Analytical Toxicology and Mineral Metabolism Unit, Institute for Medical Research and Occupational Health, Ksaverska cesta 2, P.O. Box 291, HR-10001 Zagreb, Croatia.
Biol Trace Elem Res. 2011 Sep;142(3):611-22. doi: 10.1007/s12011-010-8775-1. Epub 2010 Jul 21.
Since there are no data about the protective role of selenium (Se) against cadmium (Cd)-induced oxidative damage in early life, we studied the effect of Se supplementation on antioxidative enzyme activity and lipid peroxidation (through thiobarbituric acid reactive substances; TBARS) in suckling Wistar rats exposed to Cd. Treated animals received either Se alone for 9 days (8 μmol, i.e., 0.6 mg Se as Na(2)SeO(3) kg(-1) b.w., daily, orally; Se group), Cd alone for 5 days (8 μmol, i.e., 0.9 mg Cd as CdCl(2) kg(-1) b.w., daily, orally; Cd group), or pre-treatment with Se for 4 days and then co-treatment with Cd for the following 5 days (Se + Cd group). Our results showed that selenium supplementation, with and without Cd, increased SOD activity in the brain and kidney, but not in the liver and GSH-Px activity across all tissues compared to control rats receiving distilled water. Relative to the Cd group, Se + Cd group had higher kidney and brain SOD and GSH-Px activity (but not the liver), while in the liver caused increased and in the brain decreased TBARS level. These results suggest that Se stimulates antioxidative enzymes in immature kidney and brain of Cd-exposed rats and could protect against oxidative damage.
由于目前尚无关于硒（Se）对镉（Cd）诱导的早期生命氧化损伤的保护作用的数据，我们研究了补充硒对暴露于 Cd 的哺乳期 Wistar 大鼠抗氧化酶活性和脂质过氧化（通过硫代巴比妥酸反应物质；TBARS）的影响。处理后的动物连续 9 天接受单独 Se 处理（8 μmol，即 0.6 mg Se 作为 Na(2)SeO(3) kg(-1) b.w.，每日口服；Se 组）、连续 5 天接受单独 Cd 处理（8 μmol，即 0.9 mg Cd 作为 CdCl(2) kg(-1) b.w.，每日口服；Cd 组），或先接受 4 天 Se 预处理，然后再与 Cd 共同处理 5 天（Se + Cd 组）。我们的结果表明，与仅接受 Cd 处理的大鼠相比，Se 补充剂（单独或与 Cd 一起）增加了大脑和肾脏中的 SOD 活性，但对肝脏和 GSH-Px 活性没有影响，在所有组织中均如此。与 Cd 组相比，Se + Cd 组的肾脏和大脑 SOD 和 GSH-Px 活性更高（但肝脏除外），而肝脏中的 TBARS 水平升高，大脑中的 TBARS 水平降低。这些结果表明，Se 刺激了暴露于 Cd 的幼鼠未成熟肾脏和大脑中的抗氧化酶，并能防止氧化损伤。
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