Ostrowski J
Arzneimittelforschung. 1979;29(6):889-94.
Rat heart mitochondria were isolated by a slightly modified method of Sordahl. The influence of carbocromen (Intensaín) on the respiratory function of the tightly coupled or uncoupled mitochondria was tested in the presence of the respiratory substrates pyruvate, alpha-ketoglutarate, D,L-palmitoylcarnitine, L-palmitoylcarnitine, and D,L-acetylcarnitine. Carbocromen (0.089--0.89 mmol/l) did not change the P/O ratio, but reduced the rate of oxygen consumption (QO2) of the coupled mitochondria by about 20% when palmitoylcarnitine was used as respiratory substrate. With ADP in excess (5 mmol/l) carbocromen decreased QO2 in state ST3 by about 35%. This drug induced reduction of QO2 is still much more evident in uncoupled mitochondria (18% with 0.045 mmol/l carbocromen, 70% with 0.89 mmol/l carbocromen). In the presence of pyruvate as substrate the respiratory function of the coupled and uncoupled mitochondria remained nearly unchanged after adding the drug. It is discussed that carbocromen could interact with the complex enzyme dependent transport of long-chain fatty acids through the mitochondrial membrane.
采用索达尔方法略作修改后分离大鼠心脏线粒体。在呼吸底物丙酮酸、α - 酮戊二酸、D,L - 棕榈酰肉碱、L - 棕榈酰肉碱和D,L - 乙酰肉碱存在的情况下，测试了卡波铬（安他心）对紧密偶联或解偶联线粒体呼吸功能的影响。卡波铬（0.089 - 0.89 mmol/l）不改变P/O比值，但当棕榈酰肉碱用作呼吸底物时，可使偶联线粒体的氧消耗率（QO2）降低约20%。当ADP过量（5 mmol/l）时，卡波铬使ST3状态下的QO2降低约35%。在解偶联线粒体中，这种药物引起的QO2降低更为明显（0.045 mmol/l卡波铬时降低18%，0.89 mmol/l卡波铬时降低70%）。以丙酮酸为底物时，加入该药物后偶联和解偶联线粒体的呼吸功能几乎保持不变。讨论了卡波铬可能与依赖复合酶的长链脂肪酸通过线粒体膜的转运相互作用。
