ACATALASEMIC AND HYPOCATALASEMIC MOUSE MUTANTS

Abstract

A strain of mice genetically deficient in blood catalase should be of considerable value in studying the possible role of hydrogen peroxide in carcinogenesis and cancerolysis, as suggested by WARBURG, GAWEHN, and GEISSLER (1957) and by HOLMAN (1957), and in assessing the possible role of H,O, in radiation lethality. That such a strain could be viable appeared probable from the work of TAKAHARA (1952), AEBI et al. (1961 ) , and SZEINBERG et al. (1963), with humans, and RADEV (1958) with guinea pigs. Therefore a large scale search for low-catalase mutants among the progeny of irradiated mice was initiated. A preliminary note announced (FEINSTEIN et al. 1964b) the successful production of a mouse litter containing individuals with blood catalase levels approximately 1 % of normal. The present communication details the search for mutants and describes five mutant lines which have been obtained. MATERIALS AND METHODS A. Initial source of mutants: Mice used as the initial source of possible mutants were discards from two experiments at Oak Ridge National Laboratory. In these experiments, designed to obtain radiation-induced visible mutations at specific loci (RUSSELL 1951), mice examined were offspring of irradiated fathers, who had received a total dose of 600R in fractionated exposures. B. Analytical techniques: Blood was drawn from the orbital sinus (RILEY 1960) and laked in an appropriate volume of cold water. In the initial screening, a recently published (FEINSTEIN et al. 1964.a) rapid, semi-quantitative blood catalase assay was used. After this stage, the quantitative perborate assay (FEINSTEIN 1949) was employed. Mice were weaned and sexed at four weeks of age. and blood catalase was assayed at six weeks.