ABSTRACT We evaluated the influence of hesperidin and vitamin C (VitC) on glycemic parameters, lipid profile, and DNA damage in male Wistar rats treated with sucrose overload. Rats were divided into six experimental groups: I-water control; II-sucrose control; III-hesperidin control; IV-VitC control; V-co-treatment of sucrose plus hesperidin; VI-co-treatment of sucrose plus VitC. We measured the levels of triglycerides, total cholesterol, HDL-c, LDL-c, fasting glucose, and glycated hemoglobin (A1C). DNA damage was evaluated in blood and brain cells using the comet assay and the micronucleus test was used to evaluate chromosomal damages in the rat bone marrow. Co-treatment with VitC, but not with hesperidin, normalized the serum glucose. No effect of co-treatments was observed on A1C. The co-treatment with VitC or hesperidin did not influence the lipid profile (p>0.05). Rats co-treated with hesperidin had a significantly lower DNA damage level in blood (p<0.05) and brain (p<0.05). Rats treated with VitC only, but not those co-treated with VitC plus sucrose, had significantly higher DNA damage in brain (p<0.05). No significant differences were observed in the results of micronucleus test (p>0.05). Hesperidin and VitC showed different effects on sucrose and DNA damage levels. While VitC lowered the serum glucose, hesperidin reduced the DNA damage.

ABSTRACT The purpose of this study was to determine the effects of the high consumption of sucrose on the levels of DNA damage in blood, hippocampus and bone marrow of rats. Male Wistar rats were treated for 4 months with sucrose (10% for 60 initial days and 34% for the following 60 days) in drinking water, and then, glycemia and glycated hemoglobin (A1C) were measured. Levels of DNA damage in blood and hippocampus were evaluated by the comet assay. The micronucleus test was used to evaluate chromosomal damages in the bone marrow. The sucrose treatment significantly increased (p<0.01) the serum glucose levels (~20%) and A1C (~60%). The level of primary DNA damage was significantly increased (p<0.05) in hippocampal cells (~60%) but not in peripheral blood leukocytes (p>0.05). Additionally, it was observed a significative increase (p<0.05) in the markers of chromosomal breaks/losses in bone marrow, as indicated by the micronucleus test. This is the first study that evaluated DNA damage induced by high sucrose concentration in the hippocampus and bone marrow of rats. Sucrose-induced DNA damage was observed in both tissues. However, the mechanism of sucrose toxicity on DNA remains unknown.

ABSTRACT This study aimed to identify the 516 G>T polymorphism of the CYP2B6 gene and evaluate its influence on central nervous system (CNS) side effect development in HIV-positive individuals undergoing Efavirenz (EFV) treatment in a population from southern Brazil. Additionally, we performed a survey on the clinical and epidemiological characteristics of our sample. In addition to medical records evaluation, whole blood of 89 individuals was analyzed for viral load, T lymphocyte count (CD4+ and CD8+), and the polymorphism. Considering the side effects of the CNS reported by individuals but without considering the genetic variables, no statistically significant association was noted between the adverse effects and the antiretroviral treatment (including or not EFV). In addition, no statistically significant difference was noted for the influence of genotype on the viral load or the number of T lymphocytes (CD4+ and CD8+) among individuals undergoing EFV treatment. This is the first study that investigated the impact of the 516 G>T polymorphism of the CYP2B6 gene among HIV-positive individuals from southern Brazil. Its clinical significance indicates the need for prospective studies in this population.

O objetivo deste estudo foi avaliar potenciais danos no DNA e citotoxicidade em técnicos de laboratório de patologia expostos a solventes orgânicos, principalmente ao xileno. Amostras de sangue periférico e células bucais foram coletadas de 18 técnicos ocupacionalmente expostos a solventes orgânicos e de 11 indivíduos não expostos aos solventes. Os técnicos foram avaliados em dois momentos: segunda-feira e sexta-feira. Danos no DNA e citotoxicidade foram avaliados usando o Ensaio Cometa e o Teste de Micronúcleos e Anomalias Nucleares. Quinze indivíduos (83,5%) do grupo exposto aos solventes queixaram-se de algum sintoma com provável relação com o contato com vapores de solventes orgânicos. Os danos no DNA no grupo exposto aos solventes foram aproximadamente 2 vezes maiores na sexta-feira do que na segunda-feira, e em ambos momentos os indivíduos desse grupo apresentaram maiores níveis de danos no DNA em relação aos controles. Não foi encontrada diferença significativa na frequência de micronúcleos nas células bucais entre os técnicos de laboratório e os indivíduos do grupo controle. Entretanto, na análise realizada na sexta-feira, os técnicos apresentaram maior frequência (aproximadamente 3 vezes) de células cariolíticas e células indicativas de apoptose (cariorréticas e picnóticas) em relação ao grupo controle. Considerando a frequência de dano e o tempo de trabalho, uma correlação positiva foi encontrada entre o grupo de indivíduos expostos aos solventes (r=0,468; p=0,05). Os resultados sugerem que técnicos de laboratório de patologia expostos de forma inadequada a solventes orgânicos possuem aumento dos níveis de danos no DNA.

