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The main objective of the present study was to investigate the toxicity of orally administered organophosphorus dimethoate pesticide in Rattus norvegicus on the basis of biochemical alterations in the blood. There was a total of eight groups: two control groups and six treatment groups. Albino rats of the exposed groups were fed simple laboratory chow along with a low dose: five milliliters were given to the T1 group; the medium dose, ten milliliters, was given to the T2 group; and the high dose, twenty milliliters, was given to the T3 group of dimethoate pesticide for thirty, sixty, or ninety days under controlled laboratory conditions. At the end of the experiment, any weight gain, changes in the blood parameters, or biochemical changes were determined. The results revealed increases in the total glucose, aspartate aminotransferase, and alanine aminotransferase levels in the exposed groups of both genders of albino rats. There were decreases in the levels of urea, uric acid and total bilirubin in the exposed groups of both genders of albino rats. These effects did not vary between the sexes. This study provides a foundation for further research on the long-term effects of dimethoate and similar pesticides, promoting the development of safer alternatives.

The western corn rootworm ( Diabrotica virgifera virgifera LeConte) (WCR) is a major insect pest of corn ( Zea mays L.) in the United States (US) and is highly adaptable to multiple management tactics. A low level of WCR field-evolved resistance to pyrethroid insecticides has been confirmed in the US western Corn Belt by laboratory dose-response bioassays. Further investigation has identified detoxification enzymes as a potential part of the WCR resistance mechanism, which could affect the performance of insecticides that are structurally related to pyrethroids, such as organophosphates. Thus, the responses of pyrethroid-resistant and -susceptible WCR populations to the commonly used pyrethroid bifenthrin and organophosphate dimethoate were compared in active ingredient bioassays. Results revealed a relatively low level of WCR resistance to both active ingredients. Therefore, a simulated aerial application bioassay technique was developed to evaluate how the estimated resistance levels would affect performance of registered rates of formulated products. The simulated aerial application technique confirmed pyrethroid resistance to formulated rates of bifenthrin whereas formulated dimethoate provided optimal control. Results suggest that the relationship between levels of resistance observed in dose-response bioassays and actual efficacy of formulated product needs to be further explored to understand the practical implications of resistance.

Multiple environmental factors acting in concert can interact and strongly influence population fitness and ecosystem composition. Studies investigating interactions usually involve only two environmental factors; most frequently a chemical and another abiotic factor such as a stressful temperature. Here we investigate the effects of three environmental factors: temperature, an insecticide (dimethoate) and interspecific co-occurrence. We expose two naturally co-occurring species of Drosophila (D. hydei and D. melanogaster ) to the different environments during development and examine the consequences on several performance measures. Results are highly species and trait specific with evidence of two- and three-way interactions in approximately 30% of all cases, suggesting that additive effects of combined environmental factors are most common, and that interactions are not universal. To provide more informative descriptions of complex interactions we implemented re-conceptualised definitions of synergism and antagonism. We found approximately equal proportions of synergistic and antagonistic interactions in both species, however the effects of interactions on performance differed between the two. Furthermore, we found negative impacts on performance in only 60% of interactions, thus our study also reveals a high proportion of cases with positive effects of interactions.

This study presents the results of research concerning the effect of single and combined application of pyrantel tartrate and dimethoate on selected antioxidative enzymes: catalase (CAT), superoxide dismutase (SOD) and glutathione peroxidase (GPx), in rat erythrocytes. Pyrantel tartrate was applied twice, at a dose of 85 mg/kg bw at a two week interval, i.e. on day 14 and 28 of the experiment, orally, in a water solution with a stomach tube. Dimethoate was administered with drinking water for 28 days at a dose of 25 mg/kg bw/day. It was found that pyrantel tartrate caused only small changes in the activity of the antioxidative enzymes under analysis. Subchronic exposure of rats to dimethoate caused a significant increase in the activity of CAT, SOD and GPx in erythrocytes, indicating the existence of strong oxidative stress. In combined intoxication, no significant effects of administering pyrantel tartrate on the activity of CAT, SOD and GPx was found in animals poisoned with dimethoate. The profile of changes was similar to that observed in rats exposed only to the organophosphorus insecticide. This may indicate a lack of interaction between the compounds used in the experiment.

Two live-trapping field experiments were carried out to assess whether exposure to an organophosphate pesticide affects the frequency with which free-living rodents are captured. Both experiments involved dosing or sham-dosing animals with dimethoate and examining the subsequent recapture rates. Experimental treatment was an ip injection of 50 mg dimethoate/kg body weight. Results from the first experiment indicated no long-term effect of dimethoate on the trappability of wood mice. In the second experiment, the frequency at which voles were recaptured was not affected significantly by dimethoate treatment. Analysis of the time interval between treatment and first capture for both wood mice and bank voles did not indicate any effect of dimethoate.

Objective To observe the effects of neuregulin1β (NRG1β) on the level of phosphorylated ERK1/2 (p-ERK1/2), and explore the therapeutic mechanism of NRG1β on the cognitive dysfunction in rats with chronic omethoate poisoning. Methods Rats with strong learning and memory ability, 50 in total, were selected by Y-electric maze test. Among which, 15 rats were randomly selected into control group, and the rest 35 rats were used to establish experimental cognitive impairment models by being injected with omethoate subcutaneously. The 30 cases of successful cognitive impairment models were randomly divided into model group and treated group consisting of 15 rats, respectively. Then rats in treated group were injected with NRG1β into their lateral ventricles, while rats in control and model groups were given equal volume of PBS simultaneously. The cognitive capacity of rats was evaluated with Y-electric maze. The morphology and ultrastructure of hippocampus were observed by hematoxylin eosin (HE) staining and transmission electron microscopy (TEM) respectively. The expression of p-ERK1/2 was determined by immunohistochemical (IHC) staining and Western blotting. Results Compared with rats in model group, the cognitive ability of rats with omethoate exposed (model and treated groups) reduced significantly, along with the obvious damage of hippocampal neurons and the expression of p-ERK1/2 decreased significantly ( P  < 0.05). And after treatment with NRG1β, the cognitive activity of treated rats was improved obviously, and the injury of hippocampal neurons was milder and the expression of p-ERK1/2 increased significantly more than those in model rats ( P  < 0.05). Conclusion In chronic omethoate poisoning rats, NRG1β can promote the phosphorylation level of ERK1/2 in hippocampal neurons, and play an important role in the improvement of cognitive function.

