Field and laboratory experiments were conducted in 1983 and 1984 to compare the degradation of dichlormid (2,2-dichloro-N,N-di-2-prophenylacetamide), dietholate (O,O-diethyl O-phenylphosphorothioate), EPTC (S-ethyl dipropyl carbamothioate), and butylate [S-ethyl bis(2-methylpropyl) carbamothioate] in soils that had or had not been previously treated with each chemical. EPTC + dichlormid, butylate + dichlormid, EPTC + dichlormid + dietholate, or butylate + dichlormid + dietholate were applied annually for 4 yr to field plots to establish treatment histories. Butylate and EPTC degradation was enhanced in soils with previous histories of butylate and EPTC, respectively. Degradation rates of dietholate were equivalent in untreated soils or soils previously treated with EPTC + dietholate or butylate + dietholate.

CGA-154281 and temperature effects on metolachlor absorption and metabolism were studied in corn seedlings grown in untreated soil or soil treated with metolachlor, CGA-154281, or both. Seedlings were grown under a cool (21/13 C, 16-h day) or warm (30/21 C, 16-h day) temperature regime and exposed to 14C-metolachlor for 10 min at either 21 or 30 C. Corn grown under the cool temperature regime absorbed slightly more 14C-metolachlor than corn grown under the warm temperature regime. Corn held at 21 C during a 10-min 14C-metolachlor exposure period metabolized metolachlor more slowly than corn held at 30 C. Decreased corn tolerance to metolachlor observed at lower temperatures may be due in part to slower metolachlor metabolism. Corn grown in the presence of metolachlor plus CGA-154281 metabolized 14C-metolachlor to the glutathione conjugate twice as fast as corn grown in the presence of metolachlor alone. The increase in metabolism rate was due to a fivefold increase in glutathione-S-transferase (GST, EC 2.5.1.18) activity and not to an increase in glutathione (GSH) content. Results are consistent with the hypothesis that CGA-154281 protects corn from metolachlor injury by enhancing GST activity, which accelerates metolachlor detoxification via GSH conjugation.

The combination of certain herbicides with insecticides can inhibit crop growth. Greenhouse studies were conducted to evaluate interaction effects of herbicides and insecticides with/without protectant, on corn and weed species. ‘Northrup King 9283’ hybrid corn showed greater sensitivity to acetanilide herbicides than ‘Cargill 7567.’ Neither the insecticides terbufos nor isazofos appeared to enhance this sensitivity. Both hybrids were sensitive to the combination of chlorimuron, nicosulfuron, or primisulfuron with terbufos. Cargill 7567 was more tolerant than Northrup King 9283 to the growth inhibiting interaction of sulfonylurea herbicides with terbufos. Imazaquin at 70 g/ha reduced height of Northrup King 9283 corn, but there was no interaction with terbufos. The protectants CGA-154281 and NA reduced corn injury from metolachlor and the combination of nicosulfuron and primisulfuron with terbufos, respectively. Nicosulfuron and primisulfuron treatments combined with metolachlor showed less corn injury than metolachlor alone, but these herbicides increased corn injury when combined with terbufos. The inclusion of terbufos did not enhance primisulfuron activity on barnyardgrass, giant foxtail, or velvetleaf.

Greenhouse studies were conducted to determine the response of six corn hybrids and two soybean varieties to acetolactate synthase (ALS) inhibitor herbicides applied with terbufos and/or piperonyl butoxide (PBO), a mixed function oxidase (MFO) inhibitor. Field experiments also were conducted to determine the response of six corn hybrids to the combination treatments, terbufos plus ALS inhibitor herbicides and/or PBO and/or antidote. PBO at 0.33 kg/ha tank-mixed with nicosulfuron and primisulfuron injured the Northrup King 9283 corn hybrid. Great Lakes 584 corn was less sensitive than Northrup King 9283 to these combination treatments. Pioneer 3377 IR corn hybrid was resistant to the combination of nicosulfuron or primisulfuron plus PBO at 2 kg/ha and also to the combination treatments of imazethapyr herbicide plus PBO even though terbufos was previously applied. ICI 8532 IT, ICI 8532, and Pioneer 3377 hybrids were injured by the combination of nicosulfuron or primisulfuron and/or terbufos and/or PBO at 2 kg/ha. ICI 8532 IT corn hybrid was not injured by the combination treatment of imazethapyr or thifensulfuron and terbufos. In the field studies, Pioneer 3377 IR and Ciba 4393 RSC hybrids were resistant to sulfonylurea and imidazolinone herbicides even when applied with PBO regardless of the presence of terbufos. All treatments of chlorimuron plus terbufos caused considerable injury to ICI 8532 IT, ICI 8532, Pioneer 3377, and Ciba 4393, but not Pioneer 3377 IR and Ciba 4393 RSC. The combination of thifensulfuron with PBO injured Elgin ‘87 soybean, but the W20 soybean was tolerant to this combination treatment. Combination of imazethapyr with PBO did not affect the growth of Elgin ‘87 soybean.

Thioproline (L-thiazolidine-4-carboxylic acid) partially protects sorghum [Sorghum bicolor (L.) Moench. ‘DK 42Y’] seedlings against the herbicides tridiphane [2-(3,5-dichlorophenyl)-2-(2,2,2-trichloroethyl)oxirane] and alachlor [2-chloro-N-(2,6-diethylphenyl)-N-(methoxymethyl)acetamide] in controlled environment chambers. Thioproline alone inhibits plant growth at concentrations above 10−5 M. Its phytotoxicity is intermediate between the two herbicide antidotes OTC (L-2-oxothiazolidine-4-carboxylic acid) and flurazole [phenylmethyl 2-chloro-4-(trifluoromethyl)-5-thiazolecarboxylate]. The two thiazolidine antidotes increased thiol content of excised corn (Zea mays L. ‘DK T 1100’) seedling roots whereas thiol content was decreased by the two herbicides. While thioproline or OTC partially offset tridiphane-induced decreases in thiol content, none of the antidotes effectively circumvented the reduced thiol content resulting from alachlor treatment.

