Vereckei A, Blázovics A, Szénási G, Kónya L, Láng I, Zsinka A, Fehér J
Semmelweis Orvostudományi Egyetem, II Belklinika, Budapest.
Orv Hetil. 1991 Mar 3;132(9):483-4, 487-8.
It was supposed that free radicals are produced during the metabolism of amiodarone and involved in the mechanism of the drug's side effects. In vitro and in vivo experiments were performed in rats to check this hypothesis. We verified that amiodarone generated free radicals in vitro by chemiluminometric method. The light emission induced by amiodarone was inhibited by dihydroquinoline type antioxidants CH 402 and MTDQ--DA in a dose dependent manner. The malondialdehyde content, --one of the end products of lipid peroxidation--was increased by in vivo amiodarone administration in the serum and liver homogenate of rats. Amiodarone treatment increased significantly the NADPH and Fe3+ induced lipid peroxidation in rat liver microsomal fractions. The protective effect of antioxidants, MTDQ--DA and silibinin were ambiguous in these in vivo "short term" experiments.
据推测,胺碘酮在代谢过程中会产生自由基,并参与药物副作用的机制。为验证这一假设,我们在大鼠身上进行了体外和体内实验。我们通过化学发光法证实胺碘酮在体外能产生自由基。二氢喹啉类抗氧化剂CH 402和MTDQ-DA能以剂量依赖的方式抑制胺碘酮诱导的发光。脂质过氧化的终产物之一丙二醛的含量,在给大鼠体内注射胺碘酮后,血清和肝脏匀浆中均有所增加。胺碘酮处理显著增加了NADPH和Fe3+诱导的大鼠肝微粒体组分中的脂质过氧化。在这些体内“短期”实验中,抗氧化剂MTDQ-DA和水飞蓟宾的保护作用并不明确。