Mitochondria: important target for drug toxicity? Stephan Krähenbühl  Journal of Hepatology  Volume 34, Issue 2, Pages 334-336 (February 2001) DOI: 10.1016/S0168-8278(00)00106-9

Fig. 1 Mitochondrial metabolism. Long-chain fatty acids are first activated by palmitoyl-CoA synthase (PCS) on the outer mitochondrial membrane (o.m.). They are then converted to the carnitine derivative by carnitine palmitoyltransferase I (CPT I) and transported across the inner mitochondrial membrane (i.m.) by carnitine translocase (CTL). In the mitochondrial matrix, they are reconverted to the CoA derivative by CPT II and undergo β-oxidation. NADH and FADH produced by β-oxidation are metabolized by the electron transport chain consisting of the enzyme complexes I, II, III and IV. Ubiquinol (UQ) and cytochrome c (Cyt c) transport electrons between complexes I or II and III, and between complexes III and IV, respectively. Complexes I, III and IV can shift protons from the mitochondrial matrix into the intermembrane space, building up a proton gradient. This gradient is necessary to produce ATP from ADP by complex V or F0F1ATPase. Beta-oxidation produces also acetyl-CoA which can be used for the formation of ketone bodies or is degraded to CO2 and H2O by the Krebs cycle. Further explanations are given in the text. Journal of Hepatology 2001 34, 334-336DOI: (10.1016/S0168-8278(00)00106-9)