Departamento de Medicina, Universidade da Região de Joinville, UNIVILLE, Rua Paulo Malschitzki, 10-Zona Industrial Norte, CEP 89201-972, Joinville, SC, Brazil; Programa de Pós-Graduação em Saúde e Meio Ambiente, Universidade da Região de Joinville, UNIVILLE, Rua Paulo Malschitzki, 10-Zona Industrial Norte, CEP 89201-972, Joinville, SC, Brazil.
Programa de Pós-Graduação em Saúde e Meio Ambiente, Universidade da Região de Joinville, UNIVILLE, Rua Paulo Malschitzki, 10-Zona Industrial Norte, CEP 89201-972, Joinville, SC, Brazil.
Biomed Pharmacother. 2017 Feb;86:686-693. doi: 10.1016/j.biopha.2016.12.011. Epub 2016 Dec 28.
We, herein, investigated the in vitro effects of galactose on thiobarbituric acid-reactive substances (TBA-RS), total sulfhydryl content, and on the activities of antioxidant enzymes, including catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px), and butyrylcholinesterase (BuChE) in the blood of 30- and 60-day-old rats. We also determined the influence of the antioxidants, trolox, ascorbic acid and glutathione, on the effects elicited by galactose on the parameters tested. Galactose was added to the assay at final concentrations of 0.1, 3.0, 5.0 and 10.0mM. Control experiments were performed without the addition of galactose. Rats were sacrificed by decapitation without anesthesia and a blood sample was removed for analysis. Galactose, at 3.0mM, 5.0mM and 10.0mM, enhanced TBA-RS in the plasma of 60-day-old rats, while 10.0mM galactose reduced total sulfhydryl content in the plasma of 30-day-old rats; 5.0mM and 10.0mM galactose enhanced CAT activity in the erythrocytes of 30- and 60-day-old rats and 10.0mM galactose reduced SOD activity in the erythrocytes of 60-day-old rats. Galactose did not alter BuChE activity. Data showed that at the pathologically high concentration (greater than 5.0mM), galactose induces lipid peroxidation, reduces total sulfhydryl content and alters antioxidant defenses in the blood of rats. Trolox, ascorbic acid and glutathione addition prevented most alterations in oxidative stress parameters that were caused by galactose. Our findings lend support to a potential therapeutic strategy for this disease, which may include the use of antioxidants for ameliorating the damage caused by galactose.
我们在此研究了半乳糖对 30 日龄和 60 日龄大鼠血液中硫代巴比妥酸反应物质（TBA-RS）、总巯基含量以及抗氧化酶（包括过氧化氢酶（CAT）、超氧化物歧化酶（SOD）和谷胱甘肽过氧化物酶（GSH-Px）和丁酰胆碱酯酶（BuChE））活性的体外影响。我们还测定了抗氧化剂 Trolox、抗坏血酸和谷胱甘肽对半乳糖对所测试参数产生的影响的影响。半乳糖终浓度为 0.1、3.0、5.0 和 10.0mM 时加入测定。未添加半乳糖进行对照实验。大鼠未经麻醉断头处死，取血样进行分析。3.0mM、5.0mM 和 10.0mM 半乳糖增强了 60 日龄大鼠血浆中的 TBA-RS，而 10.0mM 半乳糖降低了 30 日龄大鼠血浆中的总巯基含量；5.0mM 和 10.0mM 半乳糖增强了 30 日龄和 60 日龄大鼠红细胞中的 CAT 活性，而 10.0mM 半乳糖降低了 60 日龄大鼠红细胞中的 SOD 活性。半乳糖没有改变 BuChE 活性。数据表明，在病理高浓度（大于 5.0mM）下，半乳糖诱导脂质过氧化，降低总巯基含量并改变大鼠血液中的抗氧化防御。Trolox、抗坏血酸和谷胱甘肽的添加阻止了半乳糖引起的大多数氧化应激参数的改变。我们的研究结果支持了针对这种疾病的潜在治疗策略，该策略可能包括使用抗氧化剂来改善半乳糖引起的损伤。
