Abstract

Increases in UV-B irradiance lead to many specific damaging effects upon the plants including damage of the thylakoid membrane, partial inhibition of PS II, decrease of chloroplast ATPase activity, loss of enzyme activities in the calvin cycle and alterations in pigment synthesis (1). Under natural conditions enhanced UV-B light is always accompanied by high intensities of photosynthetic active radiation (PAR). Damaging effects due to photoinhibitory PAR and UV-B light which lead to several oxygen radical species (2) could be reduced by photoprotection mechanisms. One of these protection mechanisms is the xanthophyll cycle. In higher plants and green algae violaxanthin is converted to zeaxanthin in the violaxanthin cycle under strong light, whereas diatoms are able to form diatoxanthin from diadinoxanthin via the diadinoxanthin cycle (3). The deepoxidised xanthophylls diatoxanthin and zeaxanthin seem to be able to convert PS II from a light harvesting state to a state where excess excitation energy is effectively dissipated as heat. This protection cycle against high light could be a potential UV-B target. The deepoxidation of diadinoxanthin is carried out by the membrane bound diadinoxanthin deepoxidase which is activated by lumen acidification and requires ascorbate as a cosubstrate. Diatoxanthin epoxidase catalyses the back reaction and is bound to the stromal side of the thylakoid membrane.

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