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Cytoprotective and anticancer properties of coenzyme Q versus capsaicin
Author(s) -
Galati Giuseppe,
O'Brien Peter J.
Publication year - 2003
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.5520180222
Subject(s) - capsaicin , rotenone , chemistry , mitochondrion , apoptosis , cytotoxicity , lipid peroxidation , inner mitochondrial membrane , reactive oxygen species , cytotoxic t cell , membrane potential , mitochondrial respiratory chain , programmed cell death , biophysics , respiratory chain , biochemistry , microbiology and biotechnology , pharmacology , oxidative stress , biology , in vitro , receptor
Abstract Coenzyme Q (CoQ) is an essential component of the mitochondrial electron transport chain and serves as an electron donor and acceptor in mitochondrial energy‐linked respiration. CoQ 1 was shown to prevent ROS formation and cell death in complex 1 inhibited cells. Low concentrations of capsaicin like CoQ 1 inhibited ROS formation but CoQ 1 was more effective at restoring the mitochondrial membrane potential collapse caused by complex 1 inhibitors such as rotenone. At low concentrations, capsaicin acts as a CoQ mimic by protecting against rotenone induced ROS formation and mitochondrial membrane potential collapse. Lipid peroxidation in isolated rat hepatocytes induced by cumene hydroperoxide and chloroacetaldehyde was also prevented. At higher concentrations, capsaicin and CoQ 1 became cytotoxic. Hep G2 cells were more susceptible than hepatocytes. The cytotoxic mechanism for both capsaicin and CoQ 1 was shown to involve a collapse of the mitochondrial membrane potential, however, only capsaicin caused ROS formation. The capsaicin side chain was required for capsaicin induced cytotoxicity. The anticancer properties of CoQ 1 and capsaicin should prove useful for inducing tumor cell apoptosis.