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 and field experiments were conducted to determine the effectiveness of dichlormid, R-29148, CGA-92194, flurazole, naphthalic anhydride, and MON-5500 as herbicide antidotes for triallate in wheat and to determine triallate antagonism by seed-applied fungicides and insecticides. Seed treatment of MON-5500 at 0.063% wt/wt was the most effective antidote for triallate in wheat in both greenhouse and field. Dichlormid and R-29148 at 0.5% wt/wt were more effective as antidotes for triallate in wheat than either CGA-92194 or naphthalic anhydride. Flurazole, as a seed treatment, did not reduce triallate injury to wheat Dichlormid or R-29148 at 2.2 kg ai ha–1 applied broadcast to soil and incorporated reduced injury to wheat from triallate at 1.1 kg ai ha–1 and also reduced injury to oats from 0.3 kg ha–1 triallate. Seed treatments of carboxin at 0.2% wt/wt or imazalil at 0.008% wt/wt antagonized triallate and decreased injury to wheat from triallate at 0.6 kg ha–1. Maneb plus lindane or mancozeb treatment of wheat seed increased injury from triallate.

The antidotes dichlormid, MON-4660, CGA-154281, R-29148, and MON-13900 were tested in the greenhouse to protect Zea mays L. (corn) against RPA 201772 injury. High rates of RPA 201772 injured four Z. mays hybrids > 30%. R-29148 and MON-13900 were the most effective of the five antidotes evaluated. R-29148 applied at rates ⩾ 45 g ha−1 provided excellent protection against RPA 201772 injury and also prevented injury to Z. mays from diketonitrile, the active metabolite of RPA 201772. In laboratory studies, R-29148 did not alter absorption of 14C-RPA 201772 from soil; however, R-29148 significantly enhanced the rate of RPA 201772 metabolism and inactivation in Z. mays. The mixed function oxidase inhibitor piperonyl butoxide (PBO) increased RPA 201772 injury on all hybrids. These results demonstrate that Z. mays tolerance to RPA 201772 can be enhanced with the use of antidotes such as R-29148 and MON-13900, that R-29148 protects Z. mays from RPA 201772 and diketonitrile by the enhancement of metabolism, and that oxidative reactions may be involved in the metabolism of RPA 201772 in Z. mays.

The influence of acetamide herbicide applications on efficacy of CGA-43089 [α-(cyanomethoximino)-benzacetonitrile] in grain sorghum [Sorghum bicolor (L.) Moench] was studied under field conditions. Acetamide herbicides applied preplant and incorporated on a Haynie very fine sandy loam caused more grain sorghum injury in 1979 than in 1978. Reductions in plant population, plant height and yield, along with delay in maturity, were severe for acetochlor [2-chloro-N-(ethoxymethyl)-6′-ethyl-O-acetotoluidide], metolachlor [2-chloro-N-(2-ethyl-6-methylphenyl)-N-(2-methoxy-1-methylethyl)acetamide], and alachlor [2-chloro-2′,6′-diethyl-N-(methoxymethyl)acetanilide]; moderate for diethatyl [N-(chloroacetyl)-N-(2,6-diethylphenyl)glycine], xylachlor [2-chloro-N-(2,3-dimethylphenyl)-N-(1-methylethyl)acetamide], and butam [2,2-dimethyl-N-(1-methylethyl)-N-(phenylmethyl)propanamide]; and did not occur for propachlor (2-chloro-N-isopropylacetanilide) treatments. Acetamide herbicides caused less grain sorghum injury on a Reading silt loam than on a Haynie very fine sandy loam in 1979. CGA-43089 applied as a seed treatment protected grain sorghum grown on soils treated with metolachlor, alachlor, diethatyl, or xylachlor. Metolachlor-triazine combinations at five locations in Kansas reduced yields at two locations. CGA-43089 provided protection from metolachlor injury at those two locations.

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.

