Quantification of lowered cholesterol oxidation in guinea pigs with latent vitamin C deficiency

Fifty‐two male guinea pigs fed on a scorbutigenic diet were divided into a control group (10 mg ascorbicacid per animal per day) and a group with latent vitamin C deficiency (2 weeks on the scorbutigenic diet only, followed by a maintaining dose of 0.5 mg ascorbic acid per animal per day). After 13 weeks, 26‐14C‐cholesterol was administered intraperitoneally to all the animals, in which the14C excretion in the expired CO2 and the urine and cholesterol specific activity in the blood serum and liver were then studied at intervals of 24 hr and 1, 3, 5, 7, 9 and 11 weeks. The ascorbic acid concentration in the liver and spleen of the control animals was five times higher than in vitain C‐deficient animals. The total cholesterol concentration in serum and liver was significantly higher in the vitamin C‐deficient guinea pigs. A two‐pool analysis of the disappearance curves of serum cholesterol specific activity showed that the size of the cholesterol pool A (blood and tissues with rapid cholesterol exchange) was greater in the vitamin C‐deficient animals. The rate of the transformation of cholesterol to bile acids was estimated as the ratio of14CO2 expired to liver cholesterol specific activity. Latent vitamin C deficiency caused significant slowing down of this process (controls: 11.8±0.6; vitamin C deficiency: 8.3±0.4 mg/24 r/500 g w/w). A significant correlation between the liver ascorbic acid concentration and the rate of cholesterol transformation to bile acids was found. The results demonstrate that ascorbic acid is necessary for a normal course of cholesterol catabolism. In latent vitamin C deficiency, the rate of cholesterol catabolism slows down and cholesterol consequently accumulates in the blood and liver of vitamin C‐deficient guinea pigs.