Kinetin is thought to be synthesized within the cell as a result of oxidative damage processes. In such conditions DNA undergoes degradation, and as a result of oxidation of the deoxyribose 5' carbon, furfural is formed. In fact, the main target of deoxyriboside oxidation is C1' carbon, which results in 5-methylene-2-furanone formation. Furfural yield reaches 15% of deoxyribose C5' oxidation products. It reacts with adenine in DNA, forms the Schiff base, and, following intramolecular rearrangement and dehydration, kinetin results [5, 6].
When kinetin occurs in DNA, the DNA polymerase incorporates thymine opposite to the modified base on the complementary strand; however, in the vicinity of kinetin misincorporation occurs. The presence of cytokinin in DNA induces con-formational changes. Increased risk of mutation is lowered by activation of a repair mechanism that excises kinetin .
Cytokinins are present in plants as free bases, nucleosides, or nucleotide derivatives. Interconversion between these forms is maintained by enzymes involved to purine metabolism . Cytokinin modifications include O-xylosylation, O-glucosylation, and N-glucosylation. All these forms are inactive. O-glucosylation provides resistance to cytokinin oxidase cleavage of the N6 side chain. The reaction is reversible and the molecule can be converted to the active form by P-glucosidases. It could serve as a storage form of inactive cytokinin. Adenine ring glucosylation could occur at N3, N7, and N9 sites. Like N9-glucoside, N7-glucoside is resistant to glucosidases since they cannot be converted to the active forms. Therefore N-glucosylation is considered to be an irreversible pathway of cytokinin inactiva-tion [9, 11]. Cytokinins can be modified by cleavage of the side chain by cytokinin oxidase. The reaction leads to irreversible degradation .
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