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Mitochondrial reactive oxygen species generation by the SDHC V69E mutation causes low birth weight and neonatal growth retardation.
- Source :
-
Mitochondrion [Mitochondrion] 2011 Jan; Vol. 11 (1), pp. 155-65. Date of Electronic Publication: 2010 Oct 18. - Publication Year :
- 2011
-
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.<br /> (Copyright © 2010 Elsevier B.V. and Mitochondria Research Society. All rights reserved.)
- Subjects :
- Animals
Animals, Newborn
Disease Models, Animal
Gene Expression Regulation
Humans
Infant, Low Birth Weight
Infant, Newborn
Mice
Mice, Transgenic
Mitochondrial Diseases pathology
NIH 3T3 Cells
Succinate Dehydrogenase genetics
Tetracycline pharmacology
Transgenes genetics
Transgenes physiology
Growth Disorders etiology
Mitochondria metabolism
Mitochondrial Diseases etiology
Mutation
Reactive Oxygen Species metabolism
Succinate Dehydrogenase metabolism
Subjects
Details
- Language :
- English
- ISSN :
- 1872-8278
- Volume :
- 11
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Mitochondrion
- Publication Type :
- Academic Journal
- Accession number :
- 20870041
- Full Text :
- https://doi.org/10.1016/j.mito.2010.09.006