Objective. Cognitive impairment reduces quality of life and is related to vascular and neurodegenerative disorders. However, there is also a close relationship between these diseases and oxidative stress. Thus, the purpose of this study was to assess whether inflammation and oxidative damage are associated with low cognitive performance in the elderly with different housing conditions. Methods. The study groups consisted of 32 institutionalized and 25 noninstitutionalized Brazilian elderly subjects. Oxidative damage, inflammation markers, and cognitive function were evaluated. Results. The results demonstrated pronounced oxidative stress in the institutionalized elderly group, which also had a lower antioxidant status compared to noninstitutionalized subjects. High levels of proinflammatory cytokines were also observed in the institutionalized elderly. Furthermore, the raised levels of inflammatory markers were correlated with increased oxidative stress, and both were associated with low cognitive performance. However, based on multiple linear regression analysis, oxidative stress appears to be the main factor responsible for the cognitive decline. Conclusions. The findings suggest that individuals with lower antioxidant status are more vulnerable to oxidative stress, which is associated with cognitive function, leading to reduced life quality and expectancy.

Toluene is an organic solvent used in numerous processes and products, including industrial paints. Toluene neurotoxicity and reproductive toxicity are well recognized; however, its genotoxicity is still under discussion, and toluene is not classified as a carcinogenic solvent. Using the comet assay and the micronucleus test for detection of possible genotoxic effects of toluene, we monitored industrial painters from Rio Grande do Sul, Brazil. The putative involvement of oxidative stress in genetic damage and the influences of age, smoking, alcohol consumption, and exposure time were also assessed. Although all biomarkers of toluene exposure were below the biological exposure limits, painters presented significantly higher DNA damage (comet assay) than the control group; however, in the micronucleus assay, no significant difference was observed. Painters also showed alterations in hepatic enzymes and albumin levels, as well as oxidative damage, suggesting the involvement of oxidative stress. According to multiple linear regression analysis, blood toluene levels may account for the increased DNA damage in painters. In summary, this study showed that low levels of toluene exposure can cause genetic damage, and this is related to oxidative stress, age, and time of exposure.

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BACKGROUND: Anti-mullerian hormone (AMH) is a marker of ovarian function and reserve and reflects the number and size of antral follicles. The objective of this study was to evaluate the effect of FSH suppression on AMH levels, during the late luteal phase of human menstrual cycle, with the use of oral contraceptives pills (OCP). METHODS: Twenty normovulatory infertile women were included in the study. On the third day of a spontaneous menstrual cycle, the patients were submitted to a transvaginal ultrasound examination and blood sample collection. From the 20th day of this menstrual cycle, the patients took daily OCP, containing 0.030 mg of ethinyl-estradiol plus 0.15 mg of desogestrel. On the third day of the following cycle, the measurements were repeated. RESULTS: After OCP use, the levels of FSH and estradiol were significantly reduced (P < 0.001). The number of antral follicles measured on both occasions did not differ, although after OCP use, the follicles presented significantly lower diameters (mean 4.4 1 1.7 mm before OCP versus 3.5 1 1.2 mm after OCP P < 0.001). The levels of AMH were significantly reduced after pituitary suppression, with a median (inter-quartile range) of 3.02 ng/mL (1.21-6.39) before OCP and 2.22 ng/mL (0.9-3.11) after OCP, P 5 0.04. CONCLUSIONS: The short administration of OCP in late luteal phase caused suppression of FSH secretion during the cycle transition, leading to a more homogeneous follicular cohort. The lower AMH levels observed, although simultaneous with FSH suppression, were probably not a direct effect of the reduced FSH levels, but were more likely a consequence of the lower production by the arrested follicular cohort.