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Buprenorphine and Methadone as Opioid Maintenance Treatments for Heroin-Addicted Patients Induce Oxidative Stress in Blood

机译:丁丙诺啡和美沙酮作为阿片类药物上瘾患者的维护治疗方法诱导血液中的氧化应激

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Buprenorphine and methadone are two substances widely used in the substitution treatment of patients who are addicted to opioids. Although it is known that they partly act efficiently towards this direction, there is no evidence regarding their effects on the redox status of patients, a mechanism that could potentially improve their action. Therefore, the aim of the present investigation was to examine the impact of buprenorphine and methadone, which are administered as substitutes to heroin-dependent patients on specific redox biomarkers in the blood. From the results obtained, both the buprenorphine (n=21) and the methadone (n=21) groups exhibited oxidative stress and compromised antioxidant defence. This was evident by the decreased glutathione (GSH) concentration and catalase activity in erythrocytes and the increased concentrations of thiobarbituric acid reactive substances (TBARS) and protein carbonyls in the plasma, while there was no significant alteration of plasma total antioxidant capacity (TAC) compared to the healthy individuals (n=29). Furthermore, methadone revealed more severe oxidant action compared to buprenorphine. Based on relevant studies, the tested substitutes mitigate the detrimental effects of heroin on patient redox status; still it appears that they need to be boosted. Therefore, concomitant antioxidant administration could potentially enhance their beneficial action, and most probably, buprenorphine that did not induce oxidative stress in such a severe mode as methadone, on the regulation of blood redox status.
机译:丁丙诺啡和美沙酮是两种广泛用于替补阿片类药物的患者的替代治疗的物质。虽然已知它们部分行动朝向这个方向,但没有证据表明它们对患者的氧化还原地位的影响,这是一种可能改善行动的机制。因此,本研究的目的是检查丁丙诺啡和美沙酮的影响,该蛋白质依赖于海洛因依赖性患者的血液中的特定氧化还原生物标志物。从得到的结果中,丁丙诺啡(N = 21)和美沙酮(N = 21)组显示出氧化应激和受损的抗氧化剂防御。通过在红细胞中降低的谷胱甘肽(GSH)浓度和过氧化氢酶活性和血浆中的硫尿嘧啶酸反应性物质(TBARS)和蛋白质羰基浓度的增加,这是显而易见的,而血浆总抗氧化能力(TAC)没有显着改变对健康的人(n = 29)。此外,与丁丙诺啡相比,美沙酮揭示了更严重的氧化剂作用。基于相关研究,测试的替代品减轻海洛因对患者氧化还原状态的不利影响;似乎似乎他们需要提升。因此,伴随的抗氧化剂给药可能潜在地增强它们的有益作用,并且最多可能是在血氧化还原状态的调节下,不诱导氧化胁迫的丁丙诺啡。

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