A field trial was conducted in 1988 and 1989 to confirm the efficacy of naphthalic anhydride (NA) for providing full-season protection of corn from imazethapyr applied at various times and rates. NA applied as a 1% by weight dust to corn seed caused 6% injury 2 weeks after treatment (WAT) in 1989; however, plants recovered within 6 WAT and grain yield was not affected. Imazethapyr applied to corn untreated with NA resulted in greater than 30% injury for all treatments in both years except PRE in 1988. NA reduced phytotoxicity from all imazethapyr applications in 1989 and from PPI, early POST, and 4- to 5-leaf stage (mid-POST) applications in 1988. Despite the safening effect, corn injury was still observed 6 WAT in NA-treated corn for all imazethapyr applications in both years except early POST in 1988. Higher yields were produced from NA-treated than untreated corn with imazethapyr applied PPI in both years, PRE in 1989, early POST in both years, and mid-POST in 1988. Safened corn treated PPI and early POST yielded the same as the safened corn in the control in both years. Imazethapyr applied at the 8- to 10-leaf stage caused total yield loss regardless of NA treatment. Drought conditions may have caused the lower corn injury and yield loss from imazethapyr observed in 1988 compared to 1989.

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.

Use of R-25788 (N,N-diallyl-2,2-dichloroacetamide) eliminated early-season corn (Zea mays L. '501D′) injury, stand loss, and yield reduction caused by EPTC (S-ethyl dipropylthiocarbamate) at 3.4, 6.7, and 13.4 kg/ha. R-25788 also eliminated early-season corn injury from butylate (S-ethyl diisobutylthiocarbamate) at 9.0 kg/ha. R-25788 did not consistently prevent corn yield reduction from 2,4-D [(2,4-dichlorophenoxy)acetic acid] or EPTC + 2,4-D. R-25788 had no effect on weed control from any of the herbicides evaluated nor any effect by itself on corn injury or corn yield. No corn injury or yield reductions occurred from vernolate (S-propyl dipropylthiocarbamate) at rates up to 6.7 kg/ha or alachlor [2-chloro-2′, 6′-diethyl-N-(methoxymethyl)acetanilide] at rates up to 13.4 kg/ha. Early-season corn injury frequently did not result in reduced corn yield.

Flurazole [phenylmethyl 2-chloro-4-(trifluoromethyl)-5-thiazolecarboxylate] and acetochlor [2-chloro-N-(ethoxymethyl)-N-(2-ethyl-6-methylphenyl)acetamide] were examined in the laboratory and greenhouse for effects on grain sorghum [Sorghum bicolor (L.) Moench ‘G-522 DR’]. Flurazole did not protect against acetochlor-induced inhibition of primary root growth when sorghum was grown in distilled water, but some safening occurred after 8 days when nutrients were available. Flurazole did not protect primary roots completely. In the presence of nutrients, however, flurazole stimulated growth of the mesocotyl roots and protected the second adventitious root system.

BAS-145-138 considerably muted the herbicidal effect of the sulfonylurea herbicides on corn. Decreases of 54 and 52% in shoot fresh and dry weight caused by 10 μM chlorsulfuron were countered almost completely by 1.5 mM BAS-145-138 with only a 10% loss in fresh weight and a 3% loss in dry weight. Similar strong antidotal influence by BAS-145-138 on chlorimuron was observed. BAS-145-138 partially protected corn against sulfometuron. Shoot fresh weight of corn treated with 0.2 μM sulfometuron was inhibited 88%, whereas adding 0.5 or 1.5 mM BAS-145-138 reduced inhibition to 52 and 24%, respectively.

Laboratory studies demonstrated that naptalam safens cucumber against the phytotoxic effects of chloramben. In petri dish studies, cucumber seedlings grown from seeds exposed to chloramben plus naptalam had greater shoot growth, root growth, and dry weight than seedlings grown from seeds exposed to chloramben alone. Naptalam also partially reversed the reduction in dry weight of various plant parts caused by exposure of roots of hydroponically grown seedlings to chloramben. More radioactivity from root-applied 14C-chloramben remained in cucumber roots and less was translocated to shoots with a 14C-chloramben plus naptalam treatment than with a 14C-chloramben alone treatment. Naptalam appeared to influence chloramben metabolism. In various plant parts, concentrations of chloramben and its metabolites differed between the two treatments.

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.

Tridiphane [2-(3,5-dichlorophenyl)-2-(2,2,2-trichloroethyl)oxirane] inhibited growth of seedling corn (Zea mays L. ‘DK T 1100’), wheat (Triticum aesetivum L. ‘Arthur’), and sorghum (Sorghum vulgare Pers. ‘DK 42Y’) in growth chamber experiments. These inhibitions were partially circumvented by simultaneous treatment with OTC (L-2-oxothiazolidine-4-carboxylic acid). Tridiphane, atrazine [6-chloro-N-ethyl-N′-(1-methylethyl)-1,3,5-triazine-2,4-diamine], and OTC each increased levels of low molecular weight thiols (glutathione) in intact roots of treated corn seedlings, but only OTC did in excised roots. Tridiphane and atrazine caused a decrease in thiol content of excised roots. Tridiphane treatments reduced the amount of glutathione S-transferase activity extractable from corn roots, and this reduction was circumvented partially by OTC applied in combination with tridiphane. These data present evidence that tridiphane interference with cysteine or glutathione metabolism can be reversed by increasing cellular content of cysteine.