The uptake and metabolism of fenitrothion during forest tree seed germination and seedling growth.

Fenitrothion (0,0-dimethyl-0-(4-nitro-m-tolyl) phosphorothioate) was absorbed by germinating seeds of eastern white pine; Pinus strobus L. (Moench) Voss, white spruce; Picea-qlauca L., and yellow birch; Betula alleghaniensis L., from an aqueous solution containing 10 ppm of the pesticide. Metabolism of the pesticide was examined in young seedlings with OC14H3 labelled fenitrothion. Fenitrothion was shown to be detoxified by dealkylation in white pine via a glutathione dependent S-alkyl transferase enzyme to form desmethyl fenitrothion and S-methyl glutathione. Dealkylation was also found in white spruce and yellow birch seedlings. The pesticide was activated to form fenitro-oxon, which is more toxic than the parent compound. The desmethyl form was shown to be reactivated via alkylation by fenitrothion to form S-methyl fenitrothion which is a more potent cholinesterase inhibitor than the parent compound. Treatment of the seeds at higher concentrations of 1000 ppm fenitrothion inhibited germination of yellow birch seeds but not white pine or spruce. Severe depletion of tissue glutathione levels was shown to be related to toxicity in yellow birch which absorbed much higher levels of pesticide than the two coniferous species. Fenitrothion and seven derivatives of the compound were tested for mutagenicity via alkylation of replicating DNA in an indicator strain of Salmonella typhimurium, sensitive to base-pair substitutions caused by alkylating agents. No mutagenic activity was evident for fenitrothion or its derivatives in this system