Alteration in cell permeability as a mechanism of action of certain quinone pesticides.

The permeability of the Chlorella pyrenoidosa membrane was studied by following the efflux of (14)C-intracellular material from cells which had been allowed to incorporate (14)CO(2) photosynthetically. It was observed that the efflux increased upon treatment with low concentrations (3-30 muM) of 2, 3-dichloro-1, 4-naphthoquinone (dichlone), 2-amino-3-chloro-1, 4-naphthoquinone (06K-quinone), and 2, 3, 5, 6-tetrachloro-1, 4-benzoquinone (chloranil). Dichlone caused a greater loss of intracellular material than chloranil or 06K-quinone. The rate of loss as well as the total loss of (14)C increased with an increase in the concentration of the quinones. In the dichlone-treated cells, the leakage was observed within 1 minute of the addition of the chemical and the effect on cell permeability was irreversible. Cells exposed to dichlone in the light or under anaerobic conditions released significantly greater amounts of (14)C-material than cells treated in the dark or under aerobic conditions. The aqueous ethanol-soluble fraction of the cell was found to be the source of the released material. The proportion of the ethanol-soluble (14)C that leaked out of the cell varied with the time of (14)C-assimilation prior to treatment with dichlone. In the dichlone-treated cells, practically all the (14)C-sucrose, alanine, glutamine, serine, and glycine leaked out, whereas glutamic, aspartic, succinic, and fumaric acids were lost only partially. Essentially no (14)C-lipids were lost from the cells during dichlone treatment.The extreme rapidity of the effect of dichlone on permeability and the low concentrations at which dichlone acted suggest that the cell membrane may be a primary site of action of dichlone, and that the metabolic changes observed in dichlone-treated Chlorella may be due to the changes in the cell membrane structure.