Atlante A, Passarella S
Centro di Studio sui Mitocondri e Metabolismo Energetico, CNR, 70126 Bari, Italy.
Int J Mol Med. 1998 Mar;1(3):601-3. doi: 10.3892/ijmm.1.3.601.
The mitochondrial myopathy associated with long-term AZT therapy limits the clinical efficacy of this drug in AIDS therapy. Thus, in order to determine how AZT can affect mitochondria bioenergetics, the capability of AZT to both uncouple oxidative phosphorylation and inhibit electron flow in isolated rat liver mitochondria was investigated. The failure of AZT to oxidize intramitochondrial pyridine nucleotides, to stimulate mitochondrial swelling in K+-acetate plus valinomycin or to cause ATP hydrolysis shows that AZT is not an uncoupler.
与长期齐多夫定治疗相关的线粒体肌病限制了该药物在艾滋病治疗中的临床疗效。因此,为了确定齐多夫定如何影响线粒体生物能量学,研究了齐多夫定在分离的大鼠肝线粒体中解偶联氧化磷酸化和抑制电子流的能力。齐多夫定不能氧化线粒体内的吡啶核苷酸,不能在乙酸钾加缬氨霉素中刺激线粒体肿胀,也不能引起ATP水解,这表明齐多夫定不是解偶联剂。