Representative herbicides of the substituted ureas, uracils, s-triazines, benzonitriles, and bipyridyls, which are potent inhibitors of photosynthetic electron transport, markedly accelerated photooxidations (chlorophyll bleaching and lipid peroxidation) normally occurring in isolated intact chloroplasts. Other herbicides, which are not potent inhibitors of photosynthesis, did not accelerate photooxidations. The photooxidations, whether in the presence or absence of herbicides, were completely prevented by exogenously supplied NADH or NADPH but not by sucrose or mannitol. Herbicide-induced injury to barley (Hordeum vulgare L.) seedlings treated with paraquat (1,1′-dimethyl-4,4′-bipyridinium ion) was diminished by allowing the seedlings to absorb NADPH. These results provide additional support to the hypothesis that depletion of the source of reducing potential (NADPH) is responsible for chloroplast photooxidations and plant death following treatment with photosynthesis-inhibiting herbicides.
