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American Journal of Clinical Nutrition, Vol 24, 1238-1245, Copyright © 1971 by The American Society for Clinical Nutrition, Inc.

Lowered cholesterol catabolism in guinea pigs with chronic ascorbic acid deficiency

Emil Ginter Ph.D., C.Sc.1, Jozef Ccaronervencaron Ing.1, Rudolf Nemec Ing.1, and Ladislav Mikuscaron 1

1 From the Institute of Human Nutrition Research, Bratislava, Czechoslovakia

Chronic ascorbic acid deficiency was provoked in male guinea pigs by 14-day administration of a scorbutigenic diet followed by peroral administration of a maintenance dose of vitamin C (0.5 mg/animal per day). A control group was fed the same scorbutigenic diet supplemented perorally by 10 mg vitamin C/animal per day. The experiments lasted 5 to 7 months. The course of weight curves was not affected significantly by hypovitaminosis C.

Hypovitaminosis C caused a substantial decrease in vitamin C levels in tissues of guinea pigs and accumulation of total cholesterol in the liver. Hypovitaminosis C did not affect fecal excretion of 14C in the fraction of neutral sterols in guinea pigs injected intraperitoneally with cholesterol-4-14C, and it slightly decreased fecal excretion of 14C bile acids (during 20 days following administration of labeled cholesterol). Twenty days after application of cholesterol-4-14C more 14C was found in the blood serum and thoracic aorta of hypovitaminotic guinea pigs than in the control group. Three days after intraperitoneal injection of cholesterol-4-14C, less 14C in the fraction of bile acids was found in liver and gallbladder bile of hypovitaminotic guinea pigs than in the control group. Chronic hypovitaminosis C decreased significantly the oxidation of intraperitoneally injected cholesterol-26-14C to 14CO2 during 10 days following administration of labeled cholesterol.

The results prove that in guinea pigs with chronic ascorbic acid deficiency, the catabolism of cholesterol to bile acids is significantly decreased. A working hypothesis is postulated that ascorbic acid is required for cholesterol hydroxylation during its transformation to bile acids.




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Copyright © 1971 by The American Society for Nutrition