Effect of glutathione depletion on tissue and plasma prostacyclin and thromboxane in rats.
Effect of glutathione depletion on tissue and plasma prostacyclin and thromboxane in rats.
复制标题
谷胱甘肽消耗对大鼠组织和血浆前列环素和血栓素的影响。
DOI：
10.1016/0006-2952(92)90611-l
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发表时间：
1992
影响因子：
5.8
通讯作者：
Bottje,WG
中科院分区：
文献类型：
--
作者：
Maynard,PM;Graupner,WG;Bottje,WG
实验旨在确定用l-丁硫氨酸亚磺酰亚胺 (BSO) 或马来酸二乙酯 (DEM) 消耗谷胱甘肽 (GSH) 对雄性 Sprague-Dawley 大鼠组织和血浆前列环素 (6-ketoPGF1α) 和血栓素 (TxB2) 水平的影响。尽管将肝脏 GSH 消耗至对照的 34%，但不同水平（0.4、0.8 和 1.2 g/kg 体重）的 BSO 对肝、肾、肺或心脏组织的 6-ketoPGF1α 和 TxB2 水平或门脉或动脉血浆中 6-ketoPGF1α 的循环水平没有影响。当用 3-甲基胆蒽 (3-MC) 预处理大鼠以诱导细胞色素 P450 时，BSO（0.8 g/kg 体重）对组织或血浆前列腺素水平也没有影响，但未诱导大鼠的肝脏 6-ketoPGF1α 略有但显着增加。相比之下，DEM（1 mL/kg体重）将肝、肾和肺组织GSH分别消耗至对照的12%、50%和30%，与这些组织和右心室心脏穿刺获得的血浆中6-酮PGF1α的升高相关。用 3-MC 预处理大鼠对对照或 DEM 处理大鼠的组织 GSH 或前列腺素水平没有显着影响，但 6-ketoPGF1α 血浆水平与未诱导大鼠相比较低。有或没有3-MC预处理的DEM与肾组织中TxB2增加相关，而DEM仅在非诱导大鼠的肺组织中升高TxB2。看来除了 GSH 消耗之外，可能还需要其他因素来提高体内血浆和/或组织 6-ketoPGF1α 水平。
Experiments were designed to determine the effects of glutathione (GSH) depletion withl-buthionine sulfoximine (BSO) or diethyl maleate (DEM) on tissue and plasma prostacyclin (6-ketoPGF1α) and thromboxane (TxB2) levels in male Sprague-Dawley rats. Despite depleting hepatic GSH to as much as 34% of control, BSO at various levels (0.4, 0.8 and 1.2 g/kg body wt) had no effect on hepatic, renal, pulmonary or cardiac tissue levels of 6-ketoPGF1αand TxB2or circulating levels of 6-ketoPGF1αin portal or arterial plasma. When rats were pretreated with 3-methylcholanthrene (3-MC) to induce cytochrome P450, BSO (0.8 g/kg body wt) also had no effect on tissue or plasma prostanoid levels with the exception of a slight, but significant, increase in hepatic 6-ketoPGF1αin non-induced rats. In contrast, depletions of hepatic, renal and pulmonary tissue GSH by DEM (1 mL/kg body wt) to 12, 50 and 30% of control, respectively, were associated with elevations of 6-ketoPGF1αin these tissues and in plasma obtained by right ventricular heart puncture. Pretreatment of rats with 3-MC had no significant effect on tissue GSH or prostanoid levels in controls or DEM-treated rats but plasma levels of 6-ketoPGF1αwere lower in comparison to non-induced rats. DEM with or without 3-MC pretreatment was associated with increased TxB2in renal tissue, whereas DEM elevated TxB2only in pulmonary tissue from non-induced rats. It appears that factors besides GSH depletion may be required to raise plasma and/or tissue 6-ketoPGF1αlevelsin vivo.