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首页> 外文期刊>Chemico-biological interactions >In vitro glutathione peroxidase mimicry of ebselen is linked to its oxidation of critical thiols on key cerebral suphydryl proteins - A novel component of its GPx-mimic antioxidant mechanism emerging from its thiol-modulated toxicology and pharmacology
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In vitro glutathione peroxidase mimicry of ebselen is linked to its oxidation of critical thiols on key cerebral suphydryl proteins - A novel component of its GPx-mimic antioxidant mechanism emerging from its thiol-modulated toxicology and pharmacology

机译：ebselen的体外谷胱甘肽过氧化物酶模拟与其关键脑巯基蛋白上关键硫醇的氧化有关-GPx模仿抗氧化机制的新成分来自其硫醇调节的毒理学和药理学

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The antioxidant mechanism of ebselen in rats brain is largely linked with its glutathione peroxidase (GPx) rather than its peroxiredoxin mimicry ability. However, the precise molecular dynamics between the GPx-mimicry of ebselen and thiol utilization is yet to be fully clarified and thus still open. Herein, we investigated the influence of dithiothreitol (DTT) on the antioxidant action of ebselen against oxidant-induced cerebral lipid peroxidation and deoxyribose degradation. Furthermore, the critical inhibitory concentrations of ebselen on the activities of sulphydryl enzymes such as cerebral sodium pump, δ-aminolevulinic acid dehydratase (δ-ALAD) and lactate dehydrogenase (LDH) were also investigated. We observe that ebselen (at ≥42 μM) markedly inhibited lipid peroxidation in the presence and absence of DTT, whereas it inhibited deoxyribose degradation only in the presence of DTT. Furthermore, under in vitro conditions, ebselen inhibited the thiol containing enzymes; cerebral sodium pump (at ≥40 μM), δ-ALAD (≥10 μM) and LDH (≥1 μM) which were either prevented or reversed by DTT. However, the inhibition of the activities of these sulphydryl proteins in diabetic animals was prevented by ebselen. Summarily, it is apparent that the effective in vitro inhibitory doses of ebselen on the activity of the sulphydryl proteins are far less than its antioxidant doses. In addition, the presence of DTT is evidently a critical requirement for ebselen to effect its antioxidant action against deoxyribose degeradation and not lipid peroxidation. Consequently, we conclude that ebselen possibly utilizes available thiols on sulphydryl proteins to effect its GPx mimicry antioxidant action against lipid peroxidation in rat brain homogenate.
机译：依卜硒仑在大鼠脑中的抗氧化机制很大程度上与其谷胱甘肽过氧化物酶（GPx）有关，而不是其过氧化物酶模拟能力。然而，依柏精的GPx模拟和硫醇利用之间的精确分子动力学尚未完全阐明，因此仍然是未知的。在本文中，我们研究了二硫苏糖醇（DTT）对依伯硒仑抗氧化剂诱导的脑脂质过氧化和脱氧核糖降解的抗氧化作用的影响。此外，还研究了依布硒仑对诸如脑钠泵，δ-氨基乙酰丙酸脱水酶（δ-ALAD）和乳酸脱氢酶（LDH）之类的硫代硫酸酯酶活性的关键抑制浓度。我们观察到依布硒仑（≥42μM）在存在和不存在DTT的情况下均显着抑制脂质过氧化，而仅在存在DTT的情况下才抑制脱氧核糖降解。此外，在体外条件下，依布硒啉抑制了含硫醇的酶。 DTT预防或逆转了脑钠泵（≥40μM），δ-ALAD（≥10μM）和LDH（≥1μM）。但是，依布硒仑可防止对糖尿病动物中这些巯基蛋白活性的抑制。综上所述，依布硒仑对巯基蛋白质活性的有效体外抑制剂量显然远小于其抗氧化剂剂量。此外，DTT的存在显然是依布硒仑要实现其抗脱氧核糖脱铁而不是脂质过氧化的抗氧化作用的关键要求。因此，我们得出结论，依布硒仑可能利用巯基蛋白质上的可用硫醇来影响其GPx模仿抗大鼠脑匀浆中脂质过氧化的抗氧化作用。

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