Quinclorac controls crabgrass (Digitaria spp.) in cool- and warm-season turfgrass species. Herbicide-resistant smooth crabgrass [Digitaria ischaemum (Schreb.) Schreb. ex Muhl.] biotypes have evolved due to recurrent usage of quinclorac. Two Mississippi populations (MSU1 and MSU2) of D. ischaemum were characterized using standard greenhouse dose–response screens to assess their resistance relative to known susceptible populations. Subsequent investigations explored mechanisms of resistance, including examining cyanide accumulation, glutathione S-transferase (GST) activity, and the potential involvement of cytochrome P450s in MSU1, MSU2, and a susceptible (SMT2). Resistant populations MSU1 and MSU2 required 80 and 5 times more quinclorac, respectively, to reach 50% biomass reduction than susceptible populations. The SMT2 biotype accumulated three times more cyanide than the resistant MSU1 and MSU2 populations. GST activity was elevated in resistant MSU1 and MSU2 populations. Furthermore, quinclorac concentrations in treated resistant populations were elevated when plants were pretreated with the P450 inhibitor malathion. These findings suggest a non–target site based mechanism of resistance involving the accumulation of cyanide. This may provide a scientific basis for understanding the occurrence of quinclorac-resistant D. ischaemum, although further research is needed to investigate potential target-site mechanisms of resistance.

Cotton and soybean growers were offered new technologies in 2016, expanding in-crop herbicide options to include dicamba or 2,4-D. Within 3 yr of commercialization, dicamba use in these crops increased 10-fold, and growers began to report Palmer amaranth escapes in dicamba-tolerant production systems in western Tennessee. In 2020, Palmer amaranth seed was collected from eight Tennessee locations where growers witnessed poor control following dicamba. Greenhouse experiments were conducted to evaluate the response of these Palmer amaranth populations to dicamba. In 2021, field experiments were conducted on two tentative dicamba-susceptible populations in Georgia, on three confirmed dicamba-resistant populations in Tennessee, and on a tentative dicamba-susceptible population in Texas to evaluate cotton response following dicamba and to examine if malathion insecticide (a cytochrome P450 inhibitor) would improve weed control and not reduce cotton yield when applied in conjunction with dicamba. Palmer amaranth populations collected in 2020 survived dicamba in the greenhouse at 1, 2, and 4 times the labeled rate. Five Palmer amaranth populations exhibited 15% to 26% survival to the labeled dicamba rate (560 g ha−1) in the greenhouse. These findings were reinforced in the field when research on three of those populations in 2021 showed 55% control with the labeled dicamba rate and 69% control with 2 times the labeled rate. This demonstrates that the dicamba resistance allele or alleles were passed between generations. This result was not consistent in the Macon County, GA, or Worth County, GA, locations, where malathion improved dicamba control of 15- to 38-cm-tall Palmer amaranth. Cotton injury was observed when malathion was applied in combination with dicamba. These results further document the evolution of dicamba-resistant Palmer amaranth in Tennessee. Moreover, the nonreversal of resistance phenotype by malathion may suggest that the resistance mechanism is something other than metabolism.

Malathion is an insecticide that is used to control arboviruses and agricultural pests. Adolescents that are exposed to this insecticide are the most vulnerable as they are in the critical period of postnatal sexual development. This study aimed to evaluate whether malathion damage can affect sperm function and its respective mechanisms when adolescents are exposed during postnatal sexual development. Twenty-four male Wistar rats (PND 25) were divided into three experimental groups and treated daily for 40 d: control group (saline 0.9%), 10 mg/kg (M10 group), or 50 mg/kg (M50 group) of malathion. At PND 65, the rats were anesthetized and euthanized. Testicles were collected for the evaluation of gene expression. Sperm cells from the epididymis were used for evaluation of the oxidative profile or spermatic function. Data showed that a lower dose of malathion downregulated the gene expression of androgen receptors and testosterone converter enzyme 17-β-HSD in the testis. The acrosomal integrity of sperm cells was compromised in the M50 group, but not the M10 group. The mitochondrial activity was not impaired by exposure. Finally, although no alterations in malondialdehyde and glutathione levels were observed, malathion, at both doses, increased antioxidant enzyme catalase activity and, at a higher dose, superoxide dismutase activity. The present study showed that low doses of malathion considered to be inoffensive are capable of impairing sperm quality and function through the downregulation of testicular genic expression of AR enzyme 17-β-HSD and can damage the spermatic antioxidant profile during critical periods of development.

