Is the cancer protective effect correlated with growth inhibitions by green tea (−)-epigallocatechin gallate mediated through an antioxidant mechanism?

The preferential inhibition by (−)-epigallocatechin gallate (EGCg) of growth of cancer cells (e.g. HeLa) in culture correlates with the ability of EGCg to inhibit a growth-related, cell surface hydroquinone oxidase with protein disulfide-thiol interchange activity (tNOX) measured as an NADH oxidase and specifically associated with tumorigenically-transformed cells and tissues. tNOX is reduced or absent from the surface of non-cancer cells. Various oxidizing conditions known to render other antioxidants such as thiols, ascorbate and vitamin E ineffective did not reduce the effectiveness of EGCg in inhibiting either the tNOX activity or the growth of HeLa cells. Only after Fenton reaction with iron catalysis in the presence of hydrogen peroxide was the effectiveness of the EGCg reduced. We conclude that it is unlikely that the anticancer action of green tea EGCg on the tNOX protein is mediated through antioxidant properties of EGCg.