重金属のポルフィリン代謝に及ぼす実験的研究-2-特に鉛,水銀及び砒素のデルタアミノレブリン酸脱水酵素に及ぼす影響について
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Inhibition of δ-aminolevulinic acid dehydratase (δ-ALA-D) activity by lead has been generally accepted as one of the main disorders of porphyrin metabolism in lead poisoning. δ-ALA-D activity inhibited by lead in bone marrow and erythrocytes results in an increased urinary excretion of δ-ALA. If mercury or arsenite inhibits δ-ALA-D with stronger affinity for SH groups than lead, raised urinary δ-ALA concentration should be expected.<BR>This paper reports the urinary excretion patterns of δ-ALA, PBG and coproporphyrin III in mercury or arsenite poisoned rats. The inhibitory effects of these three metals on δ-ALA-D activity in liver and erythrocyte preparations were also examined.<BR>The following results were obtained.<BR>1) Urinary excretion of δ-ALA in rats poisoned with mercury or arsenite was not so remarkably raised as compared with lead poisoned rats.<BR>2) Treatment of rats with lead has been found to produce copro- and protoporphyrins in bone marrow. In mercury or arsenite poisoning bone marrow porphyrins were not elevated but small amount of porphyrins were found in liver.<BR>3) It was found that δ-ALA-D activity in liver homogenate was partially inhibited in vitro by lead, mercury or arsenite (1×10<SUP>-5</SUP>M)by approximately 10-20%. On the other hand, δ-ALA-D activity in erythrocyte hemolysate was strongly inhibited by lead but not by mercury or arsenite.
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