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Mitochondrion. 2011 Jan;11(1):155-65. doi: 10.1016/j.mito.2010.09.006. Epub 2010 Oct 18.

Mitochondrial reactive oxygen species generation by the SDHC V69E mutation causes low birth weight and neonatal growth retardation.

Author information

1
Department of Molecular Life Science, Tokai University School of Medicine, Isehara, Kanagawa, Japan.

Abstract

We have previously demonstrated that excessive mitochondrial reactive oxygen species caused by mutations in the SDHC subunit of Complex II resulted in premature death in C. elegans and Drosophila, tumors in mouse cells and infertility in transgenic mice. We now report the generation and initial characterization of conditional transgenic mice (Tet-mev-1) using our uniquely developed Tet-On/Off system, which equilibrates transgene expression to endogenous levels. The mice experienced mitochondrial respiratory chain dysfunction that induced reactive oxygen species overproduction. The mitochondrial oxidative stress resulted in excessive apoptosis leading to low birth weight and growth retardation in the neonatal developmental phase in Tet-mev-1 mice.

PMID:
20870041
DOI:
10.1016/j.mito.2010.09.006
[Indexed for MEDLINE]

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