Comparative Studies on the Inducing Effects of Cobalt Chloride and Co-Protoporphyrin on Hepatic Ornithine Decarboxylase and Heme Oxygenase in Rats
スポンサーリンク
概要
- 論文の詳細を見る
Co-protoporphyrin, like Co^<2+>, produced a significant and persistent induction of hepatic ornithine decarboxylase (ODC) as well as its known inducing effect on heme oxygenase and the decreasing effects on drug-metabolizing enzymes. The induction of ODC and heme oxygenase by Co-protoporphyrin occurred dose-dependently with the lowest effective dose of 6.25 μmol/kg. Although Co-protoporphyrin produced similar effects on ODC and heme oxygenase to Co^<2+>, there were differences in the mode of ODC induction. In particular, pretreatment with diethyl maleate failed to augment the induction of ODC by Co-protoporphyrin. Moreover, multiple administrations of Co^<2+>, but not Co-protoporphyrin, caused super-addtive induction of ODC to about 1000-fold over the controls. This super-additive induction of ODC by Co^<2+> was dependent on the doses and time intervals between two administrations. In parallel with a large induction of ODC evoked by two administrations of Co^<2+>, hepatic putrescine content was increased markedly, while spermine content was decreased as compared to the control levels. Pretreatment with Co^<2+> led to super-additive induction of ODC by subsequent administration of the metal ion itself or diethyl maleate, but not by other ODC inducers, such as Co-protoporphyrin and thioacetamide, and not by subsequent partial hepatectomy. Under these experimental conditions, the magnitudes of heme oxygenase induction were similar. ODC induced by two doses of Co^<2+> was insensitive to exogenous putrescine, but sensitive to α-difluoromethylornithine and 1,3-diaminopropane. These findings add new insight into the effects of Co^<2+> and Coprotoporphyrin on hepatic polyamine metabolism ; and the results suggest that the metal ion could cause extensive derangement of the ODC regulatory system in a manner different from the metalloporphyrin.
- 公益社団法人日本薬学会の論文
- 1989-09-01
著者
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NUMAZAWA Satoshi
Department of Biochemical Toxicology, School of Pharmacy, Showa University
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YOSHIDA Takemi
Department of Biochemical Toxicology, School of Pharmacy, Showa University
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KUROIWA YUKIO
Department of Biochemical Toxicology, School of Pharmaceutical Science Showa University
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Kuroiwa Yukio
Department Of Biochemical Toxicology School Of Pharmaceutical Sciences Showa University
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Kuroiwa Yukio
Department Of Biochemical Toxicology Faculty Of Pharmaceutical Sciences Showa University
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Yoshida Tomoko
Department Of Nuclear Engineering Nagoya University
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Yoshida T
Department Of Biochemical Toxicology School Of Pharmaceutical Science Showa University
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Numazawa Satoshi
Dep. Of Biochemical Toxicology School Of Pharmacy Showa Univ.
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Numazawa Satoshi
Department Of Biochemical Toxicology School Of Pharmaceutical Science Showa University
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Oguro T
Univ. Texas Medical Branch At Galveston Texas Usa
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Oguro Takiko
Department Of Biochemical Toxicology School Of Pharmaceutical Sciences Showa University
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Yoshida Takemi
Department Of Biochemical Toxicology School Of Pharmaceutical Science Showa University
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Yoshida Teiji
Department Of Physics Faculty Of Science Tohoku University
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Yoshida Takahiko
Department Of Environmental Health Division Of Community And Environmental Health Tokai University S
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Yoshida Takemi
School Of Pharmaceutical Sciences Showa University
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Kuroiwa Y
Department Of Biochemical Toxicology School Of Pharmaceutical Sciences Showa University
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Yoshida Takemi
Pfizer Japan Inc. Drug Safety R&d Pfizer Global R&d
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Yoshida Tomoko
Department of Biochemical Toxicology, School of Pharmacy Showa University
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