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Cytotoxicity of chlorhexidine on human osteoblastic cells is related to intracellular glutathione levels
Author(s) -
Lee T.H.,
Hu C.C.,
Lee S.S.,
Chou M.Y.,
Chang Y.C.
Publication year - 2010
Publication title -
international endodontic journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.988
H-Index - 119
eISSN - 1365-2591
pISSN - 0143-2885
DOI - 10.1111/j.1365-2591.2010.01700.x
Subject(s) - cytotoxicity , glutathione , buthionine sulfoximine , chemistry , intracellular , cell growth , pharmacology , cell culture , apoptosis , cytotoxic t cell , biochemistry , in vitro , microbiology and biotechnology , biology , genetics , enzyme
Lee T‐H, Hu C‐C, Lee S‐S, Chou M‐Y, Chang Y‐C. Cytotoxicity of chlorhexidine on human osteoblastic cells is related to intracellular glutathione levels. International Endodontic Journal , 43 , 430–435, 2010. Abstract Aim To evaluate the mechanisms of cytotoxicity of chlorhexidine (CHX) in human osteoblastic cells in vitro . Methodology Cytotoxicity, cell proliferation and collagen synthesis assays were performed to elucidate the toxic effects of CHX on the human osteoblastic cell line U2OS. To determine whether glutathione (GSH) levels were important in the cytotoxicity of CHX, cells were pre‐treated with 2‐oxothiazolidine‐4‐carboxylic acid (OTZ) to boost GSH levels or buthionine sulfoximine (BSO) to deplete GSH. Results CHX demonstrated a cytotoxic effect to U2OS cells in a dose‐dependent manner ( P < 0.05). The 50% inhibition concentration of CHX was approximately 0.005%. CHX also inhibited cell proliferation and collagen synthesis ( P < 0.05). The addition of OTZ acted as a protective effect on the CHX‐induced cytotoxicity ( P < 0.05). In contrast, the addition of BSO enhanced the CHX‐induced cytotoxicity ( P < 0.05). Conclusions The levels of CHX tested inhibited cell growth, proliferation and collagen synthesis on U2OS cells. CHX has significant potential for periapical toxicity. GSH depletion might be one of the mechanisms underlying CHX cytotoxicity.