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Background Recent epidemiological studies on workers describe that exposure to pesticides can induce oxidative stress by increased production of free radicals that can accumulate in the cell and damage biological macromolecules, for example, RNA, DNA, DNA repair proteins and other proteins and/or modify antioxidant defense mechanisms, as well as detoxification and scavenger enzymes. This study aimed to assess oxidative stress and DNA damage among workers exposed to pesticides. Methods For this purpose, 52 pesticide exposed workers and 52 organic farmers were enrolled. They were assessed: the pesticide exposure, thiobarbituric acid reactive substances (TBARS), total glutathione (TG), oxidized glutathione levels (GSSG), and 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxodG), levels. Results Correlation between pesticide exposure was positively associated with high TBARS and 8-oxodG levels (p Conclusions The present investigation results seem to indicate a mild augment in oxidative stress associated with pesticide exposure, followed by an adaptive response to increase the antioxidant defenses to prevent sustained oxidative adverse effects stress.

Beta-2-glycoprotein I (beta(2)GPI) is mainly produced by the liver and is found in plasma partially associated to lipoproteins. Although various properties have been attributed to this protein, its physiological role remains still unclear. We investigated its expression in cultured liver cells and in regenerating liver. Expression studies in HepG2 cells demonstrate that beta(2)GPI mRNA is regulated in a cell cycle-dependent manner, with very low expression in low cycling conditions and increasing levels in proliferating cells. p21 WAF-dependent growth arrest, induced by butyrate treatment, down-regulate beta(2)GPI mRNA levels. Immunolocalization in normal rat liver shows a non-homogeneous pattern, being mainly present in the centrolobular area; post-hepatectomy regenerating rat liver is uniformly immunostained and mitotic elements show the highest protein expression. Albumin gene expression, studies as control liver specific product, was not affected by sodium butyrate induced growth arrest. As previously reported for endothelial cells, beta(2)GPI behaves as survival factor for HepG2 cells: when increasing amounts of the protein (10-50 microg) have been added to serum deficient cultured liver cells a progressive reduced cell loss was observed. In conclusion, the present data demonstrate that beta(2)GPI gene expression is strictly related to the proliferative status of hepatic cells and that this protein could play a role in maintaining liver cells vitality when exposed to different stress factors such as regeneration after partial hepatectomy or growth factors depletion.