人类慢性氟中毒时红细胞谷胱甘肽代谢
Erythrocyte glutathione metabolism in human chronic fluoride toxicity.
作者信息
Saralakumari D, Rao P R
机构信息
Department of Biochemistry, Sri Krishnadevaraya University, Anantapur, India.
出版信息
Biochem Int. 1991 Jan;23(2):349-57.
Chronic exposure of humans to toxic levels of fluoride in drinking water resulted in significant increase in blood GSH content with significant increase in the activities of erythrocyte glutathione metabolising enzymes viz., gamma-glutamylcysteine synthetase (E.C. 6.3.2.2), gamma-glutamyltranspeptidase (E.C. 2.3.2.2), GST (E.C. 2.5.1.18), GSH-Px (E.C. 1.11.1.9) and GR (E.C. 1.6.4.2). The data suggested a form of adaptation on the part of the erythrocytes to counteract the oxidative stress in red blood cells of fluorotic patients.
人类长期接触饮用水中有毒水平的氟化物会导致血液中谷胱甘肽（GSH）含量显著增加，同时红细胞谷胱甘肽代谢酶的活性也显著增强，这些酶包括γ-谷氨酰半胱氨酸合成酶（E.C. 6.3.2.2）、γ-谷氨酰转肽酶（E.C. 2.3.2.2）、谷胱甘肽S-转移酶（GST，E.C. 2.5.1.18）、谷胱甘肽过氧化物酶（GSH-Px，E.C. 1.11.1.9）和谷胱甘肽还原酶（GR，E.C. 1.6.4.2）。数据表明，红细胞存在一种适应性机制，以抵消氟中毒患者红细胞中的氧化应激。
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