Malaria is a life-threatening disease caused by Plasmodium and represents one of the main public health problems in the world. Among alterations associated with the disease, we highlight the hepatic impairment resulting from the generation of oxidative stress. Studies demonstrate that liver injuries caused by Plasmodium infection are associated with unbalance of the antioxidant system in hepatocytes, although little is known about the role of antioxidant molecules such as glutathione and vitamin C in the evolution of the disease and in the liver injury. To evaluate disease complications, murine models emerge as a valuable tool due to their similarities between the infectious species for human and mice. Herein, the aim of this study is to evaluate the effect of antioxidants glutathione and vitamin C on the evolution of murine malaria and in the liver damage caused by Plasmodium berghei ANKA infection. Mice were inoculated with parasitized erythrocytes and treated with glutathione and vitamin C, separately, both at 8 mg/kg during 7 consecutive days. Our data showed that during Plasmodium infection, treatment with glutathione promoted significant decrease in the survival of infected mice, accelerating the disease severity. However, treatment with vitamin C promoted an improvement in the clinical outcomes and prolonged the survival curve of infected animals. We also showed that glutathione promoted increase in the parasitemia rate of Plasmodium-infected animals, although treatment with vitamin C has induced significant decrease in parasitemia rates. Furthermore, histological analysis and enzyme biochemical measurement showed that treatment with glutathione exacerbates liver damage while treatment with vitamin C mitigates the hepatic injury induced by the infection. In summary, the current study provided evidences that antioxidant molecules could differently modulate the outcome of malaria disease; while glutathione aggravated the disease outcome and liver injury, the treatment with vitamin C protects the liver from damage and the evolution of the condition.

中文翻译：

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抗氧化剂谷胱甘肽和维生素C对伯氏疟原虫ANKA感染所致肝损伤的差异化作用

疟疾是由疟原虫引起的危及生命的疾病，是世界上主要的公共卫生问题之一。在与疾病相关的改变中，我们强调了由氧化应激产生的肝损伤。研究表明，疟原虫引起的肝损伤感染与肝细胞抗氧化系统的失衡有关，尽管我们对谷胱甘肽和维生素 C 等抗氧化分子在疾病发展和肝损伤中的作用知之甚少。为了评估疾病并发症，小鼠模型成为一种有价值的工具，因为它们在人类和小鼠的传染性物种之间存在相似性。在此，本研究的目的是评估抗氧化剂谷胱甘肽和维生素 C 对鼠疟疾演变和伯氏疟原虫ANKA 感染引起的肝损伤的影响。小鼠接种了寄生的红细胞，并在连续 7 天内分别用 8 毫克/千克的谷胱甘肽和维生素 C 处理。我们的数据显示，在疟原虫期间感染后，谷胱甘肽治疗会显着降低受感染小鼠的存活率，从而加速疾病的严重程度。然而，维生素 C 治疗促进了临床结果的改善，并延长了受感染动物的生存曲线。我们还发现在的原虫率谷胱甘肽促进增加疟原虫- 受感染的动物，尽管用维生素 C 治疗已导致寄生虫血症发生率显着降低。此外，组织学分析和酶生化测量表明，谷胱甘肽治疗会加剧肝损伤，而维生素 C 治疗可减轻感染引起的肝损伤。总之，目前的研究提供的证据表明抗氧化剂分子可以不同地调节疟疾疾病的结果；虽然谷胱甘肽会加重疾病结果和肝损伤，但维生素 C 治疗可以保护肝脏免受损伤和病情发展。