Photoinactivation of PS2 secondary donors by PS2 cation radicals and superoxide radicals

摘要

Illumination of Mn- and Cl-depleted PS2 causes rapid irreversible inactivation of specific redox-active components on the donor side of the PS2 Reaction Center (RC). Under aerobic conditions, weak light preillumination of NH(sub 2)OH-PS2 causes rapid loss of Y(sub Z)(sup (plus minus)) formation, Y(sub Z) (yields) P(sub 680)(sup +), the A(sub T)-band thermoluminescence emission, the Y(sub Z)(sup +)-dependent (Site 1) photooxidation of exogenous e(sup (minus)) donors, and the capability to photoligate Mn(sup 2+) into the water oxidizing enzyme (photoactivation), all without significantly affecting P(sub 680)(sup +)/Q(sub A)(sup (minus)) charge separation. In contrast, aerobic high light preillumination of Mn-depleted PS2 promotes very rapid and parallel loss of photoactivation and A(sub T)-band emission capabilities significantly than loss of either Y(sub Z)(sup +)-formation or P(sub 680)(sup +)/Q(sub A)(sup (minus)) charge separation capabilities. These photodamages and those to Cl-depleted thylakoids (4,5) generally are believed to be caused by reactions between the highly oxidizing cation radicals (P(sub 680)(sup +)/Chl(sup +)) and nearby amino acid residues of D(sub 1)>D(sub 2). The reported promotion of the photodamages by e(sup (minus)) acceptors of Q(sub A)(sup (minus))/Q(sub B)(sup (minus)) their inhibition by e(sup (minus)) donors to Y(sub Z)(sup +) and their occurrence under strict anaerobic conditions all tend to support the idea of direct damage by P(sub 680)(sup +)/Chl(sup +). Our studies lead us to conclude that the photodamages to the donor side components are caused minimally by a rapid mechanism requiring both superoxide and PS2 cation radicals; and by a slower mechanism driven by the PS2 cation radicals only.