AlCl₃induces lymphocyte apoptosis in rats through the mitochondria-caspase dependent pathway

Abstract

To investigate apoptosis mechanisms in lymphocytes induced by aluminum trichloride (AlCl3) through the mitochondria-caspase dependent pathway, the spleen lymphocytes of rats were cultured with RPMI-1640 medium and exposed to AlCl3·6H2O in the final concentrations of 0 (control group, CG), 0.3 (low-dose group, LG), 0.6 (mid-dose group, MG), and 1.2 (high-dose group, HG) mmol·L(-1) for 24 h, respectively. Mitochondrial transmembrane potential (ΔΨm), cytochrome C (Cyt C) protein expression in cytoplasm, Caspase-3 and Caspase-9 activity, Bcl-2, Bax, Caspase-3 and Caspase-9 mRNA expressions, DNA ladder and lymphocytes apoptosis index were detected. The results showed that Cyt C protein expression in cytoplasm, Caspase-3 and Caspase-9 activity, Bcl-2, Bax, Caspase-3 and Caspase-9 mRNA expressions, the ratio of Bcl-2 and Bax mRNA expression, lymphocytes apoptosis index increased, while ΔΨm decreased in the AlCl3-treated groups compared with those in CG. The results indicate that AlCl3 induces lymphocyte apoptosis in rats through the mitochondria-caspase dependent pathway.

The Protective Effects of Melatonin on Aluminum-Induced Hepatotoxicity and Nephrotoxicity in Rats

“…Thus, AlCl3 may cause hepatic and renal apoptosis by reducing Bcl-2 expression. Our results are in agreement with those of Li et al [ 45 ].…”

Neuroprotective efficacy of the bacterial metabolite, prodigiosin, against aluminium chloride‐induced neurochemical alternations associated with Alzheimer's disease murine model: Involvement of Nrf2/HO‐1/NF‐κB signaling

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Glycosylation of anthocyanins enhances the apoptosis of colon cancer cells by handicapping energy metabolism

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