2,4-Dichlorophenol induces apoptosis in primary hepatocytes of grass carp (Ctenopharyngodon idella) through mitochondrial pathway

- 2,4-DCP could induce apoptosis in primary hepatocytes of grass carp.
- The apoptosis induced by 2,4-DCP is mediated by the mitochondrial pathway.
- 2,4-DCP-induced apoptosis was regulated by the Bax/Bcl-2 ratio.
- ALC, a mitochondria protecting agent, was used to ascertain the mechanism of 2,4-DCP induced apoptosis.

2,4-Dichlorophenol (2,4-DCP), a major type of chlorophenols, has been widely used to produce some herbicides and pharmaceuticals, yet due to its incomplete degradation and bioaccumulation characteristics, it is toxic to aquatic organisms. Apoptosis is one of the most severe outcomes of cell poisoning and injury. So far, the potential molecular mechanism of 2,4-DCP-induced apoptosis has not been reported. This study showed that 2,4-DCP significantly induced apoptosis in primary hepatocytes of grass carp (Ctenopharyngodon idella). 2,4-DCP exposure upregulated mRNA of caspase-3, reduced the mitochondrial membrane potential (Δψm), increased intracellular reactive oxygen species (ROS) and the Bax/Bcl-2 ratio, while protection of mitochondria with acetyl-l-carnitine hydrochloride (ALC) rescued 2,4-DCP-induced apoptosis, restored the Δψm and reduced the Bax/Bcl-2 ratio. Taken together, this is the first study that has identified that 2,4-DCP exposure induced apoptosis through the mitochondria-dependent pathway in primary hepatocytes of grass carp.