The mechanism of the production of diabetes in animals given injections of alloxan has been the subject of much study in recent years. Since the original publication of Dunn, Sheehan & McLetchie (1943) it has been established that the diabetes is pancreatic in origin but the chemical mechanisms involved have remained in doubt. Leech & Bailey (1945), using the arsenophosphotungstic acid method, were among the first to observe a precipitous but temporary fall in the concentration of glutathione in the blood of rabbits after the intra- venous injection of diabetogenic amounts of alloxan. Since then other workers (Bruckmann & Wertheimer, 1947; Binet, Wellers & Marquis,1949; Collin-Williams, Renold & Marble, 1950) have reported similar falls in glutathione in the blood of rats and guinea pigs after alloxan injection, though the guinea pigs do not develop diabetes (West & Highet, 1948). On the basis of these observations upon blood glutathione concentration and other circumstantial evidence, Lazarow (1949) suggested that alloxan forms an addition com- pound with sulphydryl groups in the ,B cells of the islets of Langerhans, so causing death of these cells.
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Bhattacharya et al. (1956) studied this question.