Two strains of crownvetch (Coronilla varia L. # CZRVA) rhizobia were cultured in vitro with various rates of atrazine [6-chloro-N-ethyl-N′-(1-methylethyl)-1,3,5-triazine-2,4-diamine] and bifenox [methyl 5-(2,4-dichlorophenoxy)-2-nitrobenzoate]. Growth, measured turbidimetrically over 48 h, was similar for both strains. Atrazine and bifenox significantly reduced bacterial growth after 14 and 36 h, respectively, only at the highest concentrations tested (463 μM atrazine and 292 μM bifenox). Since growth of crownvetch rhizobia was apparently not affected by rates of atrazine or bifenox above reasonable soil solution concentrations, it is likely that herbicidal effects on nodulation were due to toxicity to the host plant rather than toxicity to these bacteria. In a growth chamber experiment, total nodule activity (TNA) and carbon dioxide exchange rate (CER) were measured simultaneously in an effort to distinguish direct atrazine effects on nodule function from indirect effects due to inhibition of photosynthesis and a resulting decrease in photosynthate supply to nodules. When 5 and 50 mg atrazine per kg soil were applied to intact plants, CER was severely reduced within 24 h, but similar reductions in TNA were not observed until 48 h after treatment. Total nodule activity was reduced similarly by atrazine and defoliation; the application of atrazine to defoliated plants did not inhibit TNA more than did defoliation alone. The data indicate that reductions in crownvetch nodule activity by atrazine are due to inhibition of photosynthesis or other processes rather than direct toxicity to N fixation.

Cotton (Gossypium hirsutum L.) response was evaluated when propanil (3′,4′-dichloropropionanilide), thiobencarb {S-[(4-chlorophenyl)methyl] diethylcarbamothioate}, butachlor [N-(butoxymethyl)-2-chloro-2′,6′-diethylacetanilide], oxadiazon [2-tert-butyl-4-(2,4-dichloro-5-isopropoxyphenyl)-δ2-1,3,4-oxadiazolin-5-one], bifenox [methyl-5-(2,4-dichlorophenoxy)-2-nitrobenzoate], acifluorfen {5-[2-chloro-4-(trifluoromethyl)phenoxy]-2-nitrobenzoic acid}, and metribuzin [4-amino-6-tert-butyl-3-(methylthio)-as-triazin-5(4H)-one] were applied over-the-top at simulated drift rates at two growth stages during 1975 to 1979. No rate of butachlor or thiobencarb injured cotton. The order of phytotoxicity for the herbicides applied to cotyledonary cotton was propanil > metribuzin > bifenox > oxadiazon > acifluorfen > butachlor = thiobencarb. Herbicides injured cotton less at the five- or eight-node stage than at the cotyledonary stage. Injury was more severe in seasons of wet or cold weather during early plant development.

Saflufenacil (Kixor™) is a new herbicide of the pyrimidinedione chemical class for preplant burndown and selective preemergence dicot weed control in multiple crops, including corn. In this study, the mode of action of saflufenacil was investigated. For initial characterization, a series of biotests was used in a physionomics approach for comprehensive physiological profiling of saflufenacil effects. With the use of treated duckweed plants, metabolite profiling was performed based on quantification of metabolite changes, relative to untreated controls. Physiological and metabolite profiling suggested a mode of action similar to inhibitors of protoporphyrinogen IX oxidase (PPO) in tetrapyrrole biosynthetic pathway. Saflufenacil inhibited PPO enzyme activity in vitro with 50% inhibition of 0.4 nM for the enzymes isolated from black nightshade, velvetleaf, and corn. PPO inhibition by saflufenacil caused accumulations of protoporphyrin IX (Proto) and hydrogen peroxide (H2O2) in leaf tissue of black nightshade and velvetleaf. In corn, only slight increases in Proto and H2O2 were found, which reflects in planta tolerance of this crop. The results show that saflufenacil is a new PPO-inhibiting, peroxidizing herbicide.