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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.

Animal model for oxidative stress research—Catalase mutant mice