Harik S I, Hritz M A
Department of Neurology, University Hospitals of Cleveland, OH.
Biochem Pharmacol. 1993 May 25;45(10):2170-2. doi: 10.1016/0006-2952(93)90034-t.
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) is believed to induce neurotoxicity by inhibiting mitochondrial oxidative metabolism, whereas acetyl-L-carnitine (ALC) facilitates this process by transporting fatty acids into mitochondria for beta oxidation. We investigated whether large doses of ALC given by gavage for 1 week before and 1 week after MPTP could ameliorate MPTP neurotoxicity in mice. We found that ALC had no effect on MPTP-induced depletion of striatal dopamine and its metabolites.
1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPTP）被认为通过抑制线粒体氧化代谢诱导神经毒性，而乙酰左旋肉碱（ALC）则通过将脂肪酸转运到线粒体进行β氧化来促进这一过程。我们研究了在给予MPTP前1周和后1周通过灌胃给予大剂量ALC是否可以改善MPTP对小鼠的神经毒性。我们发现ALC对MPTP诱导的纹状体多巴胺及其代谢产物的耗竭没有影响。
