Acadêmica do Curso de Enfermagem da Universidade Federal do Piauí, Piauí, Brazil.
Oxid Med Cell Longev. 2009 Sep-Oct;2(4):214-21. doi: 10.4161/oxim.2.4.8876.
Ascorbic acid has many nonenzymatic actions and is a powerful water-soluble antioxidant. It protects low density lipoproteins from oxidation and reduces harmful oxidants in the central nervous system. Pilocarpine-induced seizures have been suggested to be mediated by increases in oxidative stress. Current studies have suggested that antioxidant compounds may afford some level of neuroprotection against the neurotoxicity of seizures. The objective of the present study was to evaluate the neuroprotective effects of ascorbic acid (AA) in rats, against the observed oxidative stress during seizures induced by pilocarpine. Wistar rats were treated with 0.9% saline (i.p., control group), ascorbic acid (500 mg/kg, i.p., AA group), pilocarpine (400 mg/kg, i.p., pilocarpine group), and the association of ascorbic acid (500 mg/kg, i.p.) plus pilocarpine (400 mg/kg, i.p.), 30 min before of administration of ascorbic acid (AA plus pilocarpine group). After the treatments all groups were observed for 6h. The enzyme activities as well as the lipid peroxidation and nitrite concentrations were measured using spectrophotometric methods and the results compared to values obtained from saline and pilocarpine-treated animals. Protective effects of ascorbic acid were also evaluated on the same parameters. In pilocarpine group there was a significant increase in lipid peroxidation and nitrite level. However, no alteration was observed in superoxide dismutase and catalase activities. Antioxidant treatment significantly reduced the lipid peroxidation level and nitrite content as well as increased the superoxide dismutase and catalase activities in hippocampus of adult rats after seizures induced by pilocarpine. Our findings strongly support the hypothesis that oxidative stress in hippocampus occurs during seizures induced by pilocarpine, proving that brain damage induced by the oxidative process plays a crucial role in seizures pathogenic consequences, and also imply that a strong protective effect could be achieved using ascorbic acid.
抗坏血酸具有许多非酶促作用，是一种强大的水溶性抗氧化剂。它可以保护低密度脂蛋白免受氧化，并减少中枢神经系统中的有害氧化剂。已有人提出，毛果芸香碱诱导的癫痫发作可能是由氧化应激增加介导的。目前的研究表明，抗氧化化合物可能在一定程度上提供对癫痫毒性的神经保护作用。本研究的目的是评估抗坏血酸（AA）对毛果芸香碱诱导的癫痫发作期间观察到的氧化应激的神经保护作用。Wistar 大鼠用 0.9%生理盐水（ip，对照组）、抗坏血酸（500mg/kg，ip，AA 组）、毛果芸香碱（400mg/kg，ip，毛果芸香碱组）和抗坏血酸（500mg/kg，ip）加毛果芸香碱（400mg/kg，ip）治疗，抗坏血酸给药前 30min 加药（AA 加毛果芸香碱组）。所有组治疗后观察 6h。采用分光光度法测定酶活性、脂质过氧化和亚硝酸盐浓度，并与生理盐水和毛果芸香碱处理动物的测定值进行比较。还评估了抗坏血酸对相同参数的保护作用。毛果芸香碱组脂质过氧化和亚硝酸盐水平显著升高。然而，超氧化物歧化酶和过氧化氢酶活性无变化。抗氧化治疗显著降低了脂质过氧化水平和亚硝酸盐含量，并增加了毛果芸香碱诱导的成年大鼠海马中的超氧化物歧化酶和过氧化氢酶活性。我们的研究结果强烈支持这样一种假设，即在毛果芸香碱诱导的癫痫发作期间，海马中发生氧化应激，证明由氧化过程引起的脑损伤在癫痫发病后果中起着至关重要的作用，这也意味着使用抗坏血酸可以实现强大的保护作用。
