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Introduction: malnutrition is one of the most common health problems among children in underdeveloped countries, including Mexico. Previous studies have indicated increased genetic damage in malnourished humans and animal models, but the essential mechanisms remain unclear. In the present study, we assessed the effects of malnutrition on the frequency of micronucleus (MN) in reticulocytes (RET) from the peripheral blood of well-nourished uninfected (WN), well-nourished infected (WNI), moderately malnourished infected (UNM) and severely malnourished infected (UNS) children. Moreover, lipid peroxidation and the antioxidant status were evaluated to investigate the role of oxidative processes in malnutrition-associated genotoxicity. Methods: the antioxidant status of the study population was determined by measuring superoxide dismutase (SOD) in the red blood cells and glutathione peroxidase (GPX) in whole blood. Results: the UNS and UNM groups have increased percentages of MN-RET compared to the WNI group. Moreover, the data showed a significant increase in lipid peroxidation and a decrease in erythrocyte SOD activity and GPX activity in the malnourished group compared to the well-nourished infected children. Conclusion: the data suggest that the antioxidant system was impaired in the cells of malnourished children and that oxidative stress causes a significant increase in DNA damage, as evaluated by the MN-RET frequency.

Acetaldehyde (Ac), the main metabolite of ethanol oxidation, is a very reactive compound involved in alcohol-induced liver damage. In the present work, we studied the effect of Ac in mitochondria functionality. Mitochondria from Wistar rats were isolated and treated with Ac. Ac decreased respiratory control by 50% which was associated with a decrease in adenosine triphosphate content (28.5%). These results suggested that Ac could be inducing changes in cell redox status. We determined protein oxidation, superoxide dismutase (SOD) activity, and glutathione ratio, indicating that Ac induced an enhanced oxidation of proteins and a decrease in SOD activity (90%) and glutathione/oxidized GSH ratio (36%). The data suggested that Ac-induced oxidative stress mediated by mitochondria dysfunction can lead to cell sensitization and to a second oxidative challenge. We pretreated hepatocytes with Ac followed by treatment with antimycin A, and this experiment revealed a noticeable decrease in cell viability, determined by neutral red assay, in comparison with cells treated with Ac alone. Our data demonstrate that Ac impairs mitochondria functionality generating oxidative stress that sensitizes cells to a second damaging signal contributing to the development of alcoholic liver disease.

Aging process is often accompanied with a high incidence of cardiovascular diseases (CVD) due to the synergistic effects of age-related changes in heart morphology/function and prolonged exposure to injurious effects of CVD risk factors. Oxidative stress, considered a hallmark of aging, is also an important feature in pathologies that predispose to CVD development, like hypertension, diabetes and obesity. Approaches directed to prevent the occurrence of CVD during aging have been explored both in experimental models and in controlled clinical trials, in order to improve health span, reduce hospitalizations and increase life quality during elderly. In this review we discuss oxidative stress role as a main risk factor that relates CVD with aging. As well as interventions that aim to reduce oxidative stress by supplementing with exogenous antioxidants. In particular, strategies of improving the endogenous antioxidant defenses through activating the nuclear factor related-2 factor (Nrf2) pathway; one of the best studied molecules in cellular redox homeostasis and a master regulator of the antioxidant and phase II detoxification response.

Development of hepatic fibrosis is a complex process that involves oxidative stress (OS) and an altered balance between pro- and anti-apoptotic molecules. Since Bcl-2 overexpression preserves viability against OS, our objective was to address the effect of Bcl-2 overexpression in the hepatic stellate cells (HSC) cell-line CFSC-2G under acetaldehyde and H(2)O(2) challenge, and explore if it protects these cells against OS, induces replicative senescence and/or modify extracellular matrix (ECM) remodeling potential.To induce Bcl-2 overexpression, HSC cell line CFSC-2G was transfected by lipofection technique. Green fluorescent protein-only CFSC-2G cells were used as a control. Cell survival after H(2)O(2) treatment and total protein oxidation were assessed. To determine cell cycle arrest, proliferation-rate, DNA synthesis and senescence were assessed. Matrix metalloproteinases (MMP), tissue-inhibitor of MMP (TIMP), transglutaminases (TG) and smooth muscle a-actin (alpha-SMA) were evaluated by western blot in response to acetaldehyde treatment as markers of ECM remodeling capacity in addition to transforming growth factor-beta (TGF-beta) mRNA.Cells overexpressing Bcl-2 survived approximately 20% more than control cells when exposed to H(2)O(2) and approximately 35% proteins were protected from oxidation, but Bcl-2 did not slow proliferation or induced senescence. Bcl-2 overexpression did not change alpha-SMA levels, but it increased TIMP-1 (55%), tissue transglutaminases (tTG) (25%) and TGF-beta mRNA (49%), when exposed to acetaldehyde, while MMP-13 content decreased (47%).Bcl-2 overexpression protected HSC against oxidative stress but it did not induce replicative senescence. It increased TIMP-1, tTG and TGF-beta mRNA levels and decreased MMP-13 content, suggesting that Bcl-2 overexpression may play a key role in the progression of fibrosis in chronic liver diseases.