Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04040 (Catalase)
 3,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Estrogen-induced carcinogenesis involves enhanced cell proliferation (promotion) and genotoxic effects (initiation). To investigate the contribution of estrogens and their metabolites to tumor initiation, we examined DNA damage induced by estradiol and its metabolites, the catechol estrogens 2-hydroxyestradiol (2-OHE(2)) and 4-hydroxyestradiol (4-OHE(2)). In the presence of Cu(II), catechol estrogens formed piperidine-labile sites at thymine and cytosine residues in (32)P 5'-end-labeled DNA fragments and induced the formation of 8-oxo-7,8-dihydro-2'-deoxyguanosine. NADH markedly enhanced Cu(II)-dependent DNA damage mediated by nanomolar concentrations of catechol estrogens. Catalase and bathocuproine inhibited the DNA damage, suggesting the involvement of H(2)O(2) and Cu(I). These results suggest that H(2)O(2), generated during Cu(II)-catalyzed autoxidation of catechol estrogens, reacts with Cu(I) to form the Cu(I)-peroxide complex, leading to oxidative DNA damage, and that NADH enhanced DNA damage through the formation of redox cycle. To investigate the role of estrogens and their metabolites in tumor promotion, we examined their effects on proliferation of estrogen-dependent MCF-7 cells. Estradiol enhanced the proliferation of MCF-7 cells at much lower concentrations than catechol estrogens. These findings indicate that catechol estrogens play a role in tumor initiation through oxidative DNA damage, whereas estrogens themselves induce tumor promotion and/or progression by enhancing cell proliferation in estrogen-induced carcinogenesis.
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PMID:Catechol estrogens induce oxidative DNA damage and estradiol enhances cell proliferation. 1129 Oct 67

Number of studies indicate that the female gonadal hormone estrogen protects women against several neurodegenerative diseases and cerebral ischemia via various mechanisms. The possible protective effects of estrogen are mediated mainly by three ways; the activation of steroid receptors and/or modulation of a neurotransmitter and/or direct antioxidative action. Therefore we aimed to investigate the effects of estradiol and raloxifene on levels of nitric oxide (NO) and antioxidant enzymes in brain cortex of ovariectomized female rats. Ten Sprague-Dawley rats were used as naive controls while 32 rats were ovariectomized at 120-140 days of age. Twelve weeks after ovariectomy: (1). Ovariectomized Placebo group (n=11), was given physiologic saline. (2). Estrogen group (n=10) was given Ethynyl estradiol, 0.1 mg/kg sc. (3). Raloxifene group (n=10) was given raloxifene, 1 mg/kg sc. At the end of the treatment period (8 weeks), rats were decapitated and cortex samples were dissected. Results showed that ovariectomy caused a decrease in total nitrite-nitrate levels. The NO levels of both the estrogen and the raloxifene group were higher than the placebo group. Catalase activities did not show any significant difference between the groups, while superoxide dismutase (SOD) activities were elevated via ovariectomy. Estradiol and Raloxifene treatment had no statistically significant effect on SOD activity.
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PMID:The effects of estrogen and raloxifene treatment on the antioxidant enzymes and nitrite-nitrate levels in brain cortex of ovariectomized rats. 1258 35