Aluminum neurotoxicity effects on intracellular Ca~(2+) homeostasis in the rat cerebral cortex

来源 :Neural Regeneration Research | 被引量 : 0次 | 上传用户:abczxhzxh
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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+ α1c 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. Studies have suggested that aluminum, a neurotoxic metal, is involved in the progression of neurodegenerative diseases. Presvious studies have confirmed that aluminum affects intracellular Ca2 + homeostasis. However, it remains unclear whether aluminum increases or decreases intracellular Ca2 + concentrations. The present study demonstrates 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 + α1c to trigger calcium-induced calcium release. 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 cal cium expulsion.
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