Antidotes were evaluated for their ability to prevent corn and sorghum injury caused by imazaquin. Plant injury was reduced in both preemergence and early postemergence imazaquin applications. Naphthalic anhydride (NA) seed treatment was the most consistent compound in reducing the imazaquin injury. Seed treatment with CGA 92194 or flurazole also gave injury protection to corn and sorghum, while soil treatment with dichlormid provided the least protection from imazaquin injury. Treatment with the antidotes did not affect the acetolactate synthase (ALS) (EC4.1.3.18) activity in corn or sorghum tissues. Imazaquin treatments decreased extractable ALS activity but this decrease was eliminated, partially or totally, by the most effective antidotes. Antidote treatments had little effect on absorption and distribution of 14C in plants growing in soil treated with 14C-imazaquin. Antidote treatments increased the metabolism of 14C-imazaquin to both soluble and unextractable 14C after 24 h of exposure. The increased rate of imazaquin conversion to less toxic metabolites when antidotes were used resulted in a reduction in imazaquin injury to corn and sorghum.

Greenhouse studies were conducted to evaluate and compare herbicide safeners for protection of corn and sorghum from herbicidal injury from metolachlor, primisulfuron, and the interaction of primisulfuron with terbufos, an insecticide. With the exception of CGA-133205 which killed corn, the safeners oxabetrinil, flurazole, naphthalic anhydride, dichlormid, and R-29148 protected against significant injury from the interaction between primisulfuron (40 g ai ha−1) and terbufos (9.8 kg ha−1 equivalent to 750 g per 1000 m of row) and from metolachlor (6.7 kg ai ha−1). No primisulfuron-terbufos interaction was observed in sorghum and none of the safeners protected sorghum from primisulfuron injury. PRE application of the antioxidants, piperonyl butoxide and metyrapone, increased primisulfuron injury to corn. Piperonyl butoxide by itself did not influence the growth of corn seedlings, but metyrapone caused slight injury. The increased injury from piperonyl butoxide plus primisulfuron applied at 40 g ha−1 was protected by naphthalic anhydride, flurazole, and R-29148, whereas at 80 g ha−1 protection was provided by flurazole and R-29148. None of the safeners tested protected against increased injury from metyrapone. Naphthalic anhydride was also an effective safener against increased corn injury when 3000 ppm piperonyl butoxide was applied foliarly 3 d prior to primisulfuron application. 14C-Primisulfuron absorption by corn was not influenced by piperonyl butoxide or the safener, naphthalic anhydride. However, metabolism of 14C-primisulfuron was inhibited by piperonyl butoxide. This inhibition was not totally reversed by the safener, naphthalic anhydride.

Sorghum [Sorghum bicolor (L.) Moench. ‘G-623 GBR’] bioassays indicated that shoot growth was more susceptible to metolachlor [2-chloro-N-(2-ethyl-6-methylphenyl)-N-(2-methoxy-1-methylethyl)acetamide] and more responsive to the antidote CGA-92194 {α-[(1,3-dioxolan-2-yl-methoxy)-imino] benzeneacetonitrile} than root growth. Seed treatment with CGA-92194 increased seedling shoot tolerance to metolachlor approximately tenfold. CGA-92194 seed treatment enhanced shoot absorption of 14C-metolachlor approximately twofold. Metolachlor was initially metabolized to the glutathione conjugate in untreated shoots and those treated with CGA-92194. However, CGA-92194 seed treatment caused accelerated metolachlor metabolism in the shoot, decreasing metolachlor content and increasing formation of the glutathione conjugate. Cyometrinil {(Z)-α[(cyanomethoxy)imino] benzeneacetonitrile}, flurazole [phenylmethyl 2-chloro-4-(trifluoromethyl)-5-thiazolecarboxylate], naphthalic anhydride (1H,3H-naphtho[1,8-cd]-pyran-1,3-dione), and dichlormid (2,2-dichloro-N,N-di-2-propenylacetamide) also protected sorghum from metolachlor injury and enhanced metolachlor absorption and metabolism. The degree of protection conferred by a particular antidote was correlated with its ability to enhance metabolism of metolachlor in shoot tissue. These results are consistent with the hypothesis that the above antidotes protect sorghum from metolachlor injury by inducing rapid detoxification of metolachlor through conjugation with glutathione.

