carcinógeno en humanos. El objetivo de este trabajo es evaluar la sensibilidad de parámetros bioquímicos y citogenéticos en la determinación de daño inducido por OE en 12 técnicos de una central de esterilización con sus correspondientes controles. Los marcadores biológicos incluyeron: hemograma; electroforesis de hemoglobina; separación electroforética de proteínas séricas; determinación de la concentración sérica de bilirrubina: total y directa; determinación de la actividad de aminotransferasas: ALAT y ASAT, lactato deshidrogenasa y fosfatasa alcalina; fraccionamiento electroforético de fosfatasa alcalina. Al mismo tiempo en cultivo de linfocitos de sangre periférica se determinó la frecuencia de aberraciones cromosómicas/célula (AC), la variación del índice mitótico (IM) y la cinética de proliferación celular expresado como índice de replicación (IR). El análisis del fraccionamiento de la fosfatasa alcalina, reveló la presencia de fosfatasa alcalina placentaria en seis de los individuos expuestos. Asimismo, en los estudios de genotoxicidad, se observó un incremento estadísticamente significativo de la frecuencia de AC (p < 0,01) y una disminución tanto del IM (p < 0,0001) como del IR (0,001). Estos datos corroboran los efectos tóxicos del OE y demuestran la importancia de implementar una batería de marcadores biológicos en los estudios de monitoreo humano

Efecto carcinógeno del metronidazol en colon de ratas / Carcinogenic effect of metronidazol in colon of rats

El propósito del presente estudio fue evaluar el efecto carcinógeno del metronidazol para el adenocacinoma de colon en ratas. Un total de 100 ratas de la cepa Wistar fueron asignados aleatoriamente en dos grupos. El grupo experimental estuvo integrado por animales que recibieron metronidazol oralmente, 50 mg/kg/día por 10 días, repitiéndose el tratamiento cada 15 días en tres ocasiones. El grupo control recibió solución fisiológica oralmente. Después de 12 meses de observación se realizó colectomía total en busca de datos histológicos de adenocarinoma. Se determinó el nivel sérico de antígeno carcinoembrionario. En ninguno de los grupos estudiados se encontró evidencia de displasia o cáncer de colon. En el grupo experiemental, 8 por ciento de las ratas desarrollaron hiperplasia mamaria, mientras que en el grupo control fue de 0 por ciento. Las ratas tratadas con metronidazol tuvieron un nivel sérico más alto de antígeno carcinoembrionario en relación al grupo control, 10.6 ñ 1.6 ng/mL vs 1.4 ñ 1.6 ng/mL, respectivamente (p< 0.05). Estos resultados demuestran que el tratamiento con metronidazol no tiene efecto carcinógeno después de 12 meses de observación

Rapid detection of chemical carcinogens by measuring RNA released from microsomes in post-mitochondrial supernatant.

Incubation of carcinogens with post-mitochondrial supernatant (PMS) and NADPH releases ribosomes from microsomes resulting in increased RNA concentration in post-microsomal supernatant. However, non-carcinogens fail to do so. Enhanced concentration of RNA in test over control samples can provide a useful index for the carcinogenicity of environmental pollutants.

Algunos aspectos epidemiológicos del cáncer gástrico y su relación con helicobacter pylori en Chile / Some epidemiological factors of gastric cancer and it relation with helicobacter pylori in Chile

El patógeno bacteriano mas común del tracto gastrointestinal en el ser humano es el Helicobacter pylori, un microorganismo que produce inflamación de la mucosa gástrica, que en un subgrupo de individuos facilita la progresión de la ulceración. Ciertos factores ambientales, como alto consumo de nitratos y determinados factores genéticos pueden estar involucrados en la progresión de la inflamación a displasia. En Chile, mas de la mitad de los adolescentes y un alto porcentaje de niños son seropositivos a H. pylori

