DEOXYRIBOSE BREAKDOWN BY THE ADRIAMYCIN SEMI-QUINONE AND H2O2 - EVIDENCE FOR HYDROXYL RADICAL PARTICIPATION

DEOXYRIBOSE BREAKDOWN BY THE ADRIAMYCIN SEMI-QUINONE AND H2O2 - EVIDENCE FOR HYDROXYL RADICAL PARTICIPATION
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DOI:
10.1016/0014-5793(82)81222-2
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发表时间:
1982-01-01
期刊:
影响因子:
3.5
通讯作者:
WINTERBOURN, CC
WINTERBOURN, CC
中科院分区:
生物学3区
文献类型:
--
作者:
BATES, DA;WINTERBOURN, CC

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我们报告了我们的发现,阿霉素半醌(通过黄嘌呤氧化酶还原药物产生)和H2O2在N2中的反应导致脱氧核糖降解为硫代巴比妥酸反应性色原。羟基自由基清除剂抑制了脱氧核糖的分解,为羟基自由基的参与提供了证据。在空气中检测到反应,但在空气中的效率低于在N2中。脱氧核糖降解不需要金属催化剂,并抑制超氧化物歧化酶在空气中,但不N2。与DNA中脱氧核糖的类似反应可能在阿霉素的抗肿瘤作用中具有重要意义。
We report our finding that the reaction between the adriamycin semiquinone (produced by reduction of the drug by xanthine oxidase) and H2O2in N2causes deoxyribose degradation to a thiobarbituric acid-reactive chromogen. Deoxyribose breakdown was inhibited by scavengers of hydroxyl radicals, providing evidence for the participation of hydroxyl radicals. The reaction was detected in air, but was less efficient in air than in N2. Deoxyribose degradation did not require a metal catalyst, and was inhibited by superoxide dismutase in air, but not N2. A similar reaction with deoxyribose in DNA may be of major importance in the antitumour action of adriamycin.