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首页> 外文期刊>Cell biology international. >Human erythrocyte delta-aminolevulinate dehydratase inhibition by monosaccharides is not mediated by oxidation of enzyme sulfhydryl groups.
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Human erythrocyte delta-aminolevulinate dehydratase inhibition by monosaccharides is not mediated by oxidation of enzyme sulfhydryl groups.

机译：单糖对人红细胞δ-氨基乙酰丙酸酯脱水酶的抑制作用不由巯基酶的氧化介导。

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摘要

The heme pathway enzyme delta-aminolevulinate dehydratase is a good marker for oxidative stress and metal intoxication. This sulfhydryl enzyme is inhibited in such oxidative pathologies as lead, mercury and aluminum intoxication, exposure to selenium organic species and diabetes. Oxidative stress is a complicating factor in diabetes, inducing non-enzymatic glucose-mediated reactions that change protein structures and impair enzyme functions. We have studied the effects of high glucose, fructose and ribose concentrations on delta-ALA-D activity in vitro. These reducing sugars inhibited delta-ALA-D with efficacies in the order fructose=ribose>glucose. The possible mechanism of glucose inhibition was investigated using lysine, DTT, and t-butylamine. Oxidation of the enzyme's critical sulfhydryl groups was not involved because DTT had no effect. We concluded that high concentrations of reducing sugars or their autoxidation products inhibit delta-ALA-D by a mechanism not related to thiol oxidation. Also, weare not able to demonstrate that the formation of a Schiff base with the critical lysine residue of the enzyme is involved in the inhibition of delta-ALA-D by hexoses.
机译：血红素途径酶δ-氨基乙酰丙酸酯脱水酶是氧化应激和金属中毒的良好标志。这种巯基酶在铅，汞和铝中毒，硒有机物暴露和糖尿病等氧化性疾病中受到抑制。氧化应激是糖尿病的一个复杂因素，会诱导非酶促葡萄糖介导的反应，从而改变蛋白质结构并损害酶的功能。我们已经研究了高葡萄糖，果糖和核糖浓度对体外δ-ALA-D活性的影响。这些还原糖以果糖＝核糖＞葡萄糖的顺序抑制δ-ALA-D。使用赖氨酸，DTT和叔丁胺研究了葡萄糖抑制的可能机制。由于DTT没有作用，因此不涉及酶的关键巯基的氧化。我们得出的结论是，高浓度的还原糖或其自氧化产物会通过与硫醇氧化无关的机制抑制delta-ALA-D。同样，还不能证明带有关键的赖氨酸残基的席夫碱的形成与己糖对δ-ALA-D的抑制有关。

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