Dolińska M, Hilgier W, Albrecht J
Department of Neurotoxicology, Polish Academy of Sciences, Warszawa, Poland.
Neurosci Lett. 1996 Jul 26;213(1):45-8. doi: 10.1016/0304-3940(96)12827-5.
The uptake of [3H]glutamine (GLN) to non-synaptic mitochondria isolated from rat cerebral hemispheres was measured in the absence or presence of 3 mM ammonium ion (ammonium chloride; ammonia). Ammonia increased Vmax of the saturable component of GLN uptake by > 20%, without affecting K(m), but did not change a non-saturable component of GLN transport representing diffusion or uptake mediated by a very low affinity carrier. Since GLN is an idiogenic osmole, its increased uptake may contribute to the swelling of astrocytic mitochondria and, subsequently, to a decrease in cerebral energy metabolism usually associated with acute hyperammonemic states. The result is consistent with the recent view that GLN accumulating in the brain in hyperammonemic conditions contributes to ammonia neurotoxicity.
在不存在或存在3 mM铵离子（氯化铵；氨）的情况下，测量了从大鼠大脑半球分离出的非突触线粒体对[3H]谷氨酰胺（GLN）的摄取。氨使GLN摄取的可饱和成分的Vmax增加了20%以上，而不影响K(m)，但并未改变GLN转运的非饱和成分，该成分代表由极低亲和力载体介导的扩散或摄取。由于GLN是一种内源性渗透溶质，其摄取增加可能导致星形胶质细胞线粒体肿胀，进而导致通常与急性高氨血症状态相关的脑能量代谢降低。该结果与最近的观点一致，即在高氨血症条件下在大脑中积累的GLN会导致氨神经毒性。
