Orr, G. L; Hess, F. D. Mechanism of action of the diphenyl ether herbicide acifluorfen-methyl in excised cucumber (Cucumis sativus) cotyledons. Plant Physiol. 1982, 69, 502-507. Ridley, S. M. Interaction of chloroplasts with inhibitors. Effects of two diphenyl ether herbicides, fomesafen and nitrofluorfen, on electron transport and some comparisons with dibromothymoquinone, diuron and paraquat. Plant Physiol. 1983, 72, 461-468.

Triclopyr, [(3,5,6-trichloro-2-pyridinyl)oxy]acetic acid, and its ethylene glycol butyl ether ester (EGBE), equivalent to 3.5 mg of the acid, were applied, separately, to the top layers of columns (40 cm X 8.9 cm i.d.) packed with a loam soil or with quartz sand. Water, equivalent to 2.5 cm of precipitation, was leached through each column every second day. After 54 days, residues were found only in the top 10-cm layers of the soils; they were triclopyr and the metabolites 3,5,6-trichloro-2-pyridinol (TP) and 2methoxy-3,5,6-trichloropyridine, accounting for about 5, 85, and 10%, respectively, of the total of the residues which, in turn, was equivalent to 65% of the amount applied initially to the top layers. No residues were detected in the lower soil layers or the eluates. Triclopyr-treated sand: Found were 10 and 65%, respectively, in the sand and the eluates after 54 days. EGBE-treated sand: All residues were in the eluates after only 34 days. All residues from sand and eluates were in the form of triclopyr, except a few eluates from the latter treatment with traces of EGBE or TP.

No abstract

Acephate was resistent to hydrolysis in distilled, buffered water at pH 4.0 to 6.9, but not at pH 8.2, held for 20 days at 20 or 30 degrees C. The maximum conversion to methamidophos was 4.5% of the added acephate at pH 8.2 and 20 degrees C. The persistence of acephate in two natural waters, held at 9 degrees C for up to 42 and 50 days varied: 80% were recovered from pond water after 42 days, and 45% from creek water after 50 days. Rates of acephate degradation increased greatly when treated water samples were incubated in the presence of sediments, but not if water and sediment were autoclaved prior to treatment and incubation. The greatest conversion to methamidophos, 1.3% of the added acephate, had occurred after 42 days in pond water without sediment. Under the same conditions, carbaryl was less persistent than acephate in the natural waters: 18 to 20% were recovered from pond water after 42 days, and 37 to 40% from creek water after 50 days. The presence of sediment did not affect its degradation significantly. But more than 55% were recovered after 50 days if water and sediment were autoclaved prior to treatment and incubation. Neither acephate, methamidophos, nor carbaryl could be shown to escape from water into the atmosphere.

Acephate was incubated in distilled water of three different pH's at 37 degrees C for 7 days. Three hydrolytic products were formed: methamidophos, O,S-dimethyl phosphorothiolate (DMPT), and O-methylacetyl phosphoramidothiolate (OMPT). A single dose of acephate was also fed to mice, and their livers were excised and analyzed for metabolic products up to 30 hours. Three products were detected: methamidophos, DMPT, and S-methylacetyl phosphoramidothiolate (SMPT). The anticholinesterase properties of acephate, methamidophos, DMPT, SMPT, and OMPT were determined. Only acephate and methamidophos had measurable inhibitory effects on the mouse erythrocyte enzyme, methamidophos being about ten times more effective than acephate. The amount of methamidophos formed in the water and mouse liver was too low to have any direct effect on the toxicity of acephate. Acephate toxicity to aquatic insects would depend on its persistence in water, its uptake by the insects, its conversion to methamidophos, and the combined inhibitory effect of acephate and methamidophos on the cholinesterase enzyme. The toxicity of acephate to mammals would depend on the direct anticholinesterase effect of the chemical and to a small extent on methamidophos.