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首页> 外文期刊>Life sciences >IS INTESTINAL CYTOSOLIC GLUTATHIONE S-TRANSFERASE AN ALTERNATIVE DETOXIFICATION PATHWAY IN TWO-THIRDS HEPATECTOMIZED RATS
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IS INTESTINAL CYTOSOLIC GLUTATHIONE S-TRANSFERASE AN ALTERNATIVE DETOXIFICATION PATHWAY IN TWO-THIRDS HEPATECTOMIZED RATS

机译：是肠道脂质体谷胱甘肽S-转移酶在三类肝癌大鼠中的替代性解毒途径

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The present study was designed to investigate the effect of partial (two-thirds) hepatectomy (PH) on hepatic and intestinal glutathione S-transferases (GSTs) activities. A significant decrease of cytosolic hepatic GSTs activity was observed after the PH. The lowest value of hepatic GSTs was obtained 48 h after the surgery. On the other hand, intestinal GSTs activities increased after PH, reaching the highest values 48 h after the hepatic lobes resection. The hepatic GSTs activities diminution was attributed, in part, to the high accumulation of bile acids in the liver tissue of hepatectomized rats, also demonstrated by a higher retention of [C-14] taurocholate. The kinetic analysis performed with 1-chloro-2,4-dinitrobenzene (CDNB) as substrate showed two sets of parameters, indicating the presence of isozymes of high and low affinities. Vmax(1) and Vmax(2) were lower in PH rats suggesting a non competitive inhibition mechanism. The inhibitory effect of bile acids decreased during liver regeneration process of hepatectomized rats dissapearing at 7 days after PH. Conversely, in non regenerating rats (GABA treated) the inhibitory mechanism was still observed at 7 days after the surgery. The increase of intestinal GSTs activities (isozymes of high and low affinities) was attributed to tile presence of polyamines, mainly putrescine, produced during tile hepatic regeneration process. In this regard, it was showed that GABA treatment, which inhibits polyamine synthesis, completely abolished the increase on intestinal GSTs activities. Finally, the treatment with exogenous putrescine showed that in hepatectomized and sham-operated rats. the polyamine induced GSTs activities in both tissues. In PH rats, the putrescine dependent increase of hepatic GSTs was masked by the inhibitor effect of bile acids. In addition, a summation effect of endogenous and exogenous putrescine was probably tile reason of the induction of intestinal GSTs after PH. The GSH/GSSG ratio did not change during the treatments, as well as the microsomal GST activity of both tissues. The work points out the hypothetical detoxification power of the intestine during the hepatocellular insufficiency which follows a two-thirds hepatectomy. [References: 35]
机译：本研究旨在调查部分（三分之二）肝切除术（PH）对肝和肠谷胱甘肽S-转移酶（GSTs）活性的影响。 PH后观察到胞质肝GSTs活性显着降低。术后48小时获得最低的肝GST值。另一方面，PH后肠GST活性增加，肝叶切除后48小时达到最高值。肝脏GSTs活性的降低部分归因于肝切除大鼠肝脏组织中胆汁酸的高积累，这也由[C-14]牛磺胆酸盐的较高保留率所证实。以1-氯-2,4-二硝基苯（CDNB）为底物进行的动力学分析显示了两组参数，表明存在高亲和力和低亲和力的同工酶。 PH大鼠中的Vmax（1）和Vmax（2）较低，提示非竞争性抑制机制。在PH后7天消失的肝切除大鼠肝再生过程中，胆汁酸的抑制作用降低。相反，在非再生大鼠（经GABA处理）中，在术后7天仍观察到抑制机制。肠道GST活性（高亲和力和低亲和力的同工酶）的增加归因于在瓷砖的肝再生过程中产生的多胺（主要是腐胺）的存在。在这方面，已经表明抑制多胺合成的GABA处理完全消除了肠道GST活性的增加。最后，外源性腐胺的治疗表明，在肝切除和假手术的大鼠中均如此。多胺诱导两个组织中的GST活性。在PH大鼠中，胆汁酸的抑制作用掩盖了腐胺依赖性肝GST的增加。此外，内源性和外源性腐胺的总和效应可能是PH后诱导肠GSTs的原因。在治疗期间，GSH / GSSG比率以及两个组织的微粒体GST活性均未改变。这项工作指出了在三分之二的肝切除术后肝细胞供血不足期间肠的假定解毒能力。 [参考：35]

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