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)

Oxygen radicals have been considered to be important regulatory molecules in Helicobacter pylori-induced gastric ulceration and carcinogenesis. H. pylori-induced inflammation has been shown to be associated with cyclooxygenase-2 (COX-2) expression in experimental animals and human patients. This study aimed to determine if H. pylori produces oxygen radicals and induces COX-2 expression in gastric epithelial cells. A further aim was to resolve whether or not the H. pylori-induced COX-2 expression could be inhibited by mannitol, a known hydroxyl radical scavenger, and superoxide dismutase (SOD), an antioxidant enzyme, which was used as a positive control. A human gastric epithelial cell line, AGS, treated with or without mannitol or SOD, was incubated in the presence or absence of H. pylori. mRNA expression and protein levels for COX-2 were determined by Northern blot and Western blot analysis, respectively. Levels of the COX-2 products, 6-keto-prostaglandin F(1alpha) (6-keto-PGF(1alpha)) and thromboxane B(2) (TXB(2)) and H(2)O(2) were measured in the medium. The results showed that H. pylori induced H(2)O(2) production, COX-2 mRNA and protein expression and increased the levels of 6-keto-PGF(1alpha) and TXB(2). The H. pylori-induced COX-2 expression and the increase in the COX-2 products were inhibited by both mannitol and SOD. The inhibitory effect of mannitol on H. pylori-induced COX-2 expression suggests the possible involvement of oxygen radicals in the transcriptional regulation of the inflammatory mediators in gastric epithelial cells.
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PMID:Effect of mannitol on Helicobacter pylori-induced cyclooxygenase-2 expression in gastric epithelial AGS cells. 1239 40

Oxidative stress is implicated in the pathophysiology of a number of chronic diseases including atherosclerosis, diabetes, cataracts and accelerated aging. The aim of this study was to elucidate the protective role of vitamin E supplementation when oxidative stress is induced by CCl4 administration, using the rat as a model. Rats were fed diets for four weeks either with or without dl-alpha-tocopherol acetate supplementation. Half of the rats (n = 9) from each of the diet groups were then challenged with CCl4 at the completion of the four week diet period. Plasma levels of 8-iso-PGF(2alpha), antioxidant micronutrients and antioxidant enzyme activities were measured to examine changes in oxidative stress subsequent to the supplementation of dl-alpha-tocopherol in the diet. Plasma alpha-tocopherol (vitamin E) concentrations were higher for the groups supplemented with dl-alpha-tocopherol acetate, however the supplemented diet group that was subsequently challenged with CCl4 had significantly lower (p <0.001) plasma alpha-tocopherol concentration than the dl-alpha-tocopherol acetate diet group that was not challenged with CCl4. Total plasma 8-iso-PGF(2alpha) concentration was elevated in diet groups challenged with CCl4, however, the concentration was significantly lower (p <0.001) when the diet was supplemented with dl-alpha-tocopherol acetate. The antioxidant enzymes were not influenced by either dietary alpha-tocopherol manipulation or by the inducement of oxidative stress with CCl4. Plasma concentrations of trans-retinol (vitamin A) were reduced by CCl4 administration in both the dl-alpha-tocopherol acetate supplemented and unsupplemented diet groups. The results of this study indicate that dl-alpha-tocopherol acetate supplementation was protective of lipid peroxidation when oxidative stress is induced by a pro-oxidant challenge such as CCl4.
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PMID:Vitamin E supplementation in the mitigation of carbon tetrachloride induced oxidative stress in rats. 1277 Jun 45

Rickettsiae, a diverse group of obligately intracellular gram-negative bacteria, include etiologic agents of the spotted fever and typhus groups of diseases. Rocky Mountain spotted fever and boutonneuse fever, due to Rickettsia rickettsii and R. conorii, respectively, are characterized by widespread infection of the vascular endothelium, microvascular injury, and vasculitis. Cultured human endothelial cells (EC) are highly susceptible to infection and respond by altering the expression of adhesion molecules, regulatory cytokines, and the antioxidant enzyme heme oxygenase (HO). In the vasculature, HO regulates the cyclooxygenase (COX) enzymes, among which the inducible isozyme COX-2 facilitates the synthesis of prostaglandins (PGs). Using in vitro and ex vivo models of infection, we demonstrate here that R. rickettsii infection of human EC causes robust induction of COX-2 mRNA and protein expression but has no apparent effect on the constitutive COX-1 isoform. Cells infected with viable rickettsiae consistently displayed significantly increased secretion of 6-keto-PGF(1alpha) and PGE(2). R. rickettsii-induced COX-2 was sensitive to inhibitors of de novo transcription and the pyridinylimidazole-based compound SB 203580, suggesting that this transcriptional host cell response involves signaling through p38 mitogen-activated protein kinase. PG production by infected cells was abrogated by NS 398 (a selective COX-2 inhibitor) and indomethacin (a pan-COX inhibitor). Immunohistochemical staining of sections of infected umbilical cords and corresponding uninfected controls revealed comparatively more intense and abundant staining for COX-2 in infected endothelia. Induction of the endothelial COX-2 system and the resultant enhanced release of vasoactive PGs may contribute to the regulation of inflammatory responses and vascular permeability changes during spotted fever rickettsioses.
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PMID:Infection of human endothelial cells with spotted Fever group rickettsiae stimulates cyclooxygenase 2 expression and release of vasoactive prostaglandins. 1692 98