The aim of this study was to evaluate potential DNA damage and cytotoxicity in pathology laboratory technicians exposed to organic solvents, mainly xylene. Peripheral blood and buccal cells samples were collected from 18 technicians occupationally exposed to organic solvents and 11 non-exposed individuals. The technicians were sampled at two moments: Monday and Friday. DNA damage and cytotoxicity were evaluated using the Comet Assay and the Buccal Micronucleus Cytome assay. Fifteen subjects (83.5%) of the exposed group to solvents complained about some symptom probably related to contact with vapours of organic solvents. DNA damage in the exposed group to solvents was nearly 2-fold higher on Friday than on Monday, and in both moments the individuals of this group showed higher levels of DNA damage in relation to controls. No statistical difference was detected in buccal cell micronucleus frequency between the laboratory technicians and the control group. However, in the analysis performed on Friday, technicians presented higher frequency (about 3-fold) of karyolytic and apoptotic-like cells (karyorrhectic and pyknotic) in relation to control group. Considering the damage frequency and the working time, a positive correlation was found in the exposed group to solvents (r=0.468; p=0.05). The results suggest that pathology laboratory workers inappropriately exposed to organic solvents have increased levels of DNA damage.

RESUMO A doença de Parkinson é caracterizada pela morte dos neurônios dopaminérgicos, principalmente na substância negra, e causa sérias disfunções locomotoras. É provável que o dano oxidativo às biomoléculas celulares esteja entre as principais causas da neurodegeneração que ocorre nessa doença. O selênio é um mineral essencial para o adequado funcionamento do encéfalo e, principalmente devido a sua atividade antioxidante, é possível que exerça um papel especial na prevenção e no manejo nutricional da doença de Parkinson. Atualmente, poucos pesquisadores têm investigado os efeitos do selênio sobre a doença de Parkinson. Entretanto, sabe-se que níveis corporais muito altos ou muito baixos de selênio podem (possivelmente) contribuir para a patogênese da doença de Parkinson, uma vez que esse desbalanço resulta no aumento dos níveis de estresse oxidativo. Dessa forma, o objetivo deste trabalho é revisar e discutir os estudos que abordaram esses tópicos e então associar as informações obtidas através deles para que esses dados e associações sejam usadas para o estabelecimento de novas pesquisas.

ABSTRACT Parkinson's disease is characterized by the death of dopaminergic neurons, mainly in the substantia nigra, and causes serious locomotor dysfunctions. It is likely that the oxidative damage to cellular biomolecules is among the leading causes of neurodegeneration that occurs in the disease. Selenium is an essential mineral for proper functioning of the brain, and mainly due to its antioxidant activity, it is possible to exert a special role in the prevention and in the nutritional management of Parkinson's disease. Currently, few researchers have investigated the effects of selenium on Parkinson´s disease. However, it is known that very high or very low body levels of selenium can (possibly) contribute to the pathogenesis of Parkinson's disease, because this imbalance results in increased levels of oxidative stress. Therefore, the aim of this work is to review and discuss studies that have addressed these topics and to finally associate the information obtained from them so that these data and associations serve as input to new research.

RESUMO Este estudo avaliou a memória de reconhecimento e os níveis de danos no DNA (sangue e hipocampo) em ratos Wistar jovens desnutridos. O experimento foi conduzido ao longo de 14 semanas com os animais divididos em grupo controle (GC, n=8) e grupo desnutrido (GD, n=12) que foi submetido a restrição calórica. O estado nutricional para desnutrição foi definido pelo Índice de Massa Corporal (IMC) de ≤0,45g/cm2 e pela pesagem dos órgãos/tecido (fígado, baço, intestino, gordura peritoneal, rim e encéfalo). O Teste de Reconhecimento de Objeto Novo avaliou a memória de reconhecimento e o Ensaio Cometa avaliou os níveis de danos no DNA. O teste t de Student, ANOVA de duas vias e a análise de correlação de Pearson foram usados e o nível de significância foi de p<0,05. O GD apresentou um menor IMC e menores pesos dos órgãos/tecido que o GC (p<0,001). Em relação à memória de curto prazo, a taxa de reconhecimento foi maior no GD (p<0,05), apenas após 4 semanas. Em relação à memória de longo prazo, novamente a taxa de reconhecimento foi maior no GD em comparação ao GC, depois de 4 semanas (p<0,001) e depois de 14 semanas (p<0,01). O GD apresentou diminuição dos níveis de danos no DNA no sangue (p<0,01) e aumento nos níveis de danos no DNA no hipocampo (p<0,01). Concluiu-se neste estudo que a desnutrição pela restrição calórica não causou prejuízo na memória de reconhecimento, porém induziu danos no DNA no hipocampo.

ABSTRACT This study evaluated the recognition memory and the levels of DNA damage (blood and hippocampus) in undernourished young Wistar rats. The experiment was conducted along 14-week with rodents divided in control group (CG, n=8) and undernourished group (UG, n=12) which was submitted to caloric restriction. Nutritional status for undernutrition was defined by Body Mass Index (BMI) ≤0.45g/cm2 and by weighting the organs/tissue (liver, spleen, intestine, peritoneal fat, kidney and encephalon). The Novel Object Recognition Test assessed recognition memory and the Comet Assay evaluated the levels of DNA damage. Student t test, 2-way ANOVA and Pearson's correlation analysis were used and the significance level was of p<0.05. The UG showed lower BMI and organ/tissue weights than CG (p<0.001). In short-term memory, the recognition rate was higher in the UG (p<0.05), only after 4 weeks. In the long-term memory, again recognition rate was higher in the UG than the CG, after 4 weeks (p<0.001) and 14 weeks (p<0.01). The UG showed decreased levels of DNA damage in the blood (p<0.01) and increased levels in the hippocampus (p<0.01). We concluded in this study that the undernutrition by caloric restriction did not cause impairment in recognition memory, however induced DNA damage in the hippocampus.