Chiarani Fábria, Bavaresco Caren S, Dutra-Filho Carlos S, Netto Carlos Alexandre, Wyse Angela T S
Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Rua Ramiro Barcelos, 2600-Anexo, Porto Alegre, RS, Brazil.
Metab Brain Dis. 2008 Mar;23(1):123-32. doi: 10.1007/s11011-007-9073-2. Epub 2007 Nov 22.
The main objective of this study was to investigate the in vitro effects of sulfite, a metabolite accumulated in isolated sulfite oxidase deficiency, on Na (+), K (+)-ATPase activity and on some parameters of oxidative stress, namely thiobarbituric acid-reactive substances (TBARS) and catalase activity (antioxidant enzyme) in cerebral cortex, striatum and hippocampus from 10- and 60-day-old rats. Results showed that 500 microM sulfite significantly increased TBARS and reduced catalase activity in the cerebral structures studied from neonates and adults rats; in contrast, sulfite did not alter Na(+), K(+)-ATPase activity. Our present findings show that sulfite increases lipid peroxidation and decreases antioxidant enzyme defenses in rat brain, suggesting an induction of oxidative stress. We presumed that oxidative stress might be, at least in part, associated with the neuronal dysfunction of patients affected by isolated sulfite oxidase deficiency.
本研究的主要目的是探讨亚硫酸盐（一种在孤立性亚硫酸盐氧化酶缺乏症中积累的代谢产物）对10日龄和60日龄大鼠大脑皮层、纹状体和海马体中Na(+)、K(+)-ATP酶活性以及氧化应激的一些参数（即硫代巴比妥酸反应性物质（TBARS）和过氧化氢酶活性（抗氧化酶））的体外影响。结果表明，500微摩尔亚硫酸盐显著增加了新生大鼠和成年大鼠所研究脑区的TBARS并降低了过氧化氢酶活性；相比之下，亚硫酸盐并未改变Na(+)、K(+)-ATP酶活性。我们目前的研究结果表明，亚硫酸盐会增加大鼠大脑中的脂质过氧化并降低抗氧化酶防御能力，提示氧化应激的诱导。我们推测，氧化应激可能至少部分与受孤立性亚硫酸盐氧化酶缺乏症影响患者的神经元功能障碍有关。
