Mercuric chloride effects on adult rat oval cells-induced apoptosis

Abstract

In the present investigation, the toxicity of mercuric chloride (HgCl 2 ) was evaluated in adult oval cells isolated from rat utilizing the 2-acetylaminofluorene/partial hepatectomy technique. Isolated oval cells were incubated with 5 mM of HgCl 2 for 8 hr to elucidate in vitro cytotoxic responses. Recently, autophagic cell death was found in rat hepatocytes in vitro within 30 min of incubation with 5 mM of mercury (Hg) which triggered apoptosis and necroptosis in a time-dependent manner. Nuclear degradation occurred within 30 min of incubation and progressed with time until 8 hr. Apoptosis evidenced by activation of caspase-dependent pathway between 30 min to 8 hr of incubation was mediated via interchange of death domain signaling pathways. Receptor-interacting protein played a positive role to modulate the death domain receptors in the scenario of apoptotic death of oval cells until 6 hr. Autophagic marker proteins ATG12 and LC3B exerted a significant role in triggering apoptosis in 5 mM Hg-treated oval cells. No apparent expression of apoptosis-inducing-factor (AIF) and HMGB1 indicated absence of caspase-independent apoptosis and necrosis in the rat oval cells between 30 min and 8 hr. Thus a low concentration of Hg modulates programmed cell death in adult rat oval cells by altering expression of proteins involved in the molecular mechanisms of cellular functions.

CDP‐choline circumvents mercury‐induced mitochondrial damage and renal dysfunction

“…Previous reports indicate that permeability transition pore opening underlies the progression of the apoptotic mitochondrial pathway, providing a mechanism for cytochrome c detachment from the cytosol side of the inner membrane (Liu et al, ). Additionally, apoptotic cell death has been involved in Hg 2+ toxicity (Chatterjee et al, ; Vergílio et al, ). In consequence, we explored the possibility that CDP‐choline could protect against cytochrome c detachment after Hg 2+ ‐induced oxidative stress.…”