Effect of dietary protein against excess vitamin A induced hepatotoxicity in rats

P. K. Karar, G. Agarwal, S. Agarwal, M. Devgan
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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.
膳食蛋白质对过量维生素A引起的大鼠肝毒性的影响
维生素A缺乏症是一种严重的营养缺乏症。在大多数情况下,维生素A缺乏与蛋白质营养不良有关。由于缺乏运输蛋白,过量的维生素A无法运输。本研究旨在探讨日粮中蛋白质需求量对大鼠过量维生素A致肝毒性的保护作用。在3种不同蛋白质水平(6%、18%和30%)的基础上,连续30天口服正常和过量维生素A (4000 IU/kg和40000 IU/kg)。低蛋白饲粮中肝脏维生素A水平显著升高,血浆维生素A水平显著降低,肝脏脂质水平较高。过量服用维生素A导致血清和肝脏RBP水平显著下降。低蛋白状态下过量维生素A显著诱导肝脏氧化应激,导致血清中肝酶标志物转氨酶、总胆红素和直接胆红素水平升高。由于缺乏转运蛋白,脂质滞留在肝脏中,加剧了脂肪肝的形成。还测量血脂和脂蛋白水平,以评估维生素过多症患者的肝功能;一种维生素储存水平异常高,可导致中毒症状的状态。
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