Influence of Cadmium on Nerve Cells of the Brain and the Neuroprotective Effect of Ca2+ Chelator and N-Acetyl-L-Cysteine

This paper discussed the mechanism of damage and apoptosis caused by cadmium (Cd) to the nerve cells of the brain and the influence of Cd on the mRNA expression of Bcl-2 and NO synthase (NOS) genes. In addition, the protective influence of BAPTA-AM and N-Acetyl-L-cysteine (NAC) to the nerve cells was analyzed. Experiments were conducted to measure cell survival and concentrations of Ca2+ and ROS under different concentration of cadmium acetate. The results showed that with the increase in the concentration of cadmium acetate, the survival of nerve cells declined dramatically, while the intercellular Ca2+ and ROS concentrations increased significantly. This indicated considerable damage caused by Cd to the nerve cells. The mRNA expression of Bcl-2 decreased significantly with the increase in Cd concentration, while the mRNA expression of Bax increased to varying degrees. At a higher concentration of Bcl-2, Bcl-2/Bax heterodimer was detected in nerve cells, which slowed down the apoptosis of the cells; at a low concentration of Bcl-2, Bcl-2/Bax homodimer was formed, thus accelerating the apoptosis of the nerve cells. Fluorescence staining showed that the nerve cells in the control group were intact, uniformly stained and had elliptical nuclei. For the experimental group, the nuclei in most cells shrank in size or even became fragmented due to the presence of Cd. BAPTA-AM reversed the sudden increase of Ca2+ concentration in the nerve cells treated by Cd, while NAC reduced cell apoptosis by inhibiting the breaking and mutation of the DNA strand in cells. Compared with BAPTA-AM, NAC exhibited less significant inhibitory effect on Cd-induced cell apoptosis and offered limited neuroprotective effect on nerve cells.