Abstract
Experiments were conducted to determine the mechanism of resistance to atrazine (2-chloro-4-ethylamino-6-isopropylamino-s-triazine) in a Wisconsin velvetleaf (Abutilon theophrastiMedicus) biotype (WRB1) and to determine if the same mechanism is responsible for atrazine resistance in a Maryland velvetleaf biotype (MRB). Atrazine equally inhibited photosynthetic electron transport by isolated thylakoids of WRB1 and a Wisconsin atrazine-susceptible velvetleaf accession (WSA1), suggesting that the mechanism of atrazine resistance is not a less-sensitive site of atrazine action in photosystem II. WRB1 and WSA1 seedlings did not differ in uptake of hydroponically fed [14C]atrazine or nutrient solution over a 12-hr time course, but atrazine uptake was greater in WRB1 than MRB. Concentration of radioactivity was greater in WRB1 than WSA1 stems at both 6 and 12 hr of atrazine exposure, but was less in WRB1 than WSA1 leaves at 12 hr of exposure. These results suggest that decreased translocation of atrazine to leaves is a factor in the mechanism of resistance in WRB1. WSA1, WRB1, and MRB all metabolized atrazine via glutathione conjugation andN-dealkylation, as well as producing nonextractable residues. Compared to WSA1, both WRB1 and MRB metabolized more atrazine in stems and leaves. Predominant extractable metabolites in the two resistant biotypes were the glutathione,L-cysteine, andN-acetyl-L-cysteine conjugates of atrazine, metabolites produced in the glutathione conjugation pathway. Concentration of nonextractable residues was greater in WRB1 than WSA1 stems at both 6 and 12 hr of atrazine exposure. Thus, increased atrazine metabolism was the major factor accounting for WRB1 resistance to atrazine. Furthermore, in WRB1 and MRB, atrazine metabolism was qualitatively and quantitatively similar, after consideration of the lower atrazine uptake by MRB than WRB1. Hence, resistance in both of these geographically isolated velvetleaf biotypes results from increased glutathione conjugation of atrazine.
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