Abstract
A circadian cycle in hepatic UDP-glucuronic acid (UDP-GA) concentration was observed in mice that was essentially the reverse of those seen for hepatic glycogen and UDP-glucose. That is, hepatic UDP-GA levels were highest during the fasting period and lowest during the feeding period. However, there was no significant difference between the half-lives or the apparent rates of glucuronidation for either acetaminophen or salicylamide at 8 a.m. and 5 p.m. Therefore, the previously-reported circadian variation in acetaminophen toxicity is probably due to circadian variation in hepatic glutathione levels rather than in hepatic glucuronidation capacity.
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