Häussinger D, Sies H, Gerok W
J Hepatol. 1985;1(1):3-14. doi: 10.1016/s0168-8278(85)80063-5.
In the rat liver acinus area synthesis and glutaminase activity are predominantly localized in the periportal area, whereas glutamine synthetase activity and the transport system for glutamate in the plasma membrane are perivenous. Detoxification of ammonium ions at low concentrations occurs exclusively by glutamine synthesis, but not by urea formation. Therefore, the two pathways of ammonia detoxification in the liver acinus represent the sequence of a low-affinity, but high-capacity system (urea synthesis) and a high-affinity system (glutamine synthesis). In agreement with this finding, obtained in experiments with the metabolically- and structurally-intact perfused rat liver, is also an almost complete inhibition of perivenous glutamine synthesis without impairment of periportal urea synthesis. This was shown after induction of a perivenous liver cell necrosis following CCl4 pretreatment with the consequence of a diminished hepatic ammonia extraction. Periportal glutaminase and perivenous glutamine synthetase are simultaneously active, resulting in an intercellular (as opposed to intracellular) glutamine cycle, being under the control of hormones, pH and portal ammonia and glutamine concentrations. The intercellular glutamine cycle provides an effective means for almost complete conversion of portal ammonium ions to urea by additional substrate supply of periportal urea synthesis, by periportal glutamine degradation and by the perivenous re-synthesis of glutamine from ammonia which escaped urea synthesis. Because urea synthesis, in contrast to glutamine synthesis, is a major pathway for the removal of bicarbonate, the switching of ammonia detoxification from urea synthesis to glutamine synthesis in acidosis or vice versa in alkalosis points to an important role of the liver in maintaining pH homeostasis. The acid-base-induced changes of the route of hepatic ammonia detoxification and therefore bicarbonate removal are performed by the regulatory properties of the enzymes of the intercellular glutamine cycle.
在大鼠肝腺泡区,合成和谷氨酰胺酶活性主要定位于门静脉周围区域,而谷氨酰胺合成酶活性以及质膜中谷氨酸转运系统则位于肝静脉周围区域。低浓度铵离子的解毒仅通过谷氨酰胺合成进行,而非通过尿素形成。因此,肝腺泡中氨解毒的两条途径代表了一个低亲和力但高容量系统(尿素合成)和一个高亲和力系统(谷氨酰胺合成)的顺序。与在代谢和结构完整的灌注大鼠肝脏实验中获得的这一发现一致的是,肝静脉周围谷氨酰胺合成几乎完全受到抑制,而门静脉周围尿素合成未受损害。在用四氯化碳预处理诱导肝静脉周围肝细胞坏死并导致肝脏氨摄取减少后,这一点得到了证实。门静脉周围谷氨酰胺酶和肝静脉周围谷氨酰胺合成酶同时活跃,导致细胞间(而非细胞内)谷氨酰胺循环,该循环受激素、pH值以及门静脉氨和谷氨酰胺浓度的控制。细胞间谷氨酰胺循环通过门静脉周围尿素合成的额外底物供应、门静脉周围谷氨酰胺降解以及从逃脱尿素合成的氨中肝静脉周围重新合成谷氨酰胺,为将门静脉铵离子几乎完全转化为尿素提供了一种有效手段。因为与谷氨酰胺合成不同,尿素合成是去除碳酸氢根的主要途径,酸中毒时氨解毒从尿素合成切换到谷氨酰胺合成,或碱中毒时反之,这表明肝脏在维持pH值稳态中起重要作用。肝氨解毒途径以及因此碳酸氢根去除的酸碱诱导变化是由细胞间谷氨酰胺循环酶的调节特性完成的。