BAS 145 138, CGA 154 281, and 1,8 naphthalic anhydride were evaluated as seed treatments to safen 'Silver Xtra Sweet,’ ‘How Sweet It Is,’ ‘Zenith,’ and 'Sweetie 76’ sweet corn against nicosulfuron injury. Nicosulfuron POST injured sweet corn by causing slight leaf chlorosis and leaf base widening in Sweetie 76 and severe plant injury and total yield loss in Silver Xtra Sweet. Naphthalic anhydride or CGA 154 281 provided limited or no safening activity, respectively, and resulted in plant height reduction when applied alone. BAS 145 138 reduced nicosulfuron injury to Silver Xtra Sweet and prevented visible injury from nicosulfuron in How Sweet It Is, Zenith, and Sweetie 76.

Field studies were conducted in 1989 and 1990 to determine if corn seed treated with naphthalic anhydride (NA) at 0.5% (w/w) would result in a reduction in corn injury caused by clomazone applied preplant incorporated (PPI) or preemergence (PRE) at 0.56 and 0.70 kg a.i. ha–1. NA significantly reduced corn injury, especially where clomazone was incorporated. Plant population, height, ear number, and grain yield also were higher in plots where NA was used. In most instances, corn injury was less and plant population, height, ear number, and grain yield were higher in plots where clomazone was applied PRE compared with PPI.

Field studies were conducted for 3 yr near Mead, NE, to evaluate the effectiveness of seed safeners CGA-92194 [N-(1,3-dioxalon-2-yl-methoxy)iminobenzeneacetonitrile], NA (1,8-naphthalic anhydride), and R-29148 (2,2-dimethyl-5-methyldichloroacetyloxazolidine) to reduce herbicide injury to big bluestem (Andropogon gerardii Vitman), indiangrass [Sorghastrum nutans (L.) Nash], intermediate wheatgrass [Agropyron intermedium (Host.) Beauv.], sideoats grama [Bouteloua curtipendula (Michx.) Torr.], and switchgrass (Panicum virgatum L.) from preplant-incorporated butylate [5-ethyl bis-(2-methylpropyl)carbamothioate] and metolachlor [2-chloro-N- (2-ethyl-6-methylphenyl) -N- (2-methoxy-l-methylethyl)acetamide], applied at 4.5 and 2.2 kg ai/ha, respectively. Big bluestem stands were satisfactory, regardless of herbicide or safener treatment, although stands were reduced by NA treatment with either herbicide. Indiangrass stands varied by year, with protection from both herbicides by R-29148 in 1984 and by NA in 1985. All safeners reduced injury to intermediate wheatgrass from metolachlor and to a lesser extent from butylate; acceptable stands were obtained with metolachlor treatment when unsafened. Sideoats grama was nearly eliminated with either herbicide, regardless of safener. Switchgrass treated with NA produced stands two- to threefold higher than other safened or unsafened seed in metolachlor plots and equal to unsafened seed in the weeded control plots.

Greenhouse and field studies were conducted to determine the influence of herbicide rate, hybrid variability, and soil moisture on the effectiveness of CGA-154281 in protecting corn seedlings from metolachlor injury. High rates of metolachlor caused significant injury to seedlings of sensitive corn hybrids. However, with metolachlor plus CGA-154281, very few injury symptoms were observed, even with the 7.8 kg ha–1 rate and the most sensitive hybrid. Corn seedlings were not injured by metolachlor plus CGA-154281 at the highest soil moisture level evaluated, whereas those treated with metolachlor alone showed 70% injury. Metolachlor injury increased as soil moisture content increased. In the greenhouse, CGA-154281 did not protect any of the eight weed species tested against injury by 2.2 kg ha–1 metolachlor. In laboratory studies, CGA-154281 did not alter the absorption of 14C-metolachlor during an 8-h period. Qualitative comparison of the metabolism of metolachlor in the presence or absence of the protectant indicated that metolachlor was metabolized to a more polar metabolite, believed to be a glutathione conjugate. However, CGA-154281 significantly enhanced the rate of metabolism of metolachlor in three of the four hybrids tested. Metolachlor metabolism activity may already have been functioning at a maximum level in the unaffected hybrid.