Seymen Hakki Oktay, Civelek Sabiha, Seven Arzu, Yigit Gunnur, Hatemi Husrev, Burcak Gulden
Barbaros mah. Sedef Sok. Onur Sitesi, 9/23 Uskudar, Istanbul, Turkey 81150.
Yonsei Med J. 2004 Jun 30;45(3):413-8. doi: 10.3349/ymj.2004.45.3.413.
This study was designed to investigate the effects of iron supplementation on the parameters of oxidative stress in the skeletal muscle tissue of hyperthyroidism induced rats. Hyperthyroidism was found to cause an increase in thiobarbituric acid-reactive substances (TBARS) and copper zinc superoxide dismutase (Cu, Zn SOD) activity, but decreases in the glutathione-peroxidase (GSH Px) activity and glutathione (GSH). Iron supplementation caused an increase in TBARS and a decrease in GSH. Iron supplementation in hyperthyroid rats attenuated the hyperthyroid state, but lowered the plasma ferritin level, which is considered an indicator of thyroid hormone action. Iron supplementation caused no additional increase in the TBARS in hyperthyroid rats, ameliorated the decrease in GSH content and abolished the induction of Cu, Zn SOD. Our findings suggested no increase, but a decrease, in the risk of oxidative stress in iron supplemented hyperthyroid rats. Whether supplementation of iron would have similar effects in humans should be further investigated in clinical studies.
本研究旨在探讨补充铁剂对甲状腺功能亢进诱导的大鼠骨骼肌组织氧化应激参数的影响。结果发现,甲状腺功能亢进会导致硫代巴比妥酸反应性物质(TBARS)增加和铜锌超氧化物歧化酶(Cu, Zn SOD)活性升高,但谷胱甘肽过氧化物酶(GSH Px)活性和谷胱甘肽(GSH)降低。补充铁剂会使TBARS增加,GSH减少。补充铁剂可使甲状腺功能亢进大鼠的甲状腺功能亢进状态得到缓解,但会降低血浆铁蛋白水平,而血浆铁蛋白水平被认为是甲状腺激素作用的一个指标。补充铁剂不会使甲状腺功能亢进大鼠的TBARS进一步增加,可改善GSH含量的降低,并消除Cu, Zn SOD的诱导。我们的研究结果表明,补充铁剂的甲状腺功能亢进大鼠氧化应激风险没有增加,反而降低。补充铁剂在人类中是否会有类似作用,应在临床研究中进一步探讨。