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)

It has been well established that diet high in cholesterol and saturated fatty acids could significantly elevate plasma cholesterol levels and also increase the risk of cardiovascular diseases. We hypothesize that repeated systemic Escherichia coli (E. coli) in conjunction with hypercholesterolemia, leads to development of oxidative stress that may affect the development and progression of inflammatory CVD. Swiss albino mice (4 weeks old) were randomly assigned to high cholesterol diet (HCD) or normal laboratory diet (NLD) groups. At 10 weeks of age, mice were inoculated intravenously with E. coli or vehicle for 24 weeks. Serum cholesterol, low density lipoprotein, C reactive protein levels, blood glucose level and selective antioxidant enzymes throughout the systemic infection period in murine aorta, heart and liver during hypercholesterolemia, were examined. Serum cholesterol levels were elevated in HCD-fed mice, compared to NLD. The blood colony forming units (CFU) of E. coli suggested persistence of systemic infection. The antioxidant enzyme levels were elevated in E. coli infected groups as compared to controls. The myeloperoxidase content of aortic tissue was significantly higher in all groups infected with E. coli. Our study suggests that during hypercholesterolemia, repeated systemic E. coli infection induces an endogenous antioxidant response that serves to modulate vascular inflammation leading to cardiovascular diseases.
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PMID:Repeated systemic Escherichia coli infection enhances anti-oxidant response in hypercholesterolemic mice inducing cardiovascular inflammation. 1922 70

Waterlogging usually results from overuse or poor management of irrigation water and is a serious constraint due to its damaging effects. RAP2.6L (At5g13330) overexpression enhances plant resistance to jasmonic acid, salicylic acid, abscisic acid (ABA) and ethylene in Arabidopsis thaliana. However, it is not known whether RAP2.6L overexpression in vivo improves plant tolerance to waterlogging stress. In this study, the RAP2.6L transcript was induced by waterlogging or an ABA treatment, which was reduced after pretreatment with an ABA biosynthesis inhibitor tungstate. Water loss and membrane leakage were reduced in RAP2.6L overexpression plants under waterlogging stress. Time course analyses of ABA content and production of hydrogen peroxide (H(2)O(2)) showed that increased ABA precedes the increase of H(2)O(2). It is also followed by a marked increase in the antioxidant enzyme activities. Increased ABA promoted stomatal closure and made leaves exhibit a delayed waterlogging induced premature senescence. Furthermore, RAP2.6L overexpression caused significant increases in the transcripts of antioxidant enzyme genes APX1 (ascorbate peroxidase 1) and FSD1 (Fe-superoxide dismutase 1), the ABA biosynthesis gene ABA1 (ABA deficient 1) and signaling gene ABH1 (ABA-hypersensitive 1) and the waterlogging responsive gene ADH1 (alcohol dehydrogenase 1), while the transcript of ABI1 (ABA insensitive 1) was decreased. ABA inhibits seed germination and seedling growth and phenotype analysis showed that the integration of abi1-1 mutation into the RAP2.6L overexpression lines reduces ABA sensitivity. These suggest that RAP2.6L overexpression delays waterlogging induced premature senescence and might function through ABI1-mediated ABA signaling pathway.
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PMID:RAP2.6L overexpression delays waterlogging induced premature senescence by increasing stomatal closure more than antioxidant enzyme activity. 2266 Oct 72

GO nanosheets have been reported to show strong cytotoxicity towards Escherichia coli (E. coli) in aqueous solution. Natural organic matters (NOMs) in water may probably coat on the surface of GO nanosheets, which possibly influence its cytotoxicity. In this study, we illustrated how humic acid (HA), a ubiquitous NOM, mitigated the toxicity of GO nanosheets towards E. coli based on the cytotoxicity mechanism of GO nanosheets. Adsorption and cell viability tests proved that HA was adsorbed by GO nanosheets and decreased the toxicity of GO nanosheets towards E. coli. It was found that HA was adsorbed on the surface of GO nanosheets by polar groups, which prevented E. coli from contacting with GO nanosheets and weakened the toxicity of GO nanosheets. Besides, HA exerted an antioxidant role in maintaining the activity of the antioxidant enzyme and decreasing the ROS generation according to the results of oxidative stress experiments. The work revealed that HA relieved the toxicity of GO nanosheets and decreased the ecological risks induced by GO nanosheets.
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PMID:Mitigation in the toxicity of graphene oxide nanosheets towards Escherichia coli in the presence of humic acid. 2725 16