The effect of d-galactose induced oxidative stress on in vitro redox homeostasis in rat plasma and erythrocytes

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• 作者：Daniela Delwing-de Lima^a ; ^b ; ^{daniela.delwing@univille.br} ; ^{danidelwing@hotmail.com} ; Silmara Brietzig Hennrich^b ; Dé ; bora Delwing-Dal Magro^d ; Juliana Gruenwaldt Maia Auré ; lio^c ; Ana Paula Serpa^a ; Thierry Waltrich Augusto^c ; Nariana Regina Pereira^c
• 关键词：Galactose ; Oxidative stress ; Antioxidants ; in vitro ; Erythrocytes ; Plasma ; Rats
• 刊名：Biomedicine & Pharmacotherapy
• 出版年：2017
• 出版时间：February 2017
• 年：2017
• 卷：86
• 期：Complete
• 页码：686-693
• 全文大小：987 K
• 卷排序：86

文摘

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 10.0 mM. 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 3.0 mM, 5.0 mM and 10.0 mM, enhanced TBA-RS in the plasma of 60-day-old rats, while 10.0 mM galactose reduced total sulfhydryl content in the plasma of 30-day-old rats; 5.0 mM and 10.0 mM galactose enhanced CAT activity in the erythrocytes of 30- and 60-day-old rats and 10.0 mM 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 5.0 mM), 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.