Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.5.2 (NQO1)
 6,196 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Modulation of biochemical markers by ascorbic acid was investigated in mice to which benzanthrone (BA) was applied topically (150 nmol/mouse) twice a week for 34 wk. After BA exposure without ascorbic acid, in the skin there were significant decreases in the activities of aryl hydrocarbon hydroxylase (AHH; 38% decrease relative to controls) and ethoxyresorufin-O-deethylase (EROD; 39%), and enhancement of the activities of quinone reductase (41% increase), tyrosinase (82%) and histidine decarboxylase (HDC; 190%). BA exposure also caused significant inhibition of hepatic AHH, EROD and glutathione-S-transferase activities, with concomitant increases in the activities of histidase (52%) and HDC (58%). Ascorbic acid given orally (5 mg/mouse) or topically (1 mg/mouse) twice weekly for 34 wk to BA-treated mice resulted in substantial protection against the effects of BA on these enzyme markers in both the skin and the liver. These results suggest that ascorbic acid could be useful in preventing the biochemical and toxicological manifestations caused by BA in laboratory animals.
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PMID:Modulation by ascorbic acid of the cutaneous and hepatic biochemical effects induced by topically applied benzanthrone in mice. 834 29