Belous A M, Lemeshko V V, Iasaĭtis A A
Biokhimiia. 1976 May;41(5):881-5.
Halidor 1-benzyl-1-(3'-dimethylaminopropoxy)-cycloheptane fumarate, activates succinate oxidation in mitochondria and inhibits reverse electron transport from succinate to NAD+ in submitochondrial partides preparations at doses of 2-10(-5)--10(-3) M. At a dose of 5--7-10(-4) M halidor cause a swelling of mitochondria incubated in 0.1 M NH4NO3. At higher concentrations (10(-3)--10(-2) M) halidor practically completely inhibits NADH and succinate oxidase activity of mitochondria and submitochondrial particles. It is suggested that vasodilating effect of halidor is due to the uncoupling of oxidative phosphorylation, thus causing a deficiency of ATP for contracting function of blood vessel muscles.
哈利多（1-苄基-1-(3'-二甲氨基丙氧基)-环庚烷富马酸盐）在2×10⁻⁵至10⁻³M的剂量下，可激活线粒体中的琥珀酸氧化，并抑制亚线粒体颗粒制剂中从琥珀酸到NAD⁺的逆向电子传递。在5至7×10⁻⁴M的剂量下，哈利多会导致在0.1M硝酸铵中孵育的线粒体肿胀。在更高浓度（10⁻³至10⁻²M）时，哈利多几乎完全抑制线粒体和亚线粒体颗粒的NADH和琥珀酸氧化酶活性。有人认为，哈利多的血管舒张作用是由于氧化磷酸化的解偶联，从而导致血管肌肉收缩功能所需的ATP不足。
