Gene expression can be activated by external oxidants which are reduce
d at the cell surface by plasma membrane electron transport. The signa
ls generated in response to the plasma membrane electron transport inc
lude activation of proton release, internal calcium changes, and chang
e in reductant/oxidant ratio in the cytosol. H2O2 generated in respons
e to ligands which bind to plasma membrane receptors can also activate
protein tyrosine kinases and gene expression. Inhibition of oxygen ra
dical generation at the cell surface in response to the mitogen, phorb
ol myristate acetate by retinoic acid is consistent with a role for th
e plasma membrane electron transport as the source for H2O2 in Balb 3T
3 cells. Agents which affect the binding of coenzyme Q to redox sites
in the plasma membrane electron transport may increase formation of se
miquinone radicals in the membrane which can be a source of oxygen rad
icals and H2O2. The generation of H2O2 by transformed cells indicates
that oncogene product expression in the plasma membrane may also incre
ase quinone-based oxygen radical generation.