Kurhaliuk N M, Serebrovs'ka T V
Ivan Franko Lviv National University, A.A. Bogomoletz Institute of Physiology Ukrainian Academy of Sciences, Kiev.
Fiziol Zh (1994). 2003;49(3):104-9.
The object of this study was to investigate the effects of exogenous succinate (SC) and alpha-ketoglutarate (KGL) on intensity of NO metabolism, lipid peroxidation and antioxidant enzymes activity in rat liver tissues under acute hypoxia (AH). Six groups of Wistar male rats participated in the study. Animals of Gr. I underwent i.p. saline injection, Gr. II--saline injection and AH (inhalation of 7% O2, 30 min). Gr. III and IY were examined after i.p. injection of SC (50 mg/kg) or KGL (200 mg/kg) and AH test; Gr. Y-after i.p. injection of SC with alpha- beta-adrenoblockers phentolamine and obzidane (2 mg each) and AH test, Gr. 6-after i.p. injection of KGL with M- and N-cholinoreceptor blockers athropine (5 mg) and benzohexonium (10 mg) and AH test. It was shown that AH provoked the decrease of NO production by 34%, the addition of SC augmented twice the nitrite anion content, the addition of KGL--in three times. KGL decreased malon dialdehyde content under AH by 32% and SC- by 25%. The least level of lipid peroxidation was registered in Gr. YI. Adrenoblockers did not influence on antioxidant enzymes activity under AH, but cholinoblockers completely eliminated the increase of SOD, catalase, glutathione peroxidase and glutathione reductase activities under KGL treatment. We conclude that nitric oxide production under alpha-ketoglutarate influence is mediated by cholinoreceptors.
本研究的目的是探讨外源性琥珀酸盐（SC）和α-酮戊二酸（KGL）对急性缺氧（AH）大鼠肝组织中一氧化氮代谢强度、脂质过氧化及抗氧化酶活性的影响。六组Wistar雄性大鼠参与了本研究。第一组动物腹腔注射生理盐水，第二组——注射生理盐水并进行急性缺氧（吸入7%氧气，30分钟）。第三组和第四组在腹腔注射SC（50毫克/千克）或KGL（200毫克/千克）后进行急性缺氧试验；第五组——在腹腔注射SC并联合α-β肾上腺素能阻滞剂酚妥拉明和阿齐旦（各2毫克）后进行急性缺氧试验，第六组——在腹腔注射KGL并联合M-和N-胆碱能受体阻滞剂阿托品（5毫克）和苯六甲铵（10毫克）后进行急性缺氧试验。结果表明，急性缺氧使一氧化氮生成量降低34%，添加SC使亚硝酸根阴离子含量增加两倍，添加KGL使亚硝酸根阴离子含量增加三倍。急性缺氧时，KGL使丙二醛含量降低32%，SC使丙二醛含量降低25%。第六组脂质过氧化水平最低。肾上腺素能阻滞剂对急性缺氧时的抗氧化酶活性无影响，但胆碱能阻滞剂完全消除了KGL处理时超氧化物歧化酶、过氧化氢酶、谷胱甘肽过氧化物酶和谷胱甘肽还原酶活性的增加。我们得出结论，α-酮戊二酸影响下的一氧化氮生成是由胆碱能受体介导的。
