Laboratoire de Physiologie Animale, Faculté des Sciences de Bizerte, 7021 Jarzouna, Tunisia; Laboratoire de Stress Oxydant, Département de Biologie Intégrée, CHU-Grenoble, France; Commissariat d' Energie Atomique DRFMC/SCIB, Laboratoire des Lésions des Acides Nucléiques, Grenoble, France.
Environ Toxicol Pharmacol. 2007 Mar;23(2):193-7. doi: 10.1016/j.etap.2006.09.001. Epub 2006 Sep 9.
The present study was undertaken to find out the effect of zinc supplementation on the antioxidant enzymatic system, lipid peroxidation and DNA oxidation in liver and kidney of static magnetic field (SMF) exposed rats. The exposure of rats to SMF (128mT, 1h/day during 30 consecutive days) decreased the activities of glutathione peroxidase (GPx), catalase (CAT) and the superoxide dismutase (SOD) in liver and kidney. By contrast, sub-chronic exposure to SMF increased the malondialdehyde (MDA) concentration in liver and kidney. Our results revealed an increase of the 8-oxo-7,8-dihydro-2'-desoxyguanosine (8-oxodGuo) in kidney of SMF-exposed rats. However, this biomarker of DNA oxidation remained unchanged in liver. Zinc supplementation (ZnCl(2), 40mg/l, per os) in SMF-exposed rats restored the activities of GPx, CAT and SOD in liver to those of control group. However, only CAT activity was restored in kidney. Moreover, zinc administration was able to bring down the elevated levels of MDA in the liver but not in the kidney. Interestingly, zinc supplementation attenuated DNA oxidation induced by SMF in kidney to the control level. Our investigations suggested that zinc supplementation minimizes oxidative damage induced by SMF in rat tissues.
本研究旨在探讨补锌对静磁场（SMF）暴露大鼠肝肾功能抗氧化酶系统、脂质过氧化和 DNA 氧化的影响。结果表明，SMF（128mT，每天 1 小时，连续 30 天）暴露降低了大鼠肝肾功能中谷胱甘肽过氧化物酶（GPx）、过氧化氢酶（CAT）和超氧化物歧化酶（SOD）的活性；相反，亚慢性 SMF 暴露增加了肝肾功能中丙二醛（MDA）的浓度。SMF 暴露大鼠肾脏中 8-氧代-7,8-二氢-2′-脱氧鸟苷（8-oxodGuo）的含量增加，但肝脏中这种 DNA 氧化的生物标志物没有变化。SMF 暴露大鼠补锌（ZnCl2，40mg/L，口服）可使肝组织中 GPx、CAT 和 SOD 的活性恢复到对照组水平，但仅使肾组织中 CAT 活性恢复正常。此外，锌处理可降低肝组织中升高的 MDA 水平，但对肾组织无效。有趣的是，补锌可将 SMF 诱导的肾组织 DNA 氧化降低至对照组水平。我们的研究表明，补锌可减轻 SMF 诱导的大鼠组织氧化损伤。
