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 BRL 3A cells. The BRL 3A cells were treated with 0, 10, 20 or 40 µmol/l cadmium acetate (CdAc2) for 12 h. Another two groups of cells were preincubated with 2 mmol/l NAC for 30 min, and then either incubated with 20 µmol/l CdAc2 for 12 h, 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 BRL 3A cells, and NAC exerted a protective effect against Cd‑induced damage.