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At least 109 records · Page 6Linked to original sources
PubMed2001

Ethylazinphos interaction with membrane lipid organization induces increase of proton permeability and impairment of mitochondrial bioenergetic functions.

Ethylazinphos increases the passive proton permeability of lipid bilayers reconstituted with dipalmitoylphosphatidylcholine (DPPC) and mitochondrial lipids. A sharp increase of proton permeability is detected at insecticide/lipid molar ratios identical to those inducing phase separation in the plane of DPPC bilayers, as revealed by differential scanning calorimetry (DSC). Ethylazinphos progressively depresses the transmembrane potential (DeltaPsi) of mitochondria supported by piruvate/malate, succinate, or ascorbate/TMPD. Additionally, a decreased depolarization induced by ADP depends on ethylazinphos concentration, reflecting a phosphorylation depression. This loss of phosphorylation is a consequence of a decreased DeltaPsi. A decreased respiratory control ratio is also observed, since ethylazinphos stimulates state 4 respiration and inhibits ADP-stimulated respiration (state 3). Ethylazinphos concentrations up to 100 nmol/mg mitochondrial protein increase the rate of state 4 together with a decrease in DeltaPsi, without significant perturbation of state 3 and carbonyl cyanide-p-trifluoromethoxyphenylhydrazone (FCCP)-uncoupled respiration. For increased insecticide concentrations, the state 3 and FCCP-uncoupled respiration are inhibited to approximately the same extent. The perturbations are more pronounced when the energization is supported by pyruvate/malate and less effective when succinate is used as substrate. The present data, in association with previous DSC studies, indicate that ethylazinphos, at concentrations up to 100 nmol/mg mitochondrial protein, interacts with the lipid bilayer of mitochondrial membrane, changing the lipid organization and increasing the proton permeability of the inner membrane. The increased proton permeability explains the decreased oxidative phosphorylation coupling. Resulting disturbed ATP synthesis may significantly underlie the mechanisms of ethylazinphos toxicity, since most of cell energy in eukaryotes is provided by mitochondria.

Animals↗
PubMed1995

Use of microcosm and fish toxicity data to select mesocosm treatment concentrations.

Data from Mixed Flask Culture (MFC) microcosms and fish single species toxicity tests were used to select treatment concentrations for littoral enclosure studies. Selected concentrations were evaluated by comparing the predicted responses to those observed in littoral enclosure studies with a pyrethroid pesticide, esfenvalerate (Lozano et al. 1989) and an organophosphate pesticide, azinphos-methyl (Knuth et al. 1992). Comparisons of the effects predicted by these laboratory studies and effects that occurred in the two littoral enclosure trials provided useful information on the accuracy associated with each prediction. Although the approach did not always predict the exact magnitude or breadth of response found in the littoral enclosures, response levels for each of the selected treatment concentrations were adequate to describe the dose-response relationship of the littoral ecosystem for the two pesticides. The evaluation suggests that selection of treatment concentrations for the two littoral enclosure studies could have been improved by using this approach.

Animals↗
PubMed1994

Comparative toxicity of azinphos-methyl to house mice, laboratory mice, deer mice, and gray-tailed voles.

A laboratory toxicity study on house mice and laboratory mice (Mus musculus), gray-tailed voles (Microtus canicaudus), and deer mice (Peromyscus maniculatus) was conducted as part of a comprehensive laboratory and field study to field validate laboratory-based risk assessment of pesticides. The single dose oral LD50 for the organophosphorus insecticide azinphos-methyl (Guthion) was 10, 11, 32, and 48 mg/kg body weight in wild house mice, laboratory mice, gray-tailed voles, and deer mice, respectively. Ten-day dietary LC50s were 277 ppm for laboratory mice, 297 ppm for gray-tailed voles, and 1,180 ppm for deer mice. All treated animals lost more weight, consumed less food, and had depressed brain cholinesterase (ChE) activity compared to controls. Five-day LC50s were significantly higher than 10-day LC50s for laboratory mice and deer mice. For all three species, animals that died during dietary LC50 tests had mean ChE activity of 50-55% while survivors had 56-70% of controls. The conclusions were that: (1) Laboratory mice were not representative of deer mice or gray-tailed voles with respect to sensitivity to azinphos-methyl, but provided a conservative estimate for risk assessment; (2) 10-day dietary LC50 tests indicate substantially greater estimates of toxicity of azinphos-methyl to rodents than do 5-day tests; and (3) brain ChE depression of 45-50% was lethal in these species.

