Iron overload can induce reactive oxygen species (ROS) burst and liver damage. Taurine can reduce ROS production and ameliorate liver injury caused by iron overload; however, the underlying molecular mechanism remains elusive. Herein, L02 cells treated with 120 M iron dextran for 48 h showed marked oxidative stress damage and significantly increased apoptosis. Taurine protected hepatocytes by stabilizing mitochondrial membranes and resisting oxidative stress damage caused by iron overload. However, transfection with siRNA Bcl-2 virus abrogated the observed protective effects. Following treatment with taurine, B cell lymphoma-2 (Bcl-2) could inhibit the opening of the mitochondrial permeability transition pore (mPTP), subsequently stabilizing the mitochondrial membrane potential by interacting with voltage-dependent anion channel 1 (VDAC1) of mPTP. The present study is the first to clarify the mechanism underlying taurine-afforded hepatocyte protection against iron overload-induced oxidative stress via Bcl-2-mediated inhibition of mPTP opening and the antiapoptotic pathway.
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| http://dx.doi.org/10.1155/2022/4135752 | DOI Listing |
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