Interaction of cytokinins with lipid-associated oxy free radicals during senescence: a prospective mode of cytokinin action

In senescence physiology, experimental data indicate causative relationships among cytokinin, lipoxygenation, anti-oxidation, and lipid-associated free radical scavenging. During both normal and induced senescence, there is a rise in lipoxygenase (LOX) which catalyzes the oxidation of polyunsaturated fatty acids containing the cis, cis-1,4-pentadiene configuration. These include linoleic and linolenic acids, which are of common occurrence in plants and inter alia may be situated in membranal phospholipids. Lipoxygenation causes the production of free radicals such as the superoxide, fatty acid, and peroxy species. Cytokinin (CK) lowers LOX and superoxide dismutase activities significantly in senescing foliage and is mimicked by the endogenous lipid antioxidant, α-tocopherol (vitamin E), in its chlorophyll-retaining and LOX-lowering effects. Further experimentation indicated that CK interaction with free radicals may occur in two ways, (i) CK may act as a direct free radical scavenger by virtue of the fact that the hydrogens of the α-carbon atom in the amine bond can be extracted, resulting in the formation of an amide: [Formula: see text][Formula: see text] (this mechanism may also, in part, explain polyamine effects), (ii) CK may serve as an incipient preventative of free radical formation by inhibiting oxidation of plant purine compounds, which at certain stages of breakdown release superoxide and hydroxyl free radicals. This effect is probably associated with a lowering of substrate affinity for xanthine oxidase. This assumption is further borne out by similar senescence-retarding effects of selective xanthine oxidase inhibitors such as allopurinol. These observations collectively indicate that prevention of free radical formation and (or) their direct scavenging should be included in the multifactorial antisencscence mode of action of cytokinin.