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Protection by exogenous pyruvate through a mechanism related to monocarboxylate transporters against cell death induced by hydrogen peroxide in cultured rat cortical neurons
Author(s) -
Nakamichi Noritaka,
Kambe Yuki,
Oikawa Hirotaka,
Ogura Masato,
Takano Katsura,
Tamaki Keisuke,
Inoue Maki,
Hinoi Eiichi,
Yoneda Yukio
Publication year - 2005
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2005.02999.x
Subject(s) - monocarboxylate transporter , viability assay , hydrogen peroxide , microbiology and biotechnology , transporter , programmed cell death , cell culture , blot , neuroprotection , biology , cell , in vitro , cortical neurons , biochemistry , chemistry , apoptosis , pharmacology , gene , genetics
In cortical neurons cultured for 3 or 9 days in vitro (DIV), exposure to hydrogen peroxide (H 2 O 2 ) led to a marked decrease in cell viability in a concentration‐dependent manner at a concentration range of 10 µ m to 1 m m irrespective of the duration between 6 and 24 h. However, H 2 O 2 was more potent in decreasing cellular viability in cortical neurons cultured for 9 DIV than in those for 3 DIV. Pyruvate was effective in preventing the neuronal cell death at 1 m m even when added 1–3 h after the addition of H 2 O 2 . Semi‐quantitative RT–PCR and western blotting analyses revealed significantly higher expression of both mRNA and protein for a particular monocarboxylate transporter (MCT) in neurons cultured for 9 DIV than in those for 3 DIV. A specific inhibitor of MCT significantly attenuated the neuroprotection by pyruvate in neurons cultured for 9 DIV, without markedly affecting that in neurons cultured for 3 DIV. These results suggest that vulnerability to H 2 O 2 may at least in part involve expression of particular MCT isoforms responsible for the bi‐directional transport of pyruvate across cell surfaces in cultured rat cortical neurons.