Department of Zoology and Biotechnology, Utkal University, Bhubaneswar, India.
Cell Biochem Funct. 2010 Mar;28(2):126-34. doi: 10.1002/cbf.1631.
Liver is a major target organ for thyroid hormone. The objective of the present study was to investigate temporal regulation of mitochondrial glutathione and protein-bound thiol redox status in hyperthyroid liver. Mitochondria were isolated from control and hyperthyroid rat liver tissues at different time intervals, i.e., 24, 72, and 120 h following treatment, and sub-fractionated into sub-mitochondrial particles (SMPs) and matrix fractions. Increased prooxidant levels were indicative of oxidative stress in hyperthyroid mitochondria. Sensitivity to membrane lipid peroxidation (LPx) was maximal after 24 h, which subsided with time. Oxidative damage to proteins was evident as high carbonylation after 72 h; thiol residue damage was an early phenomenon. Reduced and oxidized glutathione (GSH and GSSG) pools of mitochondria were progressively depleted, thereby, impairing matrix antioxidant capacity. However, adaptations to withstand oxidative challenge were elicited in both SMPs and matrix fractions over the long term. It is concluded that maintenance of appropriate intra-mitochondrial glutathione and protein-bound thiol redox status could be instrumental in attenuating thyroid hormone-induced oxidative stress.
肝脏是甲状腺激素的主要靶器官。本研究的目的是研究甲状腺功能亢进时肝脏线粒体谷胱甘肽和蛋白结合硫醇氧化还原状态的时间调节。分别在治疗后 24、72 和 120 小时从对照和甲状腺功能亢进大鼠肝组织中分离线粒体，并进行亚线粒体颗粒 (SMP) 和基质部分的亚分离。促氧化剂水平的增加表明甲状腺功能亢进的线粒体存在氧化应激。在 24 小时后，对膜脂质过氧化 (LPx) 的敏感性最大，随着时间的推移而减弱。72 小时后，蛋白质的氧化损伤表现为高羰基化；硫醇残基损伤是早期现象。线粒体的还原型和氧化型谷胱甘肽 (GSH 和 GSSG) 池逐渐耗尽，从而损害了基质的抗氧化能力。然而，在长期内，SMP 和基质部分都对氧化应激产生了适应。结论是，维持适当的线粒体谷胱甘肽和蛋白结合硫醇氧化还原状态有助于减轻甲状腺激素引起的氧化应激。
