Cytoprotective effects of triphlorethol-A against formaldehyde-induced oxidative damage and apoptosis: role of mitochondria-mediated caspase-dependent pathway.

Journal of toxicology and environmental health. Part A

PubMedID: 20954074

Zhang R, Lee IK, Kang KA, Piao MJ, Kim KC, Kim BJ, Lee NH, Choi JY, Choi J, Hyun JW. Cytoprotective effects of triphlorethol-A against formaldehyde-induced oxidative damage and apoptosis: role of mitochondria-mediated caspase-dependent pathway. J Toxicol Environ Health Part A. 2010;73(21-22):1477-89.
The toxicity of formaldehyde (HCHO) has been attributed to its ability to form adducts with DNA and proteins. Triphlorethol-A, derived from Ecklonia cava, was reported to exert a cytoprotective effect against oxidative stress damage via an antioxidant mechanism. The aim of this study was to examine the mechanisms underlying the triphlorethol-A ability to protect Chinese hamster lung fibroblast (V79-4) cells against HCHO-induced damage. Triphlorethol-A significantly decreased the HCHO-induced intracellular reactive oxygen species (ROS) production. Triphlorethol-A prevented increased cell damage induced by HCHO via inhibition of mitochondria-mediated caspase-dependent apoptosis pathway. Triphlorethol-A diminished HCHO-induced mitochondrial dysfunction, including loss of mitochondrial membrane action potential (??) and adenosine triphosphate (ATP) depletion. Furthermore, the anti-apoptotic effect of triphlorethol-A was exerted through inhibition of c-Jun NH(2)-terminal kinase (JNK), which was enhanced by HCHO. Our data indicate that triphlorethol-A exerts a cytoprotective effect in V79-4 cells against HCHO-induced oxidative stress by inhibiting the mitochondria-mediated caspase-dependent apoptotic pathway.