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Fe~(2+)-次黄嘌呤-黄嘌呤氧化酶体系产生的活性氧能诱发脱氧核糖的损伤,使之转变为硫代巴比妥酸反应物(TBAS).增加黄嘌呤氧化酶或脱氧核糖的浓度都增加TBAS的生成量.Fe~(2+)促进TBAS的生成,此促进作用随着Fe~(2+)浓度的升高而很快达到饱和.超氧化物歧化酶(SOD)或过氧化氢酶(CAT)都能抑制TBAS的生成.间接证明体系中的TBAS是由活性氧攻击脱氧核糖而形成的.并且羟自由基是起主要作用的活性氧.
Reactive oxygen species produced by the Fe ~ (2 +) - hypoxanthine-xanthine oxidase system can induce deoxyribose damage and convert it to thiobarbituric acid reactant (TBAS). Increased xanthine oxidase or deoxygenation The concentration of ribose increased the production of TBAS, and Fe 2+ accelerated the formation of TBAS, which was quickly saturated with the increase of Fe 2+ concentration. The activity of superoxide dismutase (SOD) Or catalase (CAT) can inhibit the formation of TBAS.Indirect evidence that TBAS in the system is formed by the reactive oxygen species attack deoxyribose.And hydroxyl radical is the main role of reactive oxygen species.