Abstract
Vitamin A deficiency is a serious nutritional deficiency disease. In most cases vitamin A deficiency is associated with protein malnutrition. Excess vitamin A cannot be transported for want of transport protein. We aimed to investigate the quantity of protein required in diet to protect excess vitamin A fed hepatotoxicity in rats. Normal and excess amount of vitamin A (4000 IU/kg and 40000 IU/kg)) with three different levels of dietary protein (6%, 18% and 30%) were administered orally for 30 consecutive days in rats. In low protein diet vitamin A level significantly increased in liver and decreased in plasma and, lipids level were found to be high in liver. Administration of excessive doses of vitamin A resulted in significant decrease in the levels of serum and liver RBP. Excess vitamin A in low protein state significantly induced oxidative stress in the liver, leading to increased serum levels of liver enzyme markers aminotransferases, total and direct bilirubin. Lipid remains in liver for want of transport protein and aggravates the formation of fatty liver. Both lipids and lipoprotein levels are also measured to assess the liver function in hypervitaminosis; a state where abnormally high storage levels of vitamins can lead to toxic symptoms.
Highlights
Vitamin A deficiency (VAD) has been recognized as a public-health issue in developing countries like India which has the highest clinical and sub clinical VAD among south Asian countries[1,2]
Same trend of results of Retinol Binding Protein (RBP) was seen in plasma in normal vitamin A treated rats but excess vitamin A treated rats showed reduced values compared to normal vitamin A treated rats
Insufficient protein in diet decreases the synthesis of Apo protein which in turn affects the synthesis of lipoprotein[20]
Summary
Vitamin A deficiency (VAD) has been recognized as a public-health issue in developing countries like India which has the highest clinical and sub clinical VAD among south Asian countries[1,2]. Studies indicated that persons suffering from protein malnutrition had decreased plasma level of vitamin A which was due to functional impairment in the hepatic release of vitamin A rather than body Vitamin A deficiency, reduced synthesis of Retinol Binding Protein (RBP), a transport protein for vitamin A, may be responsible for impairment in the hepatic release of vitamin A4. Retinol bound to RBP does not appear to manifest its surface active effects on biological membranes; rather the mode of transport of vitamin A may be an important determinant of the development of the manifestations of hypervitaminosis A5. Plasma lipoproteins may nonspecifically deliver vitamin A to biological membranes and leads to vitamin A toxicity[5]. Excess level of vitamin A is known to be hepatotoxic[7]. Marker enzymes AST, ALT and bilirubin were, measured to assess the hepatotoxicity
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