4.7 Article

Cadmium inhibits the electron transfer chain and induces reactive oxygen species

Journal

FREE RADICAL BIOLOGY AND MEDICINE
Volume 36, Issue 11, Pages 1434-1443

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2004.03.010

Keywords

cadmium; electron transfer chain; reactive oxygen species; mitochondria; complex III; Q cycle; free radicals

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Recent research indicates that cadmium (Cd) induces oxidative damage in cells; however, the mechanism of the oxidative stress induced by this metal is unclear. We investigated the effects of Cd on the individual complexes of the electron transfer chain (ETC) and on the stimulation of reactive oxygen species (ROS) production in mitochondria. The activity of complexes II (succinate:ubiquinone oxidoreductase) and III (ubiquinol:cytochrome c oxidoreductase) of mitochondrial ETC from liver, brain, and heart showed greater inhibition by Cd than the other complexes. Cd stimulated ROS production in the mitochondria of all three tissues mentioned above. The effect of various electron donors (NADH, succinate, and 2,3-dimethoxy-5-methyl-6-decyl-1,4-benzoquinol) on ROS production was tested separately in the presence and in the absence of Cd. ESR showed that complex III might be the only site of ROS production induced by Cd. The results of kinetic studies and electron turnover experiments suggest that Cd may bind between semiubiquinone and cytochrome b(566) of the Q(0) site of cytochrome b of complex III, resulting in accumulation of semiubiquinones at the Q(0) site. The semiubiquinones, being unstable, are prone to transfer one electron to molecular oxygen to form superoxide, providing a possible mechanism for Cd-induced generation of ROS in mitochondria. Published by Elsevier Inc.

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