ToxSci Advance Access originally published online on March 3, 2008
Toxicological Sciences 2008 103(2):354-361; doi:10.1093/toxsci/kfn046
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Neurotoxicological Evaluation of Long-Term Lanthanum Chloride Exposure in Rats
* Key Laboratory of Nuclear Analytical Techniques and Lab for Bio-Environmental Health Sciences of Nanoscale Materials, Institute of High Energy Physics, The Chinese Academy of Sciences, Beijing 100049, China
Graduate University of the Chinese Academy of Sciences, Beijing 100049, China
Institute of Nuclear Technology, Shenzhen University, Shenzhen 518060, China
1 To whom correspondence should be addressed at Key Laboratory of Nuclear Analytical Techniques, Institute of High Energy Physics, P.O. Box 918, Beijing 100049, China. Fax: +86-10-88235294. E-mail: zhangzhy{at}ihep.ac.cn.
Received December 30, 2007; accepted February 27, 2008
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Abstract |
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With their widespread application in industry, agriculture, medicine, and daily life, rare earth elements (REEs) are widely used in various fields and eventually accumulated in human body. Therefore, understanding the effects of REEs on health has become more and more important. In this work, the neurotoxicity of lanthanum (La) was evaluated. Wistar rats were exposed to lanthanum chloride through oral administration at 0, 0.1, 2, and 40 mg/kg doses from gestation day 0 through 6 months of age. Experiments were carried out to reveal the effects of La exposure on brain functions from four aspects including behavioral performance, [Ca2+]i level and the activity of Ca2+-ATPase (adenosine triphosphatase) in hippocampal cells, oxidative stress, and Nissl staining. Adverse effects were observed in 2 and 40 mg/kg dose groups and increased with dose. Morris water maze test showed that La exposure at 2 and 40 mg/kg could significantly impair the behavioral performance. (The preference for the target quadrant decreased by 16.6% and 19.4% versus control, respectively.) The neurotoxicological consequences demonstrated that the alteration in homeostasis of [Ca2+]i/Ca2+-ATPase (the ratio of [Ca2+]i vs. Ca2+-ATPase activity increased by 44% in rats of 40 mg/kg group), the inhibition to activities of antioxidant enzymes, and the subsequent cell damage (18% and 23% cell loss in CA3 subregion of rats in 2 and 40 mg/kg group, respectively) might be involved in the neurological adverse effects of REEs exposure.
Key Words: intracellular free calcium; lanthanum; Morris water maze; Nissl staining; oxidative stress; rare earth elements.