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백서에서 과량투여된 비타민A 대사에 미치는 비타민C의 영향

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 (The) influence of ascorbic acid on hypervitaminosis A in rats 
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[영문] The clinical and biochemical effect of vitamin A intoxication in rats has been extensively investigated. (Nerurkar and Saharabudka, 1956; Lois and Krause, 1959; Mathews and Beaten, 1963; Lucy and Dingle, 1965; Dua et al, 1966; Phillips, 1966; Misra, 1967) However, there have been only a few studies of mechanism of hypervitaminosis A and its detoxixation The Purpose of this study was investigation of the detoxication of vitamin A by ascorbic acid, and to seek a possible biochemical role for ascobic acid in the metabolism of vitamin A. Male albino rats weighing 123-150 g were used. The rats were fed a low protein rite diet. They were divided randomly into six groups of five rats each. They were fed various amounts of vitamin A alone, or vitamin A with vitamin C, or vitamin A with glucuronic acid (10 mg daily given as intraperitoneal injection) for 7, 14 or 24 days. The growth rate, the vitamin C content in serum and in the liver, kidney, brain, adrenal gland and intestine were determined for each group. Measurement were carried out by using the indophenol titrimetric method for vitamin C, the anti-monytrichloride method for vitamin A, and the carbazole reaction of Bowness for glucuronic acid. The results are summarized as follows: 1. Vitamin A intoxication was produced by feeding an average of 10,000 L.U. per day of the vitamin A for 7 days. 2. The maximum retention of vitamin A in the liver was about 240 mg% which indicates for limitation of the intestinal absorption of Vitamin A. 3. An excess dose of vitamin A reduced the serum and liver vitamin C content. 4. The administration of vitamin C improves the growth rate and increased the liver concentration of vitamin A in the hypervitaminosis A rat. 5. A possible role for vitamin C in hypervitaminosis A was related to its moblization into liver of vitamin A from extrahepatic areas. 6. Glucuronic acid, the precursor of vitamin C, improved the growth rate and increased the hepatic retention of vitamin A in the hypervitaminosis A rat.
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