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The paper investigates Cd2+ neurotoxicity over time by simulating Cd2+ contaminated water. Li et al. (2022) suggest that chronic Cd exposure resulted in neuron death in the hippocampus rather than a modification in neurogenesis. Furthermore, apoptosis of hippocampal neurons increased with time, as demonstrated by a rise in the number of apoptotic neurons from three to thirty months. To see if chronic Cd toxicity has the same influence on neurogenesis as severe Cd toxicity, the authors looked for newborn cells and neuronal progenitors in the hippocampus. Essentially, there was no considerable variability in the proportion of developing cells and neural progenitors between Cd-drinking mice and the comparable control group; neurogenesis was solely impacted by age.
The crucial discovery was made on essential compounds implicated in Cd toxicity, ranging from autophagy to apoptosis. According to Li et al. (2022), the phosphorylation level of p53, a tumor suppressor gene, rose dramatically between 18 and 30 months after Cd2+ deposition. Nonetheless, Sirt1, a sirtuin family member, did not alter substantially between time points in the Cd2+ groups, but it grew with time in the control group. Acetyl-p53 reduced over time in the Cd2+ group while increasing in the control group, demonstrating that Sirt1 prevents cells from apoptosis by neutralizing p53 under stressors. Furthermore, the authors emphasize that caspase-3 and Bax, both apoptotic indicators, were activated and enhanced by Cd2+ buildup from three to eighteen months.
Finally, P53 facilitates the switch from autophagy to apoptosis via JNK and Sirt1. The results showed that phosphorylation of p53 (Ser46) and acetylation of p53 were significantly reduced and that there was a dosage impact on the levels of phosphorylation and acetylation of p53 (Li et al., 2022). In addition to Sirt1 and JNK antagonists, the effect of chloroquine, an autophagy inhibitor, on Cd2+-treated primary neurons was investigated. The findings demonstrate that chloroquine has a comparable impact on neuronal autophagy and apoptosis as nicotinamide.
Reference
Li, T., Dong, S., He, J., Yang, J., Li, W., Li, S., Li, J., Du, X., Hou, Z., Li, L., Huang, Z., & Sun, T. (2022). Apoptosis, rather than neurogenesis, induces significant hippocampaldependent learning and memory impairment in chronic low Cd2+ exposure. Environmental Toxicology, 37(4), 814-824.
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