Regulation of phosphoenolpyruvate carboxykinase mRNA in mouse liver, kidney, and fat tissues by fasting, diabetes, and insulin.

Previous investigations of the phosphoenolpyruvate carboxykinase (PEPCK) gene have been conducted using rats. In a recent comparative study, we investigated, for the first time, the effects of fasting, refeeding, alloxan-induced diabetes, and insulin treatment on the levels of PEPCK mRNA in mouse liver, kidney, and adipose tissues. As in rats, fasting and diabetes induced, while insulin repressed, hepatic PEPCK mRNA. In contrast, the response of renal PEPCK mRNA to fasting, refeeding, and diabetes in mice differed quantitatively with that in rats: fasting caused a twofold increase in mice and a fourfold increase in rats. Moreover, diabetes, which induces renal PEPCK mRNA indirectly by causing acidosis in rats, was without effect in mice. In adipose tissue, the results of previous studies in both rats and mice have shown that the amount of PEPCK protein and its rate of synthesis are increased by fasting and diabetes and decreased by refeeding and insulin treatment. Thus, it was surprising to find that fasting, refeeding, alloxan-induced diabetes, and insulin treatment had no effect on adipose tissue PEPCK mRNA in either rats or mice.

Lack of clastogenic effects of irradiated glucose in somatic and germ cells of mice.

The clastogenic ability of irradiated glucose was evaluated using the micronucleus test in bone marrow cells and the chromosomal aberration assay in the spermatogonial cells of mice. Glucose was irradiated with 0.2, 2.0, 20 and 50 kGy of gamma-rays and administered to mice for various periods. No evidence of mutagenic effects was observed in somatic or germ cells.

Lack of mutagenicity of irradiated glucose in Salmonella typhimurium using host-mediated assay.

Experiments were conducted to study the ability of irradiated glucose to induce reverse mutations in S. typhimurium by host-mediated assay. The results revealed no significant increase in the frequency of reverse mutations compared to controls.

Prevention and/or reversibility by colchicine of genetic damage induced by gamma-radiation in the germ cells of mice: possible relevance to prostaglandin involvement.

Gamma radiation, known to produce genetic damage in both somatic and germ cells of experimental animals and man, can also block thromboxane A2 (TXA2) and prostaglandin E1 (PGE1) synthesis. In this communication evidence is presented that colchicine, a known TXA2 and PGE1 synthesis stimulator, can suppress the genetic damage induced in the germ cells of mice by gamma radiation. This evidence lends support to the hypothesis that an altered PG system could be responsible for mutagenesis and carcinogenesis.

Mutagenic effects of irradiated glucose in Drosophila melanogaster.

The mutagenic effects of irradiated glucose were studied using the sex-linked recessive lethal test in Drosophila melanogaster. Oregon K males of D. melanogaster reared on a medium containing 20 or 40% glucose irradiated with a dose of 0.02, 0.10, 0.20, 2 or 5 Mrad gamma-rays were scored for the induction of sex-linked recessive lethals. The results showed no significant increase in the frequency of X-lethals in Drosophila at any of the dose levels.

Induction of chromosome aberrations by phenobarbitone in the germ cells of Swiss male mice.

The cytogenetic effects of phenobarbitone were studied in the male germ cells of Swiss mice. The drug was orally administered at 42, 84 and 126 mg/kg body weight dose levels by sub-acute and chronic modes of treatment. In the treated series, the incidence of chromosome aberrations was significant at all dose levels. However, there were no significant differences between sub-acute and chronic treatments in the incidence of chromosome aberrations. The results clearly demonstrate the ability of phenobarbitone to induce chromosome damage in the germ cells of male mice.