Mono-2-ethylhexyl phthalate induced loss of mitochondrial membrane potential and activation of Caspase3 in HepG2 cells

L02 and HepG2 cells were exposed to mono-(2-ethylhexyl) phthalate (MEHP) at concentrations of 6.25–100 μM. After 48 h treatment, MEHP decreased HepG2 cell viability in a concentration-dependent manner and L02 cell viability in the 50 and 100 μM groups (p < 0.01). Furthermore, at 24 and 48 h after treatment, MEHP decreased the glutathione levels of HepG2 cells in all treatment groups and in the ΔΨm in L02 and HepG2 cells with MEHP ≥ 25 μM (p < 0.05 or p < 0.01). At 24 h after treatment, MEHP induced activation of caspase3 in all treated HepG2 and L02 cells (p < 0.05 or p < 0.01) except the 100 μM MEHP treatment group. The increase in the Bax to Bcl-2 ratio suggests that Bcl-2 family involved in the control of MEHP-induced apoptosis in these two cell types. The data suggest that MEHP could induce apoptosis of HepG2 cells through mitochondria- and caspase3-dependent pathways.

► The manuscript firstly reported about cytotoxicity of mono-2-ethylhexyl phthalate in HepG2 and L02 cells. ► Mono-2-ethylhexyl phthalate firstly caused loss of mitochondrial membrane potential in HepG2 and L02 cells. ► Mono-2-ethylhexyl phthalate firstly induced casepase 3 activity in HepG2 and L02 cells. ► Mono-2-ethylhexyl phthalate could induce apoptosis of HepG2 cells via mitochondria- and caspase 3-dependent pathways.