Chakraborty D, Bhattacharyya A, Chatterjee J, Chatterjee K, Sen A, Chatterjee S, Majumdar K, Chatterjee G C
Int J Vitam Nutr Res. 1978;48(1):22-31.
The effects of chronic polychlorinated biphenyl (PCB) compound toxicity on L-ascorbic acid metabolism in rats have been studied. PCB treatment brought about a depression in the activities of the enzymes L-gluonolactone oxidase and dehydroascorbatase along with an increased tissue levels and urinary excretion of L-ascorbic acid. PCB toxicity drastically disturbed the normal histological pattern of the liver cells and also significantly changed the hepatic lipid composition. L-ascorbic acid supplementation to the toxicated group of animals, although could not prevent the growth retardative effect of PCB, could afford a definite protection against the enzyme activity alterations and histological changes as caused by PCB toxicity.
已对慢性多氯联苯(PCB)化合物毒性对大鼠L-抗坏血酸代谢的影响进行了研究。PCB处理导致L-葡萄糖酸内酯氧化酶和脱氢抗坏血酸酶的活性降低,同时L-抗坏血酸的组织水平和尿排泄增加。PCB毒性严重扰乱了肝细胞的正常组织学模式,也显著改变了肝脏脂质组成。给中毒动物组补充L-抗坏血酸,虽然不能预防PCB的生长抑制作用,但可以对PCB毒性引起的酶活性改变和组织学变化提供一定的保护。