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The ability of a quinone to redox cycle is dependent upon the favourability of its reduction by a single electron, which can be quantitatively described by its reduction potential ( E o )

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[74] demonstrated that rice APx1/2s mutants (double mutants for cytosolic APXs) exhibited an altered redox homeostasis, as indicated by increased levels of H 2 O 2 and AsA and GSH redox states, but the antioxidative compensatory mechanism displayed by the mutants was associated with increased expression of OsGpx genes, which resulted in higher GPX activity in the cytosolic and chloroplastic fractions