TBARS公司
氧化应激
超氧化物歧化酶
过氧化氢酶
脂质过氧化
内分泌学
前列腺炎
硫代巴比妥酸
抗氧化剂
内科学
前列腺
谷胱甘肽
化学
谷胱甘肽过氧化物酶
免疫学
医学
生物化学
酶
癌症
作者
Miguel Ángel Orsilles,Mirtha Depiante‐Depaoli
出处
期刊:The Prostate
[Wiley]
日期:1998-03-01
卷期号:34 (4): 270-274
被引量:24
标识
DOI:10.1002/(sici)1097-0045(19980301)34:4<270::aid-pros4>3.0.co;2-l
摘要
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. Prostate 34:270–274, 1998. © 1998 Wiley-Liss, Inc.
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