Palmer amaranth is one of the most problematic weeds in cropping systems of North America, especially in midsouthern United States, because of its competitive ability and propensity to evolve resistance to several herbicide sites of action. Previously, we confirmed and characterized the first case of nontarget site resistance (NTSR) to fomesafen in a Palmer amaranth accession from Randolph County, AR (RCA). The primary basis of the present study was to evaluate the cross- and multiple-resistance profile of the RCA accession. The fomesafen dose-response assay in the presence of malathion revealed a lower level of RCA resistance when compared with fomesafen alone. The resistance index of the RCA accession, based on 50% biomass reduction, ranged from 63-fold (fomesafen alone) to 22-fold (malathion plus fomesafen), when compared with a 2007 susceptible, and 476-fold and 167-fold, respectively, relative to a 1986 susceptible check. The RCA accession was resistant to other protoporphyrinogen oxidase (PPO) inhibitors (i.e., flumioxazin, acifluorfen, saflufenacil) as well as the 4-hydroxyphenylpyruvate dioxygenase (HPPD) inhibitor tembotrione and acetolactate synthase (ALS) inhibitor pyrithiobac sodium. Sequencing of the ALS gene revealed no point mutations, indicating that a target-site mechanism is not involved in conferring ALS-inhibitor resistance in the RCA accession. Of the three PPO-inhibiting herbicides tested in combination with the malathion, saflufenacil resulted in the greatest biomass reduction (80%; P < 0.05) and lowest survival rate (23%; P < 0.05) relative to nontreated plants. The application of cytochrome P450 or glutathione S-transferase inhibitors with fomesafen did not lead to any adverse effects on soybean, suggesting a possible role for these compounds for management of NTSR under field conditions. These results shed light on the relative unpredictability of NTSR in conferring herbicide cross- and multiple resistance in Palmer amaranth.

Italian ryegrass has invaded wheat fields in China and is becoming a predominant, troublesome weed. Fenoxaprop-P-ethyl has been widely used for weed control on Chinese farms since the 1990s. However, overuse has led to fenoxaprop-P-ethyl resistance in Italian ryegrass in Chinese wheat fields. In this study, we identified a putative fenoxaprop-P-ethyl–resistant population of Italian ryegrass, HZYC-6, from Henan province, China. Mutations involving Asp-2078-Gly and Ile-1781-Leu substitutions were identified in the carboxyl-transferase domain of acetyl-coenzyme A carboxylase in this population, and these mutations are the likely cause of the target site–based resistance to fenoxaprop-P-ethyl. In addition, we identified cytochrome P450–mediated metabolism of herbicides (non–target site based resistance) in the HZYC-6 population, indicating that multiple mechanisms of resistance may be segregating in this population. Furthermore, HZYC-6 was also highly resistant to haloxyfop-R-methyl and quizalofop-P-ethyl, moderately resistant to clodinafop-propargyl and sethoxydim, and had low resistance to clethodim and pinoxaden.

Field and greenhouse experiments were conducted to determine the effect of selected insecticides on cotton when applied in combination with pyrithiobac. In the field, acephate, azinphos-methyl, bifenthrin, chlorpyrifos, dicrotophos, esfenvalerate, malathion, methomyl, or oxamyl was applied foliarly with the sodium salt of pyrithiobac at 70 g ae/ha. Pyrithiobac plus malathion resulted in greatest injury when compared with other treatments. There were no differences observed in fruiting characteristics of cotton. Cotton yield was lower with oxamyl, methomyl, and chlorpyrifos when applied in combination with pyrithiobac in one of three experiments. In greenhouse experiments, injury due to pyrithiobac was greater in a cool (21 C day, 13 C night) temperature than in a warm temperature (30 C day, 21 C night), but differences were less than 15%. Pyrithiobac plus malathion in the cool environment injured cotton more severely 7 DAT than either pesticide alone. Adding insecticides to pyrithiobac did not influence injury in the warm environment.

Field experiments were conducted to determine factors that predispose winter wheat to injury by sulfonylurea herbicides. Wheat was injured occasionally when herbicides were applied postemergence in November or when tank mixed with malathion. CGA 131036 at 28 or 56 g ha-1 was less injurious than chlorsulfuron or DPX-G8311 at 26 or 53 g ha-1, and preemergence treatments of chlorsulfuron and DPX-G8311 were less injurious than preplant incorporated or postemergence treatments. Wheat growth stage, minimum post-treatment daily temperature, and summed diurnal temperature fluctuations after treatment and after first post-treatment rainfall were correlated with wheat injury. Grazing and cultivar selection did not affect injury.