Towards understanding the molecular basis of thyroid cancer

Cancer is a multistep phenomenon and multiple genetic lesions are involved in the emergence of the cancerous lesion. This has best been demonstrated in colonic cancer. The authors review their work and that of others highlighting what is known about thyroid cancer. They implicate ras mutations predominantly in follicular carcinoma, rearrangement of the ret proto-oncogene in papillary carcinoma and the tumor suppressor genes p53 and retinoblastoma gene product in all stages of thyroid carcinoma. They find a low rate of ret proto-oncogene rearrangement in the Saudi population [>5%] as compared to elsewhere in the world [20%]. They find TSH receptor message abundance to be predictive of prognosis in thyroid cancer patients. Lastly, they examine whether the abundance of the antimetastatic gene nm23 message abundance negatively correlated with the tendency of thyroid tumors to metastasize and find that not to be the case in thyroid carcinoma. The study of oncogenes and tumor suppressor genes in the pathogenesis of thyroid cancer is in its infancy; however, rapid progress is being made in identifying genes participating in malignant thyroid cell transformation

Avaliaçäo do potencial carcinogênico do formocresol diluído a 1/5 e do glutaraldeído a 2 por cento no modelo experimental DMBA-induzido / The evaluation of the carcinogenic potential of 1/5 formocresol and 2 per cent glutaraldehyde in DMBA-induced model

O objetivo deste trabalho foi avaliar o potencial carcinogênico do formocresol e do glutaraldeído, nas concentraçöes utilizadas clinicamente, em testes de longa duraçäo, a partir do modelo experimental em hamsters sírius dourados para estudo da carcinogênese química bucal induzida pelo uso do DMBA a 0,5 por cento. A análise comparativa macro e microscópica das alteraçöes provocadas pela aplicaçäo tópica do formocresol diluído a 1/5 e glutaraldeído a 2 por cento sobre a mucosa lingual lateral, precedida ou näo por escarificaçäo, após 7, 13 e 20 semanas, permitiu verificar que o formocresol diluído a 1/5 e o glutaraldeído a 2 por cento induzem alteraçöes morfológicas que caracterizam displasia epitelial; näo houve induçäo à formaçäo de papilomas e carcinomas nos animais, tal como ocorreu com o DMBA a 0,5 por cento

Avaliaçäo do potencial cariogênico do formocresol diluído a 1/5 e do glutaraldeído a 2 por cento no modelo experimental DMBA-induzido / The evaluation of the cariogenic potential of 1/5 formocresol and 2 percent glutaraldehyde in DMBA-induced model

A necessidade de se avaliar o potencial cariogênico do formocresol e glutaraldeído, nas concentraçöes utilizadas clinicamente, em testes de longa duraçäo, motivou a realizaçäo deste trabalho, a partir do modelo experimental em hamsters sírios dourados para o estudo da cariogênese química bucal induzida pelo uso do DMBA a 0,5 por cento. A análise comparativa das evoluçöes macroscópica e microscópicas das alteraçöes provocadas pela aplicaçäo tópica do formocresol diluido a 1/5 e do glutaraldeído a 2 por cento sobre a mucosa lingual lateral, precedida ou näo pelo procedimento de trauma por escarificaçäo, após 7, 13 e 20 semanas, permitiu verificar que: 1) O formocresol diluído a 1/5 e o glutaldeído a 2 por cento induzem alteraçöes epiteliais hiperplásicas nos locais das aplicaçöes, mas sem modificaçöes morfológicas que caracterizam displasia epitelial; 2) Näo houve induçäo à formaçäo de papilomas e carcinomas nos animais em que foram aplicados formocresol diluído 1/5 e glutaraldeído a 2 por cento, na mucosa da borda lateral da língua de hamster, tal como foi feito com o DMBA a 0,5 por cento. Desta forma, podê-se concluir que, o formocresol diluído a 1/5 e o glutaraldeído a 2 por cento, quando comparados ao DMBA a 0,5 por cento no mesmo método de aplicaçäo, näo säo carcinógenos completos