Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.6.3.1 (NADPH oxidase)
 11,281 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although Rhodococcus spp. strains are able to degrade methoxyphenols by enzymatic means, the contact with veratric acid (3, 4-dimethoxybenzoic acid, hereafter called veratrate) is very stressful for the cells of Rhodococcus erythropolis DSM 1069 (Rh). Within 5 min of contact veratrate in phosphate buffer, the emergence of many vacuoles was observed in the cell body and respiratory bursts, with violent endogenous oxygen uptake, took place several times during the 24 h incubation. During these peaks (where the cells were in their MAX states), increased activity of NADH oxidase was noted, accompanied by maximal accumulation of vanillic and isovanillic acids (3-methoxy-4-hydroxybenzoic acid and 4-hydroxy-3-methoxybenzoic acid respectively, hereafter called vanillates) in the incubation medium, which appeared to be products of veratrate demethylation. At the troughs (cell in their MIN state), the vacuoles disappeared from the cell body, oxygen uptake was normal, and the pool of vanillates decreased while the veratrate level in the medium increased. The cells from MAX and MIN states reacted in opposite ways in the presence of either formaldehyde and GSH, or paraquate and cAMP. The NADH oxidase activity, measured as oxygen uptake against NADH in the membrane pellets of MAX and MIN stage cells, differed in their response to the exogenous presence of FAD, ATP, cAMP, catalase, GSH, H(2)O(2)and methoxyphenolic substrates. The periodic character of these events is described here. Co-operation between two multiprotein membrane complexes (NAD(P)H oxidase and 3-O/4-O-demethylases) in Rhodococcus erythropolis cells and their competition for two common substrates-NAD(P)H and O(2)-is proposed as an explanation for rhythmical nature of these reactions.
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PMID:Multiple respiratory bursts as a response to veratrate stress in Rhodococcus erythropolis cells. 1092 25

Anthocyanins are reported to have vascular bioactivity, however their mechanisms of action are largely unknown. Evidence suggests that anthocyanins modulate endothelial function, potentially by increasing nitric oxide (NO) synthesis, or enhancing NO bioavailability. This study compared the activity of cyanidin-3-glucoside, its degradation product protocatechuic acid, and phase II metabolite, vanillic acid. Production of NO and superoxide and expression of endothelial NO synthase (eNOS), NADPH oxidase (NOX), and heme oxygenase-1 (HO-1) were established in human vascular cell models. Nitric oxide levels were not modulated by the treatments, although eNOS was upregulated by cyanidin-3-glucoside, and superoxide production was decreased by both phenolic acids. Vanillic acid upregulated p22(phox) mRNA but did not alter NOX protein expression, although trends were observed for p47(phox) downregulation and HO-1 upregulation. Anthocyanin metabolites may therefore modulate vascular reactivity by inducing HO-1 and modulating NOX activity, resulting in reduced superoxide production and improved NO bioavailability.
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PMID:Phenolic metabolites of anthocyanins modulate mechanisms of endothelial function. 2568 9