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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 (Δψ) and adenosine triphosphate (ATP) depletion. Furthermore, the anti-apoptotic effect of triphlorethol-A was exerted through inhibition of c-Jun NH2-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. [ABSTRACT FROM AUTHOR]

The protective effect of Castanopsis cuspidate var. sieboldii was examined on H2O2-induced cell damage. The ethanol extract of Castanopsis cuspidate was found to scavenge 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical and reduce intracellular reactive oxygen species (ROS) generation, and thus prevent lipid peroxidation and cellular DNA damage induced by H2O2. As a result, Castanopsis extract reduced H2O2-induced cell death of V79-4 cells via inhibition of apoptosis. Castanopsis extract was also found to increase catalase activity and its protein expression. Further molecular mechanistic studies revealed that Castanopsis extract enhanced phosphorylation of extracellular signal regulated kinase (ERK) and activity of nuclear factor kappa B (NF-κB). Taken together, the results suggest that Castanopsis extract protects V79-4 cells against oxidative damage by enhancing catalase activity and modulating the ERK and NF-κB signal pathway. [ABSTRACT FROM AUTHOR]