Department of Anatomy, All India Institute of Medical Sciences, New Delhi-110029, India.
Toxicol Mech Methods. 2011 Mar;21(3):216-24. doi: 10.3109/15376516.2010.538751. Epub 2010 Dec 16.
The present work focussed on the effect of exogenous α-lipoic acid (ALA) administration on retention memory and oxidative stress markers in the hippocampus subsequent to early post-natal exposure of rat pups to sodium arsenite (NaAsO(2)). Wistar rat pups were divided into the control groups receiving either no treatment (Ia) or distilled water by intraperitoneal route (i.p.) (Ib) and the experimental groups receiving either NaAsO(2) alone (1.5 and 2.0 mg/kg body wt.) (IIa, IIb) or NaAsO(2) (1.5 and 2.0 mg/kg body wt.) followed by ALA (70 mg/kg body wt.) (IIIa, IIIb) (i.p.) from post-natal day (PND) 4-15. The initial and retention transfer latency (ITL and RTL) was determined on PND 14 and 15 using elevated plus maze. The animals were sacrificed by cervical decapitation (PND 16) and the brains were obtained. The dissected out hippocampus was processed for estimation of oxidative stress markers, glutathione (GSH), and superoxide dismutase (SOD). NaAsO(2) exposure resulted in longer RTL in animal groups IIa and IIb, thereby suggestive of arsenic-induced impairment in retention memory. RTL was significantly shorter in animal groups (IIIa, IIIb) receiving ALA following NaAsO(2), thereby suggestive of improvement in retention memory. GSH and SOD levels were significantly decreased in animals receiving NaAsO(2) alone as against group Ib and administration of ALA following NaAsO(2) increased the levels of hippocampal GSH and SOD. These observations are suggestive of the role of exogenous ALA in ameliorating the adverse effects induced by NaAsO(2) exposure of rat pups on retention memory and oxidative stress markers.
本研究集中探讨了外源性α-硫辛酸(ALA)给药对新生期大鼠暴露于亚砷酸钠(NaAsO2)后海马体保留记忆和氧化应激标志物的影响。Wistar 幼鼠分为对照组,分别接受腹腔注射生理盐水(Ia)或蒸馏水(Ib),实验组分别接受亚砷酸钠(1.5 和 2.0mg/kg 体重)(IIa、IIb)或亚砷酸钠(1.5 和 2.0mg/kg 体重)后腹腔注射 ALA(70mg/kg 体重)(IIIa、IIIb)(从出生后第 4 天到第 15 天)。在第 14 天和第 15 天使用高架十字迷宫测定初始和保留转移潜伏期(ITL 和 RTL)。动物于第 16 天断头处死,取脑。取出海马体进行氧化应激标志物谷胱甘肽(GSH)和超氧化物歧化酶(SOD)的测定。亚砷酸钠暴露导致 IIa 和 IIb 组动物 RTL 延长,提示砷诱导保留记忆损伤。在接受亚砷酸钠后给予 ALA 的 IIIa 和 IIIb 组动物 RTL 明显缩短,提示保留记忆得到改善。单独接受亚砷酸钠的动物 GSH 和 SOD 水平显著降低,而接受亚砷酸钠后给予 ALA 的动物海马体 GSH 和 SOD 水平升高。这些观察结果提示外源性 ALA 可减轻新生期大鼠暴露于亚砷酸钠对保留记忆和氧化应激标志物的不良影响。