The data suggest that the combination of metoclopramide and ketamine synergistically controls acute pain in mice. This combination could be used clinically for restraint and minor surgical interventions in mice.
The aim of the present study was to determine the acute toxicity of chlorpyrifos and deltamethrin in mice separately and to study their toxic and neurobehavioral effects. Median Lethal Doses (LD50) of chlorpyrifos and deltamethrin were determined depending on up and down method. The oral LD50 of chlorpyrifos was 193.05 mg/kg and of deltamethrin was 15.71 mg/kg in mice. The oral administration of chlorpyrifos 155 mg/kg and deltamethrin 12.56 mg/kg represent 80% of LD50 resulted in acute signs of poisoning that manifested by dyspnea, salivation and lacrimation at 100%, piloerection, straub tail, tremors, convulsions and death at 70% for chlorpyrifos and 60% for deltamethrin and writhing reflex at 20% for chlorpyrifos. Oral administration of chlorpyrifos 310 mg/kg and deltamethrin 24 mg/kg increased severity of toxicosis signs as a percentage of piloerection, straub tail, tremors, seizures and death 100%. As well as decrease the onset of tremors, convulsions and death, writhing reflex which appears at 20% for chlorpyrifos and 10% for deltamethrin. After three hours of chlorpyrifos and deltamethrin oral administration at doses represent 20% and 10% of LD50 there are significantly hypoactivation in open-field activity, significantly increased in the duration of negative geotaxis performance, significantly decreased in head pocking and swimming scores compared to control group. In conclusion we found that deltamethrin was more toxic than chlorpyrifos this is based on the LD50 value. However, the signs of toxicosis and neurobehavioral effects produced by both toxicants were not differential and could not be associated with the toxic level.
This study assessed in vitro inhibition of plasma and brain cholinesterases (ChE) by the organophosphate insecticides chlorpyrifos and dichlorvos in chicks at ages of 2, 10, 20 and 30 days. Plasma samples and whole-brain homogenates of each age group were pooled and ChE activity was determined by an electrometric method with or without the organophosphate (0.5 and 1.0 µM). ChE inhibitions were the highest in 2-and 10-day-old chicks (20-83%), followed by 5-73% inhibitions at ages of 20 and 30 days. Cholrpyrifos decreased plasma ChE activity only at the ages of 2 and 10 days by 21-75%. Dichlorvos decreased plasma ChE activity at all the ages tested (2-30 days) by 39-83%. The highest percentage of plasma ChE inhibition by chlorpyrifos and dichlorvos was in 2-day-old chicks. In the brain homogenate, chlorpyrifos decreased the ChE activity between ages 2 and 20 days by 20-62%. The highest percentage of brain ChE inhibition occurred at the age of 10 days and the least was at 20 and 30 days. Dichlorvos decreased brain ChE activity between ages 2 and 20 days by 24-74%. At the age of 30 days, only the higher concentration of dichlorvos (1 µM) decreased brain ChE activity by 27%. The data suggest an age-related differential in vitro inhibition of