Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of thioctic acid on the glutathione dependent antioxidant system and activities of enzymes, generating NADPH of rats has been investigated in rats under conditions of toxic hepatitis. Injections of thioctic acid to animals with toxic hepatitis caused the decrease of glutathione reductase and peroxidase activities to the normal level. Reduced glutathione content also tended to the control level. Administration of thioctic acid to rats with toxic hepatitis also caused the decrease of NADP-dependent isocitrate dehydrogenase and glucose-6-phosphate dehydrogenase which might be associated with decreasing need of NADPH supply for glutathione dependent antioxidant system. Thus, obtained results have shown that thioctic acid may regulate manifestations of oxidative stress and the state of the glutathione antioxidant system.
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PMID:[Thioctic acid action on glutathione-dependent antioxidant system functioning at toxic hepatitis of rats]. 1763 19

Murine hepatic cytochrome P450 2A5 (CYP2A5), unlike most CYP enzymes, is upregulated during hepatitis and hepatotoxic conditions, but the common stimulus for its induction remains unknown. We investigated the involvement of oxidative stress in the regulation of CYP2A5 expression using an oxidative stress-sensitive glucose-6-phosphate dehydrogenase (G6PD)-deficient mouse model. Treatment of deficient and wild-type mice with the prototypical CYP2A5-inducer pyrazole for 72h led to a significantly greater degree of induction of CYP2A5 mRNA, protein and activity in deficient mice, with the greatest increase observed in animals homozygous for the deficiency. However, markers of oxidative stress including protein carbonyl, 8-hydroxydeoxyguanosine, malondiadehyde and 4-hydroxyalkenal levels were unaltered with pyrazole treatment. Furthermore, CYP2A5 expression was not altered in G6PD-deficient mice treated with the pro-oxidant menadione whereas DNA, lipid, and protein markers of oxidative stress were significantly increased. The antioxidant polyethylene glycol-conjugated catalase, while decreasing oxidative stress in menadione-treated mice, did not prevent the induction of CYP2A5 by pyrazole. Finally, the ER stress marker protein, GRP78, was increased following pyrazole treatment in G6PD-deficient compared to wild-type mice. These findings do not support a central role for generalized cellular oxidative stress in the regulation of CYP2A5 and suggest that additional factors related to G6PD-deficiency, such as ER stress, may be involved.
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PMID:Expression of cytochrome P450 2A5 in a glucose-6-phosphate dehydrogenase-deficient mouse model of oxidative stress. 1806 88

Dapsone hypersensitivity syndrome (DHS) is a rare, but potentially life-threatening reaction to dapsone. We describe a 55-year-old Caucasian woman with normal glucose-6-phosphate dehydrogenase levels presenting with an extensive skin eruption, high-grade fever, pneumonitis and hepatitis, which occurred within 3 weeks after initiation of dapsone. In addition to supportive care, the patient was successfully treated with high-dose corticosteroids and antibiotics. The combination of high-grade fever, skin rash, lung and liver involvement made a dapsone hypersensitivity syndrome very likely.
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PMID:Dapsone hypersensitivity syndrome not related to G6PD deficiency. 2668 39


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