The organophosphate insecticides, malathion [S-1,2-di (ethoxycarbonyl)ethyl O, O-dimethyl phosphorodithioate], parathion (O, O-diethyl O-4-nitrophenyl phosphorothioate) and diazinon (O,O-diethyl O-2-isopropyl-6-methylpyrimidin-4-yl phosphorothioate) combined with bentazon [3-isopropyl-1H-2,1,3-benzothiadiazin-4(3H)-one 2,2-dioxide], caused severe injury to soybean [Glycine max (L.) Merr. ‘Corsoy′] and navy bean (Phaseolus vulgaris L. 'Seafarer′). Postemergence tank – mixture applications of bentazon with organophosphate or carbamate insecticides, or soil-applied organophosphate insecticides prior to bentazon treatments, did not interact with bentazon to injure corn (Zea mays L. ‘Great Lakes Hybrid 4122′). Technical grade malathion interacted with bentazon to the same extent as formulated malathion. Combination treatments of malathion with bentazon resulted in the same degree of injury whether they were applied as tank mixtures or split applications 48 h apart.

Combinations of thifensulfuron with carbaryl, chlorpyrifos, malathion, and methomyl caused soybean injury that exceeded the expected injury based on effects of herbicide and synergists applied alone. Thifensulfuron-induced injury and growth reductions generally increased as insecticide rates increased from 140 to 560 g ai ha-1. TBPT and fenarimol also synergistically enhanced thifensulfuron injury in soybeans. Yellow foxtail control by thifensulfuron was enhanced slightly by all insecticides except carbaryl. Insecticides did not enhance kochia control by thifensulfuron.

Burs of common cocklebur (Xanthium strumarium L.) obtained from Stoneville, Mississippi; Urbana, Illinois; and Lamberton, Minnesota, were used in greenhouse and growth chamber studies. The Mississippi and the Illinois strains were both classified as being in the “strumarium” complex of X. strumarium, whereas, the Minnesota strain was classified as being in the “hybrid” complex. The Minnesota common cocklebur developed branch leaves in the leaf axils of the main stem to a much greater extent than did the Mississippi and Illinois common cocklebur. The Mississippi common cocklebur was frequently more tolerant of postemergence applications of bentazon [3-isopropyl-1H-2,1,3-benzothiadiazin-4(3H)-one 2,2-dioxide] than were the Illinois and Minnesota common cockebur. The Mississippi and Illinois common cocklebur developed leaf necrosis when sprayed with an insecticide formulation containing malathion (o, o-dimethyl phosphorodithioate of mercaptosuccinate) and petroleum solvents; the Minnesota common cocklebur did not.

A waterhemp population (MCR) previously characterized as resistant to 4-hydroxyphenylpyruvate dioxygenase and photosystem II inhibitors demonstrated both moderate and high levels of resistance to acetolactate synthase (ALS) inhibitors. Plants from the MCR population exhibiting high resistance to ALS inhibitors contained the commonly found Trp574Leu ALS amino acid substitution, whereas plants with only moderate resistance did not have this substitution. A subpopulation (JG11) was derived from the MCR population in which the moderate-resistance trait was isolated from the Trp574Leu mutation. Results from DNA sequencing and ALS enzyme assays demonstrated that resistance to ALS inhibitors in the JG11 population was not due to an altered site of action. This nontarget-site ALS-inhibitor resistance was characterized with whole-plant dose–response experiments using herbicides from each of the five commercialized families of ALS-inhibiting herbicides. Resistance ratios ranging from 3 to 90 were obtained from the seven herbicides evaluated. Nontarget-site resistance to ALS has been rarely documented in eudicot weeds, and adds to the growing list of resistance traits evolved in waterhemp.

