Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cigarette smoking continues to pose a significant health burden on society. Two well-described mechanistic links associating smoking with morbidity and mortality include elevated blood lipids and increased oxidative stress. These variables have traditionally been measured while an individual is fasting, but evidence suggests that postprandial lipemia and oxidative stress provide more important information concerning susceptibility to disease, in particular cardiovascular disease. Cigarette smokers have elevated levels of biomarkers of oxidative stress at rest and experience impaired postprandial lipid and glucose metabolism. We have confirmed these findings while noting an exaggerated oxidative stress response to high-fat feeding. Smoking cessation is without question the best approach to minimizing smoking-induced ill health and disease, but success rates among those who attempt to quit are dismal. Other means to decrease a smoker's susceptibility to oxidative stress-related disease are needed. We propose that exercise may aid in attenuating postprandial oxidative stress, and we do so in 3 distinct ways. First, exercise stimulates an increase in endogenous antioxidant enzyme activity. Second, exercise improves blood triglyceride clearance via a reduced chylomicron-triglyceride half-life and an enhanced lipoprotein lipase activity. Third, exercise improves blood glucose clearance via an enhanced glucose 4 transport protein translocation and protein content, as well as insulin-insulin receptor binding and postreceptor signaling. Improvements in antioxidant status, as well as lipid and glucose processing, may aid greatly in minimizing feeding-induced oxidative stress in smokers. If so, and in accordance with the recent joint initiative of the American College of Sports Medicine and the American Medical Association, exercise may be viewed as a "medicine" for cigarette smokers at increased risk for postprandial oxidative stress. Research into this area may provide insight into the potential benefits of exercise for this purpose.
Nicotine Tob Res 2009 Jan
PMID:The role of exercise in minimizing postprandial oxidative stress in cigarette smokers. 1924 36

We analyzed superoxide dismutase (SOD), catalase (CAT), and ATPase activities in the highly nicotine-degrading strain Pseudomonas sp. HF-1 and two standard strains Escherichia coli and Bacillus subtilis in an attempt to understand antioxidant enzymes in bacteria are produced in response to nicotine, which increases the virulence of the bacteria. Nicotine had different effects on different antioxidant enzymes of different bacteria. SOD plays a more important role in resistance to nicotine stress in E. coli than it does in CAT. Multiple antioxidant enzymes are involved in combating oxidative stress caused by nicotine in Pseudomonas sp. HF-1. The contribution of a particular antioxidant enzyme for protection from nicotine stress varies with the growth phase involved. The inhibition of ATPase in Pseudomonas sp. HF-1 at the stationary phase was enhanced with increasing nicotine concentration, showing a striking dose-response relationship. Nicotine probably affected the metabolism of ATP to some extent. Furthermore, different bacteria possessed distinct SOD isoforms to cope with oxidative stress caused by nicotine.
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PMID:Antioxidant enzyme activity in bacterial resistance to nicotine toxicity by reactive oxygen species. 1929 56

Tobacco farmers are routinely exposed to complex mixtures of the compounds present in tobacco leaves, including organic and inorganic pesticides. Penetration through skin is the most significant route of uptake in occupational exposure to chemicals, including dust and liquids containing toxic and carcinogenic substances. This study evaluates the genotoxic effect of tobacco leaves with and without dermal exposure to flumetralin in Mus musculus, determining cell damage by the micronucleus test and the Comet assay as well as antioxidant enzyme activities and hematologic parameters. Nicotine was used as positive control. Blood samples were collected for 0, 3, 24 and 48 h exposure periods, and DNA damage by Comet assay and micronucleus test was evaluated for all these periods. Bone marrow and liver cells were also evaluated for the 48 h exposure period. Significant differences between Comet assay results in blood cells from animals exposed to tobacco leaves with and without pesticide were found in 24 and 48 h exposure periods in relation to negative control. Bone marrow cells from the group exposed to leaves with pesticide (48 h) also demonstrated significant increase in DNA damage. Concerning the micronucleus test, only animals exposed to tobacco leaves without pesticide (24 h) showed increase in frequency of micronuclei when compared to the negative control. Oxidative stress activities also were demonstrated for different groups. The results demonstrate the injury effect caused by tobacco leaves in different Mus musculus tissues, suggesting that the effects of dermal exposure to tobacco leaves are caused by complex mixtures present in the plant, but mainly by nicotine.
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PMID:Effects of dermal exposure to Nicotiana tabacum (Jean Nicot, 1560) leaves in mouse evaluated by multiple methods and tissues. 2068 53