Inhibition of photosynthesis and respiration by substituted 2,6-dinitroaniline herbicides: I. Effects on chloroplast and mitochondrial activities

Abstract

Effects of 12 substituted 2,6-dinitroaniline herbicides [ N-butyl- N-ethyl-α,α,α-trifluoro-2,6-dinitro- p-toluidine (benefin), 2,6-dinitro- N,N-dipropylcumidine (isopropalin), 4-(methylsulfonyl)-2,6-dinitro- N,N-dipropylaniline (nitralin), 3,5-dinitro- N 4,N 4 -dipropylsulfanilamide (ozyzalin), α,α,α-trifluoro-2,6-dinitro- N,N-dipropyl- p-toluidine (trifluralin), and seven experimental derivatives] were measured on electron transport and phosphorylation in isolated spinach ( Spinacia oleracea L.) chloroplasts and mung bean ( Phaseolus aureus Roxb.) mitochondria. In chloroplasts, the 2,6-dinitroanilines inhibited both photoreduction and coupled photophosphorylation with water as the electron donor and with ferricyanide as oxidant, and cyclic photophosphorylation with phenazine methosulfate as the electron mediator under an argon gas phase. In mitochondria, all of the 2,6-dinitroanilines except nitralin markedly inhibited phosphorylating electron transport (state 3 respiration) with malate as substrate, and most were strong inhibitors of NADH and succinate oxidation. Some also inhibited nonphosphorylating (state 4 respiration) electron transport. Interference on the energy-generating pathway was suggested by a limited stimulation of state 4 respiration measured either as a steady-state or transitional condition. However, the strong interference imposed on electron transport prevented an accurate evaluation of their effect on the energy-generating pathway. Inhibition of oxidative and photophosphorylation by the 2,6-dinitroanilines in isolated mitochondria and chloroplasts suggests that if the compounds should partition into the organelles in vivo, photosynthesis and respiration would be inhibited. Because of the dependence of biochemical and physiological processes on oxidative and photophosphorylation for the energy (ATP) needed to drive the reactions, interference with ATP production could be one of the major mechanisms through which phytotoxicity is expressed by the 2,6-dinitroanilines.