Aluminum neurotoxicity effects on intracellular Ca2+ homeostasis in the rat cerebral cortex

作者：Ren Rui; Zhang Yang; Zhang Xiaofeng; Wu Yanping; Zhang Dandan; Li Baixiang^*

来源：Neural Regeneration Research, 2010, 5(15): 1180-1184.

DOI：10.3969/j.issn.1673-5374.2010.15.011

• aluminum chloride
• Ca2+ concentration
• calcium homeostasis
• neurotoxicity

Studies have suggested that aluminum, a neurotoxic metal, is involved in the progression of neurodegenerative diseases. Previous studies have confirmed that aluminum influences intracellular Ca2+ homeostasis. However, it remains unclear whether aluminum increases or decreases intracellular Ca2+ concentrations. The present study demonstrated that Al3+ competitively binds to calmodulin (CaM), together with Ca2+, which resulted in loss of capacity of CaM to bind to Ca2+, leading to increased [Ca2+](i). Al3+ stimulated voltage-gated calcium channels on cell membranes, which allowed a small quantity of Ca2+ into the cells. Al3+ also promoted calcium release from organelles by stimulating L-Ca2+alpha(1c) to trigger calcium-induced calcium release. Although Al3+ upregulated expression of Na+/Ca2+ exchanger mRNA, increased levels of Ca2+ and Na+/Ca2+ exchanger did not maintain a normal Ca2+ balance. Al3+ resulted in disordered intracellular calcium homeostasis by affecting calcium channels, calcium buffering, and calcium expulsion.

• 出版日期2010-8-15
• 单位哈尔滨医科大学