Mesquita Casagrande Ana Caroline, Wamser Morgahna Nathalie, de Lima Daniela Delwing, Pereira da Cruz José Geraldo, Wyse Angela T S, Dal Magro Débora Delwing
Departamento de Medicina, Centro de Ciências da Saúde, Universidade Regional de Blumenau, Brazil.
Nucleosides Nucleotides Nucleic Acids. 2013;32(1):42-57. doi: 10.1080/15257770.2012.760043.
We herein investigated the in vitro effect of hypoxanthine on the activities of antioxidant enzymes such as catalase (CAT), glutathione peroxidase (GSH-Px), and superoxide dismutase (SOD) in erythrocytes, as well as on thiobarbituric acid-reactive substances (TBA-RS), in the plasma of rats. Results showed that hypoxanthine, when added to the incubation medium, enhanced CAT (10.0 μM), GSH-Px and SOD (8.5 μM and 10.0 μM) activities in erythrocytes of 15-day-old rats, reduced CAT activity (10.0 μM) and enhanced GSH-Px activity (10.0 μM) in erythrocytes of 30-day-old rats, reduced CAT activity (10.0 μM) and enhanced GSH-Px activity (8.5 μM and 10.0 μM) in erythrocytes of 60-day-old rats, as compared to controls. In addition, hypoxanthine (10.0 μM) enhanced TBA-RS levels in the plasma of 30- and 60-day old rats. Furthermore, we also tested the influence of allopurinol, trolox, and ascorbic acid on the effects elicited by hypoxanthine on the antioxidant enzymes and TBA-RS. Allopurinol and/or administration of antioxidants prevented most alterations caused by hypoxanthine in the oxidative stress parameters evaluated. Findings suggest that hypoxanthine alters antioxidant defenses and induces lipid peroxidation in the blood of rats; however, in the presence of allopurinol and antioxidants, some of these alterations in oxidative stress caused are prevented. Data indicate that, in humans, antioxidant administration might serve as a potential adjuvant therapy for ameliorating the damage caused by hypoxanthine.
我们在此研究了次黄嘌呤对大鼠红细胞中过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-Px）和超氧化物歧化酶（SOD）等抗氧化酶活性的体外影响，以及对大鼠血浆中硫代巴比妥酸反应性物质（TBA-RS）的影响。结果表明，当将次黄嘌呤添加到孵育培养基中时，其可增强15日龄大鼠红细胞中的CAT（10.0 μM）、GSH-Px和SOD（8.5 μM和10.0 μM）活性，降低30日龄大鼠红细胞中的CAT活性（10.0 μM）并增强GSH-Px活性（10.0 μM），降低60日龄大鼠红细胞中的CAT活性（10.0 μM）并增强GSH-Px活性（8.5 μM和10.0 μM），与对照组相比。此外，次黄嘌呤（10.0 μM）可提高30日龄和60日龄大鼠血浆中的TBA-RS水平。此外，我们还测试了别嘌呤醇、生育三烯酚和抗坏血酸对次黄嘌呤对抗氧化酶和TBA-RS所产生影响的作用。别嘌呤醇和/或抗氧化剂的给药可预防次黄嘌呤在评估的氧化应激参数中引起的大多数改变。研究结果表明，次黄嘌呤会改变大鼠血液中的抗氧化防御并诱导脂质过氧化；然而，在存在别嘌呤醇和抗氧化剂的情况下，可预防一些由其引起的氧化应激改变。数据表明，在人类中，给予抗氧化剂可能作为一种潜在的辅助疗法来减轻次黄嘌呤造成的损害。
