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首页> 外文期刊>Ciência Rural >Exogenous ATP administration prevents ischemia/reperfusion-induced oxidative stress and tissue injury by modulation of hypoxanthine metabolic pathway in rat ovary
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Exogenous ATP administration prevents ischemia/reperfusion-induced oxidative stress and tissue injury by modulation of hypoxanthine metabolic pathway in rat ovary

机译:外源ATP的给药通过调节大鼠卵巢次黄嘌呤的代谢途径来防止缺血/再灌注诱导的氧化应激和组织损伤

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摘要

In this study, xanthine oxidase (XO), malondialdehyde (MDA), myeloperoxidase (MPO) and glutathione (GSH) levels in the ovarian tissues of rats during the development of ischemia and postischemia-induced reperfusion were investigated, and the effect of ATP on ischemia-reperfusion (I/R) damage was biochemically and histopathologically examined. The results of the biochemical analyses demonstrated that ATP significantly reduced the level of XO and MDA and increased the amount of GSH in both ischemia and I/R-applied ovarian tissue at the doses administered. Furthermore, ATP significantly suppressed the increase in MPO activity that occurred following the application of post ischemia reperfusion in the ovarian tissue. The biochemical results obtained in the present study coincide with the histological findings. The severity of the pathological findings, such as dilatation, congestion, haemorrhage, oedema and polymorphonuclear nuclear leukocytes (PMNLs), increased in parallel with the increase observed in the products of XO metabolism. In conclusion, exogenously applied ATP prevented I/R damage by reducing the formation of XO in ischemic ovarian tissue.
机译:在这项研究中,研究了大鼠卵巢组织在缺血和缺血后诱导的再灌注过程中黄嘌呤氧化酶(XO),丙二醛(MDA),髓过氧化物酶(MPO)和谷胱甘肽(GSH)的水平,并研究了ATP对卵巢组织的影响缺血再灌注(I / R)损伤进行了生化和组织病理学检查。生化分析的结果表明,在给药剂量下,ATP显着降低了缺血和I / R施用卵巢组织中XO和MDA的水平,并增加了GSH的量。此外,ATP显着抑制了在卵巢组织中施加缺血再灌注后发生的MPO活性的增加。在本研究中获得的生化结果与组织学结果一致。病理结果的严重性(如扩张,充血,出血,水肿和多形核核白细胞(PMNL))与XO代谢产物中所观察到的增加同时增加。总之,外源施加的ATP通过减少缺血性卵巢组织中XO的形成来防止I / R损伤。

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