Mitochondrial reactive oxygen species generation by the SDHC V69E mutation causes low birth weight and neonatal growth retardation
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.
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Ishii and coworkers found that an SdhC mutation in transgenic mouse fibroblasts and conditional transgenic mice induces mitochondrial respiratory chain dysfunction and increased ROS production.
“Ishii and coworkers observed that a mutation in the SdhC subunit in transgenic mouse fibroblasts and conditional transgenic mice induces mitochondrial respiratory chain dysfunction and increased ROS production [95].”
From Differential effects of complex II on mitochondrial ROS production and their relation to cardioprotective pre- and postconditioning (2013) · cites this paper as [95]
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Self-citation
- Authors
- Ishii, T., Miyazawa, M., Onodera, A., Yasuda, K., Kawabe, N., Kirinashizawa, M., Yoshimura, S., Maruyama, N., Hartman, P. S., & Ishii, N.
- Affiliations
- Tokai University (JP)
- Tokyo Metropolitan Institute of Gerontology (JP)
- Texas Christian University (US)
- Corresponding author
- Ishii, Naoaki
- Venue
- Mitochondrion
- Publisher
- Elsevier BV
- Published
- 2011-01
- Volume
- 11
- Issue
- 1
- Pages
- 155-165
- ISSN
- 1567-7249 (ISSN-L)
- OpenAlex
- W1989368620
- Cited by
- 42
- References
- 32
- Citations by year
- 2026: 1 · 2025: 4 · 2023: 2 · 2022: 3 · 2021: 1 · 2020: 2 · 2019: 2 · 2018: 1 · 2017: 1 · 2016: 5 · 2015: 2 · 2014: 6 · 2013: 4 · 2012: 5
- FWCI
- 1.56
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Mitochondrion (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Japan Society for the Promotion of Science (22510064)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Clinical Biochemistry › Metabolism and Genetic Disorders
- Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
- Keywords
- succinate dehydrogenase, reactive oxygen species, oxidative stress, mitochondrial respiratory chain dysfunction, apoptosis, low birth weight, mev-1, premature mortality
- MeSH terms
- Animals, Animals, Newborn, Disease Models, Animal, Gene Expression Regulation, Growth Disorders, Humans, Infant, Low Birth Weight, Infant, Newborn, Mice, Transgenic, Mitochondria, Mutation, Succinate Dehydrogenase, Tetracycline, Reactive Oxygen Species, Transgenes, Mitochondrial Diseases, NIH 3T3 Cells, Mice
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