Animals↗
PubMed1994

Toxicity of Guthion and Guthion 2S to Xenopus laevis embryos.

The development of Xenopus laevis (African clawed frog) embryos exposed to the pesticide Guthion (technical grade) and Guthion 2S (commercial formulation) was evaluated in modified Frog Embryo Teratogenesis Assay--Xenopus (FETAX) tests. The embryos were exposed to five or six increasing concentrations of pesticide in 10- and 100-ml exposure volumes of test solution for 96 h. Embryos exposed in 10-ml volumes of Guthion exhibited increased mortality, increased deformation, and decreased size as compared to those exposed in 100-ml volumes. LC50s for embryos exposed in the 10-ml Guthion tests ranged from 6.1 to 6.3 mg/L as compared to 10.6 to 11.9 mg/L for those in the 100-ml tests. The percentage of deformities at 3 mg/L Guthion in test survivors in 10-ml tests ranged from 73 to 89%, while in the 100-ml tests less than 2% were deformed at the same concentration. Mean control embryo lengths at test completion were 8.2 and 10.6 mm, respectively, for 10- and 100-ml tests. The LC50 for embryos in 100 ml Guthion 2S was 1.6 mg/L active ingredient, indicating a much greater toxicity of the commercial formulation. NOAEL (No Observed Adverse Effect Level) values for Guthion and Guthion 2S ranged from 0.48 to 7.96 mg/L, depending upon basis (length, deformity, mortality) and pesticide formulation, and were many times greater than the existing water quality criterion of 0.01 microgram/L.

Abnormalities, Drug-Induced↗
PubMed1980

Developmental toxicity of guthion in rats and mice.

The purpose of this study was to assess the effects of Guthion, a pesticide with anticholinesterase activity, on development in rats and mice. A preliminary toxicity study with Guthion indicated that a 35-day LD50 dose for virgin rats and a 10-day LD50 dose for virgin mice was between 4 and 8 mg/kg/day for both species. On the basis of these data, doses of 0, 1.25, 2.5, and 5.0 mg/kg/day were selected for the developmental study, which consisted of two phases. During the first phase, pregnant rats and mice were treated for 10 days starting on gestational day 6. The high dose affected maternal welfare only in rats. Guthion did not significantly increase in a dose-related manner any of the specific anomalies observed in either rats or mice. During the second phase, pregnant rats were treated from gestational day 6 to postpartum day 21. Dams in the high dose group were more sensitive to Guthion later in gestation with the result that deaths and signs of anticholinesterase toxicity increased during this time. Guthion also adversely affected maternal welfare in this group. As a result of Guthion toxicity, only one litter survived until weaning. The inability to dissociate toxicity in adult and developing animals suggests that Guthion has little primary effect on the development of rats or mice.

Abnormalities, Drug-Induced↗
PubMed1976

Subchronic inhalation toxicity of azinphos-methyl in rats.

Azinphos-methyl was evaluated for its subchronic inhalation toxicity. The exposure of rats to concentrations of 0.195, 1.24, and 4.72 mg/m3, respectively, for 12 weeks, 6 hrs daily, 5 times weekly, resulted in effects only in those animals which inhaled aerosols of the highest concentration. This group showed a significant depression of the cholinesterase activity in plasma and erythrocytes. The males of this group had a lower body weight gain. The results are in agreement with the established maximum allowable concentration of 0.2 mg/m3.

Aerosols↗
PubMed1975

Toxicity of paired mixtures of candidate forest insecticides to rainbow trout.

The toxicities of Zectran, Dylox, Volaton, Guthion, pyrethrum extract, and the synthetic pyrethroids SBP-1382, and RU-11679 were determined individually and in paired mixtures against rainbow trout. The carbamate Zectran was the least toxic, and the synthetic pyrethroids were the most toxic. Nine of the mixtures produced less than additive toxicity (antagonism), nine produced additive toxicity, and two produced greater than additive toxicity (synergism). None of the mixture toxicities deviated markedly from additive,and only two pairs of mixtures would pose a greater toxicological hazard to fish than the respective individual chemicals.

Animals↗