Abstract
1. ODS-od/ od rats (ODS rats) hereditarily unable to synthesize ascorbic acid have no hepatic L-gulonolactone oxidase activity. In ODS rats, the dietary requirement of ascorbic acid to maintain normal growth and to prevent scurvy is about 300 mg per kilogram diet. 2. In normal rats able to synthesize ascorbic acid, the administration of several types of xenobiotics caused a marked increase in urinary excretion of ascorbic acid and in the concentrations (of ascorbic acid) in various tissues. The administration of xenobiotics increased the biosynthesis of ascorbic acid in liver, and accelerated concomitantly the turnover of ascorbic acid in body. In guinea pigs unable to synthesize ascorbic acid, the dietary requirement of ascorbic acid was increased severalfold for improving the growth depression and the mortality due to xenobiotics, such as PCB. In ODS rats, the dietary requirement of ascorbic acid was increased several-fold by the administration of xenobiotics for the maximum induction of hepatic drug-metabolizing enzymes. 3. Acute ascorbic acid deficiency caused a hypercholesterolemia and an elevation of hepatic concentration of cholesterol due to the deppression of bile acid synthesis in ODS rats fed a cholesterol-containing diet or a PCB-containing diet. Moreover, the concentration of LDL-cholesterol in serum was higher in ascorbic acid-deficient ODS rats than in ODS rats fed a diet supplemented with an appropriate amount of ascorbic acid.
