INVOLVEMENT OF PROLINE IN PROTECTING THYLAKOID MEMBRANES AGAINST FREERADICAL-INDUCED PHOTODAMAGE

Investigations were carried out to determine the involvement of prolin e in protecting thylakoid membranes against photodamage. The exposure of thylakoids isolated from the cotyledons of Brassica juncea to photo inhibitory light caused a linear increase in lipid peroxidation with t ime as measured by the assay of conjugated dienes and malondialdehyde (MDA). Proline produced a considerable reduction in the lipid peroxida tion-linked formation of both conjugated dienes and MDA in the thylako ids during exposure to strong light. This reduction in lipid peroxidat ion reflects the probable involvement of proline in the reduction of t he free radicals generated on strong light exposure. The thylakoids ex posed to strong light intensity also generated singlet oxygen (O-1(2)) and superoxide radical anion (O-2(-)). The level of these radicals in creased with the time of exposure. The presence of proline significant ly curtailed the production of O-1(2), by the thylakoids during strong illumination. However, the presence of proline did not affect the O-2 (-) induction capacity of the thylakoid membranes during strong light exposure. Peroxidation of linolenic acid micelles occurred on exposure to UV radiation. The almost total suppression of UV-induced lipid per oxidation of linolenic acid micelles in the presence of sodium azide a nd L-histidine (singlet oxygen quenchers) suggested the involvement of O-1(2) in UV-induced lipid peroxidation. The presence of proline duri ng the exposure of linolenic acid micelles to UV radiation caused a co nsiderable reduction in the formation of conjugated dienes as well as MDA. The proline-induced reduction in the peroxidation of these micell es further confirms the involvement of proline in reducing the level o f O-1(2) Our results therefore demonstrate that proline is involved in reducing the photodamage in the thylakoid membranes by scavenging and /or reducing the production of O-1(2). (C) 1997 Elsevier Science S.A.