[Studies on a melanocyte-stimulating hormone-like substance in the urine, with reference to retinitis pigmentosa].
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Adolescent↗
Biomedical subjects
S Aonuma
Publications and source records attributed to S Aonuma.
[The difference in physicochemical and chemical properties of urinary MSH-like substance from retinitis pigmentosa patient and normal adult].
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Chemical Phenomena↗
[Nursing care of a patient with pneumothorax].
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Nursing↗
[Studies on posterior pituitary hormones. (7). Effect on tryptophan metabolism].
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Animals↗
[Effects of thyroid hormone-related compounds on the respiration of Saccharomyces cerevisiae, Escherichia coli and Bacillus subtilis].
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Bacteria↗
[Studies on posterior pituitary hormones. VI. The effects of thyroid hormone related compounds upon the uterine inhibitory responses to posterior pituitary hormones].
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Animals↗
Mutation induction by okadaic acid, a protein phosphatase inhibitor, in CHL cells, but not in S. typhimurium.
Okadaic acid (OA) is a specific and strong inhibitor of protein phosphatases 1 and 2A present in eukaryotes, and a potent promoter of carcinogenesis in mouse skin. In this study, we examined the mutagenicity of OA. OA did not induce mutations in S. typhimurium TA100 and TA98, with or without a microsomal metabolic activation system. However, it was strongly mutagenic to Chinese hamster lung (CHL) cells without a microsomal activation system, as shown using diphtheria toxin (DT) resistance (DTr) as a selective marker. Treatment of CHL cells with OA at 17.5 ng/ml induced 164 DTr mutants per 10(6) survivors. A plot of the mutation frequency against the OA concentration gave a concave curve, and the mutant frequency was calculated to be 5500/10(6) survivors/micrograms, with OA in the dose range of 10-15 ng/ml. This value was about 680 times that of ethyl methanesulfonate (EMS), and comparable to that of 2-amino-N6-hydroxyadenine, one of the strongest known mutagens. Elongation factor 2 (EF-2) obtained from 4 DTr clones was not ADP-ribosylated by DT fragment A. PCR-direct sequencing revealed that the hot spot of EF-2 for EMS mutagenesis in CHO-K1 cells, the first letter of codon 717, was not a hot spot for OA mutagenesis in CHL cells.
Animals↗