氧化应激状态,作为氧化还原稳态的破坏,在反复应用选定的乙酰胆碱酯酶再激活剂-肟引起的Wistar大鼠血清中,obidoxime,评估K027、K048、K074和K075。在整个研究中,每个肟以0.1个LD50/kgim的剂量给药2次/周,持续4周.然后,最后一次肟应用后七天,脂质过氧化标记物(丙二醛,MDA),和蛋白质氧化(高级氧化蛋白质产品,AOPP),以及抗氧化酶(过氧化氢酶,CAT,超氧化物歧化酶,SOD,还原型谷胱甘肽,GSH,和氧化型谷胱甘肽,GSSG),决心。氧化应激参数,MDA和AOPP在K048-,K074-和K075-处理组(p<0.001)。在奥比肟治疗组中,CAT的活性显着升高(p<0.05),而用K027,K048和K074处理诱导SOD水平升高(p<0.01,p<0.001)。有趣的是,每个肟处理组的GSH活性均显著升高.不像,用奥比肟治疗导致GSSG水平升高(p<0.01)。作为我们之前公布的数据的延续,这些结果保证了亚急性治疗后应用肟改善了大鼠的氧化状态和进一步的不良全身毒性作用。
Oxidative stress status, as a disruption of redox homeostasis, in the blood sera of Wistar rats caused by repeated application of selected acetylcholinesterase reactivators - asoxime, obidoxime, K027, K048, K074, and K075 were evaluated. Throughout this study, each oxime in a dose of 0.1 of LD50/kg im was given 2x/week for 4 weeks. Then, seven days after the last oximes\' application, markers of lipid peroxidation (malondialdehyde, MDA), and protein oxidation (advanced oxidation protein products, AOPP), as well as the activity of antioxidant enzymes (catalase, CAT, superoxide dismutase, SOD, reduced glutathione, GSH, and oxidized glutathione, GSSG), were determined. Oxidative stress parameters, MDA and AOPP were significantly highest in the K048-, K074- and K075-treated groups (p < 0.001). The activity of CAT was significantly elevated in the obidoxime-treated group (p < 0.05), while treatment with K027, K048, and K074 induced high elevation in SOD levels (p < 0.01, p < 0.001). Interestingly, the activity of GSH in each oxime-treated group was significantly elevated. Unlike, treatment with obidoxime caused elevation in GSSG levels (p < 0.01). As a continuation of our previously published data, these results assure that applied oximes following subacute treatment ameliorated the oxidative status and further adverse systemic toxic effects in rats.