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)

A study of 4718 women 15-49 years old in southwestern Uganda's Rakai district suggests that the loss of lactobacilli and the presence of bacterial vaginosis may increase susceptibility to HIV-1. These women were part of an ongoing community-based trial of sexually transmitted disease (STD) control as a strategy for AIDS prevention. The rate of HIV-1 infection among these women was 19.5%. Moderate bacterial vaginosis was detected in 44.5% of women, while 6.4% had severe bacterial vaginosis. STD rates were 10.2% for active or recent syphilis, 22.4% for trichomonas, 2.4% for gonorrhea, and 3.6% for chlamydia. The HIV rate was lowest (14.2%) among women with normal bacterial flora and highest (26.7%) among those with severe bacterial vaginosis. The HIV-abnormal flora association was higher in younger women, for whom HIV acquisition is likely to be recent, than in older women. In multiple logistic regression analyses adjusted for age, number of sexual partners, trichomonas, and syphilis, the odds ratio (OR) for HIV-1 infection associated with any abnormal vaginal flora was 1.52 (95% confidence interval [CI], 1.22-1.90) and with all bacterial vaginosis was 1.56 (95% CI, 1.24-1.97). These adjusted ORs were 1.50 (95% CI, 1.18-1.89) for moderate and 2.08 (95% CI, 1.48-2.94) for severe bacterial vaginosis. A cross-sectional study cannot ascertain whether the abnormalities in vaginal flora occurred before or after HIV seroconversion. However, the significantly increased proportion of HIV-infected women with depleted or absent vaginal lactobacilli is consistent with in vitro studies showing that hydrogen peroxidase-producing lactobacilli in vaginal flora inhibit HIV-1 viral replication. If the ongoing prospective study suggests a causal association with HIV, treatment of abnormal flora or bacterial vaginosis with inexpensive, effective drugs such as metronidazole may be indicated.
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PMID:HIV-1 infection associated with abnormal vaginal flora morphology and bacterial vaginosis. 965 90

A homeostatic balance exists between the cellular generation of oxidant species and endogenous antioxidants under normal physiological conditions. Human Immunodeficiency Virus (HIV) infection is known to affect this balance causing oxidative stress. However, the interaction of HIV infection with a substance abuse on cellular oxidant/antioxidant system is sparse. This study was designed in order to investigate the interactive effect of morphine abuse and Simian Immunodeficiency Virus/ Simian Human Immunodeficiency Virus (SIV/SHIV) infection on plasma oxidant/antioxidant balance in rhesus macaques. Six rhesus macaques adapted to morphine dependence (20 weeks) along with three controls were infected with mixture of SHIV(KU-1B), SHIV(89.6P), and SIV(17E-Fr). Plasma samples from morphine-dependent and control macaques were analyzed for an array of oxidative stress indices after 16 weeks of infection. Morphine-dependence significantly increased plasma malondialdehyde (MDA) and 8-isoprostane levels (8-fold and 2-fold), but these animals showed higher MDA and 8-isoprostane levels after viral infection (18-fold and 4-fold) which was directly correlated with increase in viral load and decline in CD4+ cells. Plasma glutathione (GSH) level depleted (55%) with morphine dependence that was further depleted (25%) by the infection. Activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) were increased by 30% and 110%, respectively with morphine dependence, but that was decreased by the infection. Catalase (CAT) activity declined (25%) with morphine dependence that was further declined by infection. Our results clearly suggest that morphine interaction with SIV/SHIV infection causes higher oxidative tissue injury that might have implication in the pathogenesis of AIDS in morphine-dependent macaques.
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PMID:Interaction of SIV/SHIV infection and morphine on plasma oxidant/antioxidant balance in macaque. 1793