Discipline of Pharmacology, University of Adelaide, Adelaide, South Australia, Australia.
School of Pharmacy and Medical Science, University of South Australia, Adelaide, South Australia, Australia.
Pharmacol Res Perspect. 2018 Jun;6(3):e00406. doi: 10.1002/prp2.406. Epub 2018 May 22.
Perhexiline, a chiral drug, is a potent antiischemic agent whose clinical utility is limited by hepatic and neural toxicities. It inhibits mitochondrial carnitine palmitoyltransferase-1, however, excessive inhibition predisposes toward tissue steatosis. This pilot study investigated the distribution of the two enantiomers and their toxicological potential. Dark Agouti rats (n = 4 per group) were administered vehicle or 200 mg/kg daily of racemic, (+)- or (-)-perhexiline maleate orally for 8 weeks. Plasma biochemical liver function tests and Von Frey assessments of peripheral neural function were performed. Hepatic and neuronal histology, including lipid and glycogen content, was assessed using electron microscopy. Concentrations of the perhexiline enantiomers and metabolites were quantified in plasma, liver and heart. Plasma perhexiline concentrations following administration of racemate, (+)- or (-)-enantiomer were within the mid-upper clinical therapeutic range. There was extensive uptake of both enantiomers into liver and heart, with 2.5- to 4.5-fold greater net uptake of (+)- compared to (-)-perhexiline (P < .05) when administered as pure enantiomers, but not when administered as racemate. There was no biochemical or gross histological evidence of hepatotoxicity. However, livers of animals administered (+)-perhexiline had higher lipid (P < .01) and lower glycogen (P < .05) content, compared to those administered (-)-perhexiline. Animals administered racemic perhexiline had reduced peripheral neural function (P < .05) compared to controls or animals administered (-)-perhexiline. For the same plasma concentrations, differences in tissue distribution may contribute to disparities in the effects of (+)- and (-)-perhexiline on hepatic histology and neural function.
哌克昔林是一种手性药物,是一种有效的抗缺血药物,但由于其肝毒性和神经毒性,临床应用受到限制。它抑制线粒体肉碱棕榈酰转移酶-1,但过度抑制会导致组织脂肪变性。本研究旨在研究两种对映体的分布及其毒性作用。将 4 只暗纹黄鼠(每组 4 只)分别给予 vehicle 或 200mg/kg/d 消旋体、(+)-或 (-)-马来酸哌克昔林,连续灌胃 8 周。进行血浆生化肝功能检查和 Von Frey 评估外周神经功能。采用电子显微镜观察肝和神经组织学,包括脂质和糖原含量。定量检测血浆、肝和心脏中哌克昔林对映体和代谢物的浓度。给予消旋体、(+)-或 (-)-对映体后,血浆哌克昔林浓度处于中高临床治疗范围。两种对映体均广泛摄取到肝和心脏中,当以纯对映体给药时, (+)-对映体的净摄取量比 (-)-对映体高 2.5-4.5 倍(P <.05),但当以消旋体给药时则没有差异。没有生化或大体组织学证据表明肝毒性。然而,给予 (+)-哌克昔林的动物肝脏中脂质含量较高(P <.01),糖原含量较低(P <.05),而给予 (-)-哌克昔林的动物肝脏中脂质含量较低(P <.05)。给予消旋哌克昔林的动物外周神经功能降低(P <.05),与对照组或给予 (-)-哌克昔林的动物相比。在相同的血浆浓度下,组织分布的差异可能导致 (+)-和 (-)-哌克昔林对肝组织学和神经功能的影响存在差异。