Filipe P M, Fernandes A C, Saavedra J A, Manso C F
Instituto de Química Fisiológica, Faculdade de Medicina de Lisboa, Portugal.
Rev Port Cardiol. 1993 Jul-Aug;12(7-8):657-60, 602.
Free radicals have been related to the pathogenesis of some cardiovascular diseases. Several drugs used to treat these diseases were shown to have antioxidant properties. Our purpose was to evaluate if ketanserin, a selective S2 receptor antagonist with proven antihypertensive efficacy and which beneficially affects hemorheology, also is able to inhibit lipid peroxidation. Lipid peroxidation was induced in different biological systems in vitro and evaluated by the formation of thiobarbituric acid-reactive products. Ketanserin 50 microM inhibited copper-dependent lipid peroxidation in human red-cell suspensions by 40.8% and the subsequent hemolysis by 57,3%. It was less efficient in inhibiting hydrogen peroxide-dependent lipid peroxidation and hemolysis in the same system. Ketanserin 100 microM inhibited lipid peroxidation induced by a mixture of copper(II) and hydrogen peroxide in hepatic microsomal suspensions and in brain total homogenates by 86.2% and 56.7%, respectively. These results proved an antioxidant effect for ketanserin which was unknown, although its therapeutic relevance remains undetermined.
自由基与某些心血管疾病的发病机制有关。一些用于治疗这些疾病的药物已被证明具有抗氧化特性。我们的目的是评估酮色林(一种具有已证实的抗高血压疗效且对血液流变学有有益影响的选择性S2受体拮抗剂)是否也能够抑制脂质过氧化。在不同的体外生物系统中诱导脂质过氧化,并通过硫代巴比妥酸反应产物的形成进行评估。50微摩尔的酮色林可抑制人红细胞悬液中铜依赖性脂质过氧化40.8%,并抑制随后的溶血57.3%。在同一系统中,它在抑制过氧化氢依赖性脂质过氧化和溶血方面效率较低。100微摩尔的酮色林分别抑制肝微粒体悬液和脑全匀浆中由铜(II)和过氧化氢混合物诱导的脂质过氧化86.2%和56.7%。这些结果证明了酮色林具有抗氧化作用,尽管其治疗相关性仍未确定,但此前这一作用尚不为人知。