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Cadmium inhibits the activity of Complexes II and III of respiratory chain and induces ROS production in mitochondria.

Authors
Wang-YD; Fang-J; Leonard-S; Demchuk-E; Rao-KMK
Source
FASEB J 2004 Mar; 18(5)(Suppl):A1196
NIOSHTIC No.
20031576
Abstract
Cadmium (Cd), a non-transitional metal, is widely used in industry. The toxicities associated with cadmium are well known. Recent research indicates that 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 stimulation of reactive oxidative species production in mitochondria. The complexes studied are Complex I (NADH:Ubiquinone oxidoreductase), Complex II (Succinate:ubiquinone oxidoreductase), Complex III (Ubiquinol:cytochrome c oxidoreductase), and Complex IV (Cytochrome c oxidase). The activity of complexes II and III 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 or absence of Cd. Results indicate that complex III is the only place that induces ROS in the presence of Cd. Results from kinetic studies and electron turnover experiments suggest that Cd may bind between semiubiquinoe and cytochrome b566 of the Qo site of cytochrome b of complex III. This binding will result in accumulation of semiubiquinones at the Qo site of complex III. The semiubiquinones are not stable and are prone to transfer one electron to molecular oxygen to form superoxide, providing a possible mechanism for Cd-induced generation of ROS in mitochondria.
Keywords
Metal-compounds; Metal-industry; Cell-alteration; Cell-damage; Cell-growth; Cell-function; Cell-morphology; Cell-transformation; Cellular-reactions; Cellular-structures; Cellular-uptake; Cellular-transport-mechanism; Heart; Liver-cells; Liver-function; Liver-microsomal-metabolism; Brain-disorders
Contact
NIOSH, PPRB, HELD, Morgantown, WV 26505
CODEN
FAJOEC
CAS No.
7440-43-9
Publication Date
20040324
Document Type
Abstract; Conference/Symposia Proceedings
Fiscal Year
2004
NTIS Accession No.
NTIS Price
Issue of Publication
5
ISSN
0892-6638
NIOSH Division
HELD
Source Name
The FASEB Journal. Experimental Biology 2004, Washington, DC, April 17-21, 2004
State
WV
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