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Molecular medicine reports

Investigation of cadmium-induced apoptosis and the protective effect of N-acetylcysteine in BRL 3A cells.


PMID 27175572

Abstract

The aims of the present study were to investigate the effect of cadmium (Cd)‑induced apoptosis and determine the protective effect of N‑acetylcysteine (NAC) in BRLxa03A cells. The BRLxa03A cells were treated with 0, 10, 20 or 40xa0µmol/l cadmium acetate (CdAc2) for 12xa0h. Another two groups of cells were preincubated with 2xa0mmol/l NAC for 30xa0min, and then either incubated with 20xa0µmol/l CdAc2 for 12xa0h, or treated with NAC alone. The levels of apoptosis and mitochondrial membrane potential (ΔΨm) were measured using flow cytometry. Mitochondrial ultrastructural changes were detected using transmission electron microscopy. The protein levels of caspase‑3, caspase‑9, poly (ADP‑ribose) polymerase (PARP), caspase‑8, and Fas ligand (FasL) protein were measured using immunoblotting. As the dose of Cd increased, there was a significant increase in the apoptotic ratio, a significant decrease in ΔΨm, mitochondrial swelling and degeneration, and blurring, deformation and eventual collapse of the mitochondrial cristae. The protein levels of caspase‑3, caspase‑9 and PARP decreased, whereas the levels of cleaved caspase‑3, cleaved caspase‑9, cleaved caspase‑8 and FasL increased dose‑dependently in relation to Cd. NAC effectively inhibited these changes. Cd induced apoptosis through the mitochondrial and FasL pathways in the BRLxa03A cells, and NAC exerted a protective effect against Cd‑induced damage.

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