Antidotes were evaluated under greenhouse conditions for their ability to prevent injury to corn and sorghum from imazethapyr. Corn was more tolerant to imazethapyr and more effectively protected from imazethapyr toxicity than sorghum. Naphthalic anhydride (NA)3, CGA 92194, or flurazole treatment of corn seed reduced plant injury from preemergence applications of imazethapyr. Corn injury from postemergence applications of imazethapyr was decreased by seed treatment with NA or CGA 92194. Sorghum injury from preemergence applications of imazethapyr was not reduced by seed treatment with the antidotes. NA treatment of sorghum seed was the most effective antidote treatment for decreasing injury from postemergence applications of imazethapyr but the level of sorghum protection was much less than that achieved with corn. Corn seedlings grown from NA-treated and untreated seed absorbed equal amounts of 14C into the roots from nutrient solution containing 14C-imazethapyr. The NA-treated corn plants translocated less of the absorbed 14C to the shoots than the untreated plants. NA treatment of corn seeds increased the rate of imazethapyr conversion to soluble metabolites 2-and 10-fold in the corn seedling roots and shoots, respectively. The increased rate of imazethapyr metabolism in corn following NA seed treatment may be responsible for the protection from imazethapyr toxicity.

The differences in tolerance, morphology, and physiological response of diclofop-resistant and -susceptible wild oat biotypes collected from fields in Saskatchewan, Canada, were investigated under growth room and field conditions. Under herbicide-free conditions the resistant biotype had more upright leaves with about 12% less leaf area and 50% less leaf width than the susceptible biotype. A marked difference in the level of tolerance to diclofop was observed. Photosynthesis was initially significantly reduced in both biotypes after treatment with diclofop at the rate of 0.70 kg ai ha−1, but the resistant biotype was able to recover. Injury to the susceptible biotype was reduced by coating the seeds with 1,8-naphthalic anhydride. Differential foliar retention was not an important factor in selectivity of diclofop among the two biotypes.

The efficacy of the safeners naphthalic anhydride (NA), CGA-92194, and CGA-133205 as protectants of grain sorghum and of NA, R-29148, CGA-154281, and dichlormid as protectants of corn against injury from the chloroacetamide herbicide, SAN 582H, was evaluated under greenhouse conditions. SAN 582H applied alone reduced the shoot growth of ‘Funk G522DR’ and ‘Funk G623’ sorghum, but had no effect on the growth of the ‘GP-10’ genotype of sorghum. Corn (‘Northrup-King 9283’ hybrid) was considerably more tolerant than grain sorghum to SAN 582H. The rate of SAN 582H causing 50% reduction of corn shoot height (GR50) was 5.1 kg/ha as compared to 1.1 kg/ha for grain sorghum. NA applied as seed dressing at 5 or 10 g/kg seed, provided moderate protection to ‘G522DR’ and ‘G623’ sorghum and no protection to corn against SAN 582H injury. Dressing of sorghum seeds with CGA-133205 provided moderate protection to G522DR sorghum, whereas seed-applied CGA-92194 provided moderate protection to G623 sorghum against SAN 582H. The dichloroacetamide safeners R-29148, dichlormid, and CGA-154281 were all effective as protectants of corn against SAN 582H injury. These results demonstrate that, as with other chloroacetamide herbicides, the tolerance of corn and grain sorghum to SAN 582H can be enhanced with the use of safeners of the dichloroacetamide type and oxime ether type, respectively.

