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Induction of heme oxygenase‐1 protects methyl mercury‐caused cytotoxicity in cultured mouse mesangial cells
Author(s) -
Suh Chang Kook,
Cha Seok Ho
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.812.26
Subject(s) - heme oxygenase , cytotoxicity , chemistry , heme , toxicity , mercury (programming language) , kidney , viability assay , zinc protoporphyrin , pharmacology , microbiology and biotechnology , biochemistry , cell , biology , enzyme , in vitro , endocrinology , organic chemistry , computer science , programming language
The kidney is a major target organ for many trace metals, and it has been shown that many of these metals have the ability to change heme metabolism in kidney. HO‐1 is known to be induced by heavy metals, UV light, heme and so on. Among these heavy metals, mercury and methyl mercury (MeHg) are environmental toxins that cause severe neurological and renal complications in humans and experimental animals. Methyl mercury is considered a more toxic compound to mercuric chloride. Therefore we investigated the relationship between MeHg‐caused cytotoxicity and HO‐1 expression using molecular biological techniques in cultured mouse mesangial cells. The expression levels of HO‐1 mRNA and protein were increased by the treatment of MeHg, with dose‐ and time‐dependent manner. The increased HO‐1 expression was attenuated by the treatment of actinomycin D, an inhibitor of transcription, but no expressional change induced by MeHg was observed by the treatment of zinc protoporphyrin IX (ZnPP), an endogenous heme analogue that inhibits HO activity. In cell viability test using MTT assay, MeHg‐induced cytotoxicity was increased time‐dependently. This MeHg toxicity was enhanced by the treatment of ZnPP. These results show HO‐1 induction takes part in protection to MeHg toxicity in cultured mouse mesangial cells.