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Animal model for oxidative stress research-Catalase mutant mice
Da-Hong Wang1, Noriyoshi Masuoka, Shohei Kira
1Department of Public Health, Okayama University Graduate School of Medicine and Dentistry, 2-5-1 Shikata-cho, 700-8558, Okayama, Japan, dahong@md.okayama-u.ac.jp.
Abstract:
Catalase-deficient mouse strains was initially established by Feinstein et al. through a large scale screening of the progeny of irradiated C3H mice in 1966. Later, Feinstein provided the mice of catalase mutant strain C3H/AnICs(a)Cs(a) (wild-type), C3H/AnICs(b)Cs(b) and C3H/AnlCs(c)Cs(c) to Okayama University Medical School in Japan. It is known that a point mutation at amino acid 11 (from glutamine to histidine) of acatalasemic mouse catalase and a point mutation at amino acid 439 (from as paragine to serine) of hypocatalasemic mouse catalase are responsible for the catalase deficiency of acatalasemic and hypocatalasemic mice, respectively. Recently, a liver cell line from an acatalasemic mouse andEscherichia coli (E. coli) strains with murine normal, hypocatalasemic, or acatalasemic catalase have been established. The construction of these new systems would be useful for studying the effects of oxidative stress at the cellular level. In this review, we give a brief overview of recent findings of studies in utilizing the catalase-deficient mice and evaluate the possibility of these mouse strains as a candidate animal model for oxidative stress research.
Insights
Catalase-deficient mice, developed in 1966, offer valuable models for studying oxidative stress. Recent advancements include cell lines and bacterial strains, enhancing their utility in research.
Area of Science:
- Biomedical Research
- Genetics
- Biochemistry
Background:
- Catalase-deficient mouse strains were first created in 1966.
- Specific point mutations cause acatalasemic and hypocatalasemic conditions in mice.
- These strains exhibit varying levels of catalase deficiency.
Purpose of the Study:
- To review recent findings using catalase-deficient mouse models.
- To evaluate these mice as potential animal models for oxidative stress research.
- To highlight new cellular and bacterial systems for studying oxidative stress.
Main Methods:
- Establishment of catalase-deficient mouse strains (acatalasemic and hypocatalasemic).
- Identification of specific point mutations responsible for catalase deficiency.
- Development of a liver cell line from acatalasemic mice.
- Engineering Escherichia coli strains with different murine catalase variants.
Main Results:
- Catalase deficiency in mice is linked to specific amino acid substitutions.
- New cellular and bacterial models have been created for oxidative stress studies.
- These models facilitate research into the effects of oxidative stress at the cellular level.
Conclusions:
- Catalase-deficient mice are crucial tools for oxidative stress research.
- Newly developed cell lines and bacterial strains expand research capabilities.
- These models hold significant promise for advancing our understanding of oxidative stress-related conditions.