The objective of this study was to investigate the response of acetylcholinesterase (AChE) activities in Clarias gariepinus in response to Organophosphates (Ops) and carbamate exposure. The AChE activities were determined in plasma, and eye and brain homogenates of unexposed and exposed fish using Ellman's method and 5,5′-dithiobis-2-nitrobenzoic acid (DTNB) chromophore. The baseline AChE activities in plasma, eyes and brain tissues in unexposed fish were comparable between males and females (P > 0.05). Concentrations of pesticides that inhibited 50% (IC₅₀) of AChE activities in brain homogenates following in vitro exposures were 0.003, 0.03, 0.15, 190, 0.2, 0.003 and 0.002 μM for carbaryl, chlorfenvinphos, diazinon, dimethoate, fenitrothion, pirimiphosmethyl and profenofos, respectively. The in vivo dose-effect relationships were assessed using chlorfenvinphos and carbaryl at different concentrations that ranged from 0.0003 to 0.06 μM and 0.0005 to 0.05 μM, respectively. Acetylcholinesterase activities were comparable in plasma, and eye and brain homogenates from control and carbaryl-exposed fish. Following exposure of fish to chlorfenvinphos at concentrations above 0.03 μM, a significant inhibition of AChE activities in plasma (84%) and eye homogenate (50%) was observed. The AChE activities in brain homogenate were comparable between chlorfenvinphos-exposed fish and controls. Because carbaryl cause reversible inhibition of AChE activities was found to be more potent than chlorfenvinphos that cause irreversible inhibition following in vitro exposure. Contrary, carbaryl was less potent than chlorfenvinphos after in vivo exposure possibly due to more rapid biotransformation of carbaryl than chlorfenvinphos. Findings from this study have demonstrated that inhibition of AChE activity in C. gariepinus is a useful biomarker in assessing aquatic environment contaminated by anticholinesterases.

Effects of combined exposure with dimethoate (DM), HgCl2(Hg),andNaAsO2 (As)wereinvestigatedfollowinga28-day oral exposure in male Wistar rats. In preliminary experiments, the LOEL (Lowest Observed Effect Level) and NOEL (Non Observed Effect Level) doses of the substances were determined using the same experimental system [determination of body weight gain, organ weights of brain, thymus, heart, lung, kidneys, adrenals, spleen, testicles, popliteal lymph node, white blood cell (WBC) and red blood cell (RBC) count, haematocrit (Ht), mean cell volume (MCV) of RBCs, cell content of the femoral bone marrow, IgM-plaque forming cell (PFC) content of the spleen, delayed type hypersensitivity (DTH) reaction] and animal strain. In the combination studies, LOEL dose of DM (28.2 mg/kg) was combinedwithNOELdosesoftheheavymetals(HgCl2 =0.40 mg/kg, NaAsO2 =3.33 mg/kg), and vice versa (DM=7.04 mg/kg, HgCl2 =3.20 mg/kg, NaAsO2 =13.3 mg/kg). In the DM–Hg combinations, significant alterations were found versus the corresponding high-dose internal control in the body weight gain, relative liver and kidney weights, and in the PFC response. When DM was combined with As, interactions were indicated by changes of relative liver weight, MCV value, and the PFC content of the spleen. These results support the theory that the interactions between pesticides and heavy metals may modify the toxic effects of the single substances, and may also change the functional detection limits of the exposure. The changes in the functional detection limits, if they occur, can lead to false-positive and false-negative results in human epidemiological studies.

Exposure to organophosphate (OP) pesticides can occur in free‐living mammals in treated areas. Risk to nontarget animals from OPs usually is assessed with acute exposure data, but exposure of wild animals is likely to be intermittent and chronic. We compared the effects of single or repeated (hourly and daily) exposure to dimethoate on acetylcholinesterase (AChE) activity in laboratory mice to assess the suitability of standard laboratory tests for assessing risk. Mice were exposed either to a single dose (10 or 30 mg/kg) or to short‐term repeated (three hourly doses of 10 mg/kg) intraperitoneal doses of dimethoate, and brain and serum AChE activity were measured. No significant difference was found in the degree of inhibition of AChE activity following acute and short‐term repeated exposure. In a second experiment, mice were given three daily doses of 10 or 20 mg/kg of dimethoate, and both AChE activity and hepatic cytochrome P450 enzyme activity were measured. Daily exposure resulted in a dose‐dependent decline in brain and serum AChE activity, and inhibition increased progressively with successively repeated exposures. However, this effect was relatively small compared to the effect of dose. Cytochrome P450 enzyme activity (CYP2B) was inhibited in the dimethoate‐dosed mice. Our results indicate that acute dose–response toxicity studies are suitable models for predicting the likely occurrence of adverse effects from either short‐ or longer‐term exposure of wild mammals to anticholinesterase compounds. Likely differences in exposure pattern between the laboratory and the natural environment are unlikely to bias the predictive power of these studies significantly.