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6-Hydroxymelatonin converts Fe (III) to Fe (II) and reduces iron-induced lipid peroxidation.

机译:6-羟基褪黑激素将Fe(III)转化为Fe(II)并减少铁引起的脂质过氧化。

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摘要

Disorders of iron accumulation are known to produce hepatotoxicity. Agents, which can reduce Fe(3+) to a more usable form Fe(2+) could potentially limit such damage. Since it has been previously demonstrated that the pineal secretory product, melatonin, is able to bind iron, we decided to investigate the potential protective properties of the principal melatonin metabolite and degradant, 6-hydroxymelatonin (6-OHM). Using adsorptive cathode stripping voltammetry (AdCSV) we showed that Fe(3+) in the presence of 6-OHM is converted to Fe(2+). We further demonstrated that 6-OHM reduces the Fe(2+)-induced rise in lipid peroxidation in rat liver homogenates. The results imply that 6-OHM facilitates the conversion of Fe(3+) to Fe(2+) which is a more biologically usable form of iron. While such a conversion could also potentially make more Fe(2+) available for driving the Fenton reaction and the consequent generation of the dangerous hydroxyl radical, 6-OHM is able to quench these radicals, thereby providing tissue protection.
机译:已知铁蓄积障碍会产生肝毒性。可以将Fe(3+)还原成更有用的形式Fe(2+)的物质可能会限制这种破坏。由于先前已证明松果体分泌产物褪黑激素能够结合铁,因此我们决定研究主要褪黑激素代谢产物和降解物6-羟基褪黑激素(6-OHM)的潜在保护特性。使用吸附阴极溶出伏安法(AdCSV),我们表明存在6-OHM的Fe(3+)转化为Fe(2+)。我们进一步证明了6-OHM可以降低Fe(2+)诱导的大鼠肝脏匀浆脂质过氧化反应的上升。结果表明6-OHM促进了Fe(3+)到Fe(2+)的转化,而Fe(2+)是生物学上更有用的铁形式。虽然这样的转换还可能潜在地使更多的Fe(2+)用于驱动Fenton反应以及随后生成的危险羟基自由基,但6-OHM能够淬灭这些自由基,从而提供组织保护。

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