Japanese foxtail is a predominant tetraploid grass weed in wheat and oilseed rape fields in eastern China. In China, pyroxsulam is mainly used to manage annual grass weeds, especially those resistant to acetyl coenzyme A carboxylase (ACCase)-inhibiting herbicides. Using dose–response studies, a pyroxsulam-resistant population, ACTC-1, was identified with a resistance index value of 58. Additionally, ACTC-1 was cross-resistant to sulfonylureas, imidazolinones, triazolopyrimidines, pyrimidinyl-benzoates, and sulfonylaminocarbonyl-triazolinones and multiresistant to ACCase and photosystem II inhibitors. Sequence analysis revealed four gene fragments encoding acetolactate synthase (ALS) from ACTC-1, and three from JNXW-1, a pyroxsulam-sensitive population. An Asp-376-Glu substitution was found in ALS1;2 and an Ile-2041-Asn in Acc1;1, which may be responsible for its resistance to pyroxsulam and ACCase inhibitors, respectively. In vitro assays of ALS activity revealed that in ACTC-1, the sensitivity of ALS to pyroxsulam was lower, and the basal ALS activity was twofold higher than that of sensitive population JNXW-1. Additionally, the combined application of pyroxsulam with malathion or piperonyl butoxide increased the sensitivity of ACTC-1 to pyroxsulam, although it could not completely overcome the resistance. It was inferred that both target-site-based resistance and nontarget-site-based resistance may be involved in the resistance to pyroxsulam.

Ninety-seven inbred lines of sunflower were screened in the field by treatment with a combination of imazamox and malathion, an inhibitor of cytochrome P450 monooxygenases (P450s), to identify sunflower lines with natural tolerance to the herbicide reversed by malathion. One tolerant line, named TolP450-1, was selected and characterized in the field and in the greenhouse to evaluate its response to the herbicides imazamox, prosulfuron, and atrazine at different plant development stages (germination, emergence, and third difoliate) with and without malathion. For all herbicides and all development stages analyzed, TolP450-1 showed significantly higher tolerance compared with the susceptible line RHA266. In all cases, the tolerance was reversed by malathion. This sunflower line, tolerant to multiple herbicides, may be useful in helping to manage herbicide-resistant weeds by allowing additional herbicides to be used in this oilseed crop.

Resistance to protoporphyrinogen oxidase (protox)-inhibiting herbicides was identified in a population of common waterhemp that had been treated with acifluorfen for several years. The protox-resistant biotype of common waterhemp was approximately 34, 82, 8, and 4 times more resistant than a susceptible common waterhemp biotype to acifluorfen, lactofen, fomesafen, and sulfentrazone, respectively. The resistant biotype also showed a high level of resistance to acetolactate synthase–inhibiting herbicides thifensulfuron and imazethapyr but not to glyphosate or paraquat. An organophosphate insecticide was applied with acifluorfen or lactofen to determine if metabolism could be the mechanism of resistance. No differences were observed between resistant plants treated with an organophosphate plus a protox-inhibiting herbicide and plants treated with a protox-inhibiting herbicide alone.

Overuse of acetolactate synthase (ALS)–inhibiting herbicides in rice has led to the evolution of halosulfuron-resistant rice flatsedge in Arkansas and Mississippi. Resistant accessions were cross-resistant to labeled field rates of ALS-inhibiting herbicides from four different families, in comparison to a susceptible (SUS) biotype. Resistance index of Arkansas and Mississippi accessions based on an R/S ratio of the lethal dose required for 50% plant mortality (LD50) to bispyribac-sodium, halosulfuron, imazamox, and penoxsulam was ≥ 21-fold. Control of Arkansas, Mississippi, and SUS accessions with labeled field rates of 2,4-D, bentazon, and propanil was ≥ 93%. An enzyme assay revealed that an R/S ratio for 50% inhibition (I50) of ALS for halosulfuron was 2,600 and 200 in Arkansas and Mississippi, respectively. Malathion studies did not reveal enhanced herbicide metabolism in resistant plants. The ALS enzyme assay and cross-resistance studies point toward altered a target site as the potential mechanism of resistance. Trp574–Leu amino acid substitution within the ALS gene was found in both Arkansas and Mississippi rice flatsedge accessions using the Illumina HiSeq platform, which corresponds to the mechanism of resistance found in many weed species. Field-rate applications of 2,4-D, bentazon, and propanil can be used to control these ALS-resistant rice flatsedge accessions.

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.

