Oxidative stress-related parameters in prostate of rats with experimental autoimmune prostatitis.

1998 
BACKGROUND. Oxidative stress in tissues can be provoked by an augmented metabolic rate, which may sometimes be combined with a decrease in the antioxidant capacity. METHODS. In this study we examined the primary enzymatic defense mechanisms against the damage caused by reactive oxygen species (ROS): the superoxide dismutase (SOD) and catalase activities and glutathione content, as well as the levels of total thiobarbituric acid-reactant substances (TBARS), indicative of lipid peroxidation. These studies were made in prostate homogenates of rats with experimental autoimmune prostatitis (EAP) and of control rats treated with complete Freund's adjuvant (CFA) or nontreated. RESULTS. The evaluation of antioxidant defenses revealed a significant diminution of the catalase activity in autoimmune rats without changes in SOD activity and glutathione content. TBARS levels evidenced a significant increase in prostate homogenates from autoimmune rats in relation to control rat samples. CONCLUSIONS. The results suggest that in EAP, a marked diminution of catalase activity associated with an enhanced oxidative metabolism of inflammatory macrophages might lead to oxidative damage in this autoimmune disease.
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