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Defective biosynthesis of ascorbic acid in Sod1-deficient mice results in lethal damage to lung tissue by Takujiro Homma; Yuji Takeda; Tomoyuki Nakano; Shinya Akatsuka; Daisuke Kinoshita; Toshihiro Kurahashi; Shinichi Saitoh; Ken-ichi Yamada; Satoshi Miyata; Hironobu Asao; Kaoru Goto; Tetsu Watanabe; Masafumi Watanabe; Shinya Toyokuni; Junichi Fujii is a Biochemistry, Genetics and Molecular Biology article available to read on EtoBox.
What is Defective biosynthesis of ascorbic acid in Sod1-deficient mice results in lethal damage to lung tissue about?
Superoxide dismutase 1 (Sod1) plays pivotal roles in antioxidation via accelerating the conversion of superoxide anion radicals into hydrogen peroxide, thus inhibiting the subsequent radical chain reactions. While Sod1 deficient cells inevitably undergo death in culture conditions, Sod1-knockout (KO) mice show relatively mild phenotypes and live approximately two years. We hypothesized that the presence of abundant levels of ascorbic acid (AsA), which is naturally produced in mice, contributes to the elimination of reactive oxygen species (ROS) in Sod1-KO mice. To verify this hypothesis, we employed mice with a genetic ablation of aldehyde reductase (Akr1a), an enzyme that is involved in the biosynthesis of AsA, and established double knockout (DKO) mice that lack both Sod1 and Akr1a. Supplementation of AsA (1.5 mg/ml in drinking water) was required for the DKO mice to breed, and, upon terminating the AsA supplementation, they died within approximately two weeks regardless of age or gender. We explored the etiology of the death from pathophysiological standpoints in principal organs of the mice. Marked changes were observed in the lungs in the form of macroscopic damage after the A
Who reads Defective biosynthesis of ascorbic acid in Sod1-deficient mice results in lethal damage to lung tissue?
It is typically read by researchers, students, and practitioners in Biochemistry, Genetics and Molecular Biology.
- Author
- Takujiro Homma; Yuji Takeda; Tomoyuki Nakano; Shinya Akatsuka; Daisuke Kinoshita; Toshihiro Kurahashi; Shinichi Saitoh; Ken-ichi Yamada; Satoshi Miyata; Hironobu Asao; Kaoru Goto; Tetsu Watanabe; Masafumi Watanabe; Shinya Toyokuni; Junichi Fujii
- Publisher
- Elsevier Science; Elsevier ; Elsevier BV (ISSN 0891-5849)
- Published
- 2020
- Language
- EN
- Field
- Biochemistry, Genetics and Molecular Biology (Life Sciences)