二乙基卡马嗪调节微丝狗尾草感染代理宿主小鼠抗氧化酶活性

Nevin K Govindan, Jayakumar K Kochukunju
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摘要

牛的常见丝虫病,其幼虫被称为,在血液和腹膜中发现,并引起一种称为脑脊髓线虫病的疾病。不可避免地需要及时发现和治疗这些丝虫病。由多种丝虫引起的感染传统上用乙基卡马嗪(DEC)治疗。DEC最值得注意的方面是,它似乎对丝虫病寄生虫几乎没有影响。然而,DEC可能作用于寄生虫的表面,揭开抗原。本研究旨在评价DEC对(Mf)感染小鼠抗氧化酶活性、超氧化物歧化酶(SOD)和过氧化氢酶(CAT)的影响。收集并分离Mf,注射到瑞士种小鼠体内12天。按对照组、对照组+DEC、对照组+Mf、对照组+Mf+DEC分组。结果显示,对照组+Mf+DEC腹膜液中CAT活性明显高于对照组。在Control+DEC和Control+Mf小鼠中,活性值相近。与对照组相比,对照组+Mf+DEC小鼠腹膜液中SOD活性从1天到12天保持升高。虽然DEC单独处理小鼠并没有显示出这些酶活性的任何显著增加。感染小鼠经dec处理后第3天和第5天SOD水平升高可能是由于活性氧的产生。被认为是由于细胞的生化平衡向氧化损伤倾斜而发生的,如果氧化损伤失败,自由基的去除减少导致组织损伤的结果。结果表明,DEC处理可能影响了Mf的生存,表现为抗氧化酶的增加,这可能是由于Mf的排泄产物引起的炎症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Diethylcarbamazine modulates the antioxidant enzyme activity in proxy host mice infected with the Setaria microfilariae
The common filarial worm of cattle, , whose larvae are known as , are discovered in the blood and peritoneum and cause a condition known as cerebrospinal nematodiasis. There is an unavoidable need for prompt detection and treatment of these filarial diseases. Infections caused by a variety of filarial species have traditionally been treated with diethylcarbamazine (DEC). The most notable aspect of DEC is that, , it appears to have little effect on filarial parasites. However, DEC may act on the parasite's surface, unmasking antigen. This study was initiated to evaluate the effect of DEC on the antioxidant enzyme activities, Superoxide dismutase (SOD), and Catalase (CAT) of mice infected with (Mf). was collected and the Mf was isolated and injected into Swiss-bred mice for 12 days. The animals were grouped as Control, Control +DEC, Control + Mf, and Control+Mf+DEC. The results showed that CAT activity in the peritoneal fluid of Control+Mf+DEC was found to be elevated at a higher level compared to the control. The activity in the Control+DEC and Control+Mf mice showed similar values. SOD activity in the peritoneal fluid of Control+Mf+DEC mice remained elevated from the 1 day to the 12 day compared to the control. Though DEC alone treated mice did not show any profound increase in the activity of these enzymes. The rise in SOD level during the 3 and 5 day of the DEC-treated infected mice may be due to the production of active oxygen species. Proposed to occur as a result of a tilt in the biochemical balance of the cells towards the oxidative damage, failing which decreased removal of free radicals leading to tissue damage results. The result showed that the DEC treatment may be affecting the survival of the Mf shown by the increased antioxidant enzymes which may be due to the inflammation caused by the excretory products of Mf.
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