Lake N, De Marte L
Department of Physiology, McGill University, Montreal, Quebec, Canada.
Neurochem Res. 1988 Oct;13(10):1003-6. doi: 10.1007/BF00970775.
Experimental evidence has suggested that the high endogenous levels of taurine found in the rat heart and retina are maintained to a large extent by transport processes out of the blood, rather than by endogenous biosynthesis. When these high levels are depleted, dysfunction ensues. In vitro studies have shown that beta-alanine is a good antagonist of these transport processes. The current studies were done to evaluate the feasibility of depleting heart and retinal taurine levels in vivo through treatment of adult rats either orally or with injections of beta-alanine. None of the treatments had significant effects on retinal taurine content; ventricular taurine was reduced in some situations, but the effects were not maintained, nor as large as with another transport antagonist. No functional changes were observed. Oral treatment with beta-alanine had fewer obvious side effects than injections, but all treated rats had body weights less than age-matched controls.
实验证据表明,大鼠心脏和视网膜中内源性牛磺酸的高含量在很大程度上是通过从血液中转运而非内源性生物合成来维持的。当这些高含量被耗尽时,功能障碍就会随之而来。体外研究表明,β-丙氨酸是这些转运过程的良好拮抗剂。目前的研究旨在评估通过口服或注射β-丙氨酸对成年大鼠进行体内治疗来耗尽心脏和视网膜牛磺酸含量的可行性。没有一种治疗方法对视网膜牛磺酸含量有显著影响;在某些情况下,心室牛磺酸含量有所降低,但这种影响并未持续,且不如另一种转运拮抗剂的影响大。未观察到功能变化。口服β-丙氨酸治疗的副作用比注射少,但所有接受治疗的大鼠体重均低于年龄匹配的对照组。