Determining the mechanisms of herbicide resistance in weeds allows for the development and implementation of applied management practices aimed to control and to prevent further spread of herbicide-resistant populations in crop fields. This research was conducted to determine propanil resistance and cross-resistance to other photosystem II (PSII) inhibitors in ricefield bulrush biotypes and to elucidate the mechanism of propanil resistance. To this end, propanil-resistant (R) and propanil-susceptible (S) biotypes were selected from field-collected populations after propanil spraying at the field rate, and whole-plant, dose–response experiments were conducted to evaluate cross-resistance to PSII inhibitors and interactions between propanil and the insecticides malathion and carbaryl. In addition, the psbA gene from R and S biotypes was sequenced for amino acid alterations following polymerase chain reaction (PCR) amplification. Plant survival data indicated the R biotype displayed a 14-fold increase in propanil resistance relative to the susceptible (S) biotype. In addition, the propanil-R biotype also had increased resistance to the PSII-inhibitors bromoxynil, diuron, and metribuzin but was more susceptible to bentazon than were propanil-S plants. Synergism between propanil and the insecticides carbaryl and malathion was greater in the S biotype than it was in the R biotype, indicating that, unlike propanil resistance in weedy grasses, enhanced degradation of the herbicide molecule is not a mechanism of resistance for propanil in ricefield bulrush. A Val219 to Ile substitution in the propanil-R chloroplast D1 protein was identified following sequencing of the psbA gene. This research suggests a single-point mutation at the target site causes resistance to propanil, diuron, metribuzin, and bromoxynil but increasing susceptibility to bentazon in propanil-R ricefield bulrush, a novel Val219–Ile feature. To our knowledge, this is the first instance of propanil resistance in weeds because of a mechanism other than enhanced herbicide metabolism. Tank-mixing bentazon and propanil, where permitted, can control both propanil-R and propanil-S biotypes.

The ubiquitous use of pesticides has increased concerns over their direct and indirect effects on disease dynamics. While studies examining the effects of pesticides on host–parasite interactions have largely focused on how pesticides influence the host, few studies have considered the effects of pesticides on parasites. We investigated the toxicity of six common insecticides at six environmentally-relevant concentrations to cercariae of the trematode Echinoparyphium from two populations. All six insecticides reduced the survival of cercariae (overall difference between mortality in control vs pesticide exposure = 86·2 ± 8·7%) but not in a predictable dose-dependent manner. These results suggest that Echinoparyphium are sensitive to a broad range of insecticides commonly used in the USA. The lack of a clear dose-dependent response in Echinoparyphium highlights the potential limitations of toxicity assays in predicting pesticide toxicity to parasites. Finally, population-level variation in cercarial susceptibility to pesticides underscores the importance of accounting for population variation as overlooking this variation can limit our ability to predict toxicity in nature. Collectively, this work demonstrates that consideration of pesticide toxicity to parasites is important to understanding how pesticides ultimately shape disease dynamics in nature.

Organophosphate pesticides (OPs) like malathion interfere with normal ovarian function resulting in an increased incidence of atresia and granulosa cell apoptosis that plays a consequential role in the loss of ovarian follicles or follicular atresia. The aim of present study was to assess malathion-induced (100 nM) reproductive stress, ultrastructural damage and changes in apoptosis frequency in ovarian granulosa cells of antral follicles. Transmission electron microscopy (TEM) was employed for ultrastructural characterization, oxidative stress was evaluated using thiobarbituric acid reactive substances (TBARS) assay to measure lipid peroxidation, and apoptosis was quantified via flow cytometry. By TEM, apoptosis was identified by the presence of an indented nuclear membrane with blebbing, pyknotic crescent-shaped fragmented nuclei, increased vacuolization, degenerating mitochondria, and lipid droplets. The results indicate a significant increase in malondialdehyde (MDA) level (nmols/g wet tissue) at a 100 nM dose of malathion i.e. 7.57±0.033*, 8.53±0.12*, and 12.87±0.78** at 4, 6, or 8 h, respectively, as compared with controls (6.07±0.033, p<0.01*, p<0.05**) showing a positive correlation between malathion-induced lipid peroxidation and percentage of granulosa cell apoptosis (r=1; p<0.01). The parallel use of these three methods enabled us to determine the role of malathion in inducing apoptosis as a consequence of cytogenetic damage and oxidative stress generated in granulosa cells of antral follicles.

—Organophosphorus-derived pesticides are commonly used to control Culex quinquefasciatus, the principal vector of filariasis in India. This paper reports on the susceptibility of C. quinquefasciatus from Madurai city, Tamil Nadu and its environs, to the organophosphate Malathion. It was observed that both larval and adult mosquitoes had low levels of resistance to the pesticide, with resistance ratios at LC50, LC90, and LC95 varying from 0.94 to 3.07 in larvae, and 0.93 to 34.68 in adults. This observation indicates the possibility of higher resistance developing in C. quinquefasciatus populations, the limitation of organophosphorus compounds as larvicides in mosquito breeding sites as a measure to control filariasis, and the importance of research into alternative measures for managing C. quinquefasciatus.