Metolachlor [2-chloro-N-(2-ethyl-6-methylphenyl)-N-(2-methoxy-1-methylethyl)acetamide] at 1 × 10−5 and 1 × 10−4 M increased the leakage of previously absorbed, 32P-labeled orthophosphate from the roots of onion (Allium cepa L.), a susceptible species, by 14 and 41 times the control values, respectively. A significant amount of 32P leaked from the roots of the moderately susceptible species, cotton (Gossypium hirsutum L. ‘DPL 61′) and cucumber (Cucumis sativus L. ‘Ashley′), whereas no significant loss of 32P occurred from two tolerant species, soybean [Glycine max (L.) Merr. ‘Bragg′] and corn (Zea mays L. ‘Pioneer 3369A′). At either 1 × 10−7 or 1 × 10−6 M, 1,8-naphthalic anhydride (NA) prevented 32P leakage from onion roots in the presence of 1 × 10−5 M metolachlor. High concentrations of NA [0.1% (w/v) suspensions], however, promoted 32P leakage and did not protect onion roots from the leakage induced by high concentrations (1 × 10−4 M) of metolachlor. Neither metolachlor nor alachlor [2-chloro-2′,6′-diethyl-N-(methoxymethyl)acetanilide], at 1 × 10−4 M, inhibited the uptake of acetate-2-14C or malonic acid-2-14C into excised cotton root tips or the incorporation of the precursors into lipids. Similarly, neither herbicide inhibited phospholipid synthesis by cotton root tips. Incorporation of 14C-choline chloride into phosphatidylcholine was not significantly inhibited by metolachlor.

Glasshouse research was conducted to investigate the efficacy of herbicide safeners for improving creeping bentgrass (CBG) tolerance to various herbicides. CBG injury from amicarbazone (150 g ha−1), bispyribac-sodium (110 g ha−1), fenoxaprop-p-ethyl (35 g ha−1), imazapic (45 g ha−1), quinclorac (1,050 g ha−1), or topramezone (37 g ha−1) applied in combination with the herbicide safeners naphthalic anhydride or isoxadifen-ethyl was evaluated. These safeners reduced CBG injury from topramezone only. Topramezone was then applied in combination with naphthalic anhydride, isoxadifen-ethyl, cloquintocet-mexyl (cloquintocet), fenchlorazole-ethyl, mefenpyr-diethyl, and benoxacor. These experiments determined that CBG injury was lowest from topramezone in combination with cloquintocet. Additional experiments evaluated topramezone (37 g ha−1) with several rates of cloquintocet and determined that applications at ≥ 28 g ha−1 reduced CBG injury similarly. Cloquintocet (28 g ha−1) increased topramezone I50 values against CBG, but not large crabgrass or goosegrass. The cytochrome P450 (cP450) inhibitor malathion (1000 g ha−1) reduced topramezone I50 values against CBG in one experimental run. Topramezone–cloquintocet combinations warrant further research in field settings.

Understanding pesticide metabolism in plants and microorganisms is necessary for pesticide development, for safe and efficient use, as well as for developing pesticide bioremediation strategies for contaminated soil and water. Pesticide biotransformation may occur via multistep processes known as metabolism or cometabolism. Cometabolism is the biotransformation of an organic compound that is not used as an energy source or as a constitutive element of the organism. Individual reactions of degradation–detoxification pathways include oxidation, reduction, hydrolysis, and conjugation. Metabolic pathway diversity depends on the chemical structure of the xenobiotic compound, the organism, environmental conditions, metabolic factors, and the regulating expression of these biochemical pathways. Knowledge of these enzymatic processes, especially concepts related to pesticide mechanism of action, resistance, selectivity, tolerance, and environmental fate, has advanced our understanding of pesticide science, and of plant and microbial biochemistry and physiology. There are some fundamental similarities and differences between plant and microbial pesticide metabolism. In this review, directed to researchers in weed science, we present concepts that were discussed at a symposium of the American Chemical Society (ACS) in 1999 and in the subsequent book Pesticide Biotransformation in Plants and Microorganism: Similarities and Divergences, edited by J. C. Hall, R. E. Hoagland, and R. M. Zablotowicz, and published by Oxford University Press, 2001.