作者: K E Hill , R F Burk
DOI: 10.1016/S0021-9258(18)33874-2
关键词: Internal medicine 、 Toxicity 、 Vitamin E deficiency 、 Selenium deficiency 、 Endocrinology 、 Incubation 、 Drug metabolism 、 Glutathione 、 Biology 、 Vitamin 、 Cysteine metabolism
摘要: Selenium deficiency and vitamin E both affect xenobiotic metabolism toxicity. In addition, selenium causes changes in the activity of some glutathione-requiring enzymes. We have studied glutathione isolated hepatocytes from selenium-deficient, E-deficient, control rats. Cell viability, as measured by trypan blue exclusion, was comparable for all groups during 5-h incubation. Freshly had same concentration regardless diet group. During incubation, however, selenium-deficient rose to 1.4 times that hepatocytes. The cells also released twice much into incubation medium did cells. Total (intracellular plus extracellular) flask increased 47.7 +/- 8.9 152 16.5 nmol/10(6) over 5 h compared with an increase 46.7 7.1 92.0 17.4 11.7 79.5 24.9 E-deficient This overall suggested synthesis accelerated deficiency. gamma-glutamylcysteine synthetase great liver supernatant (105,000 X g) or g). Hemoglobin-free perfused livers were used determine form its route. Selenium-deficient 4 GSH caval perfusate livers. Plasma rats found be 2-fold rats, suggesting release is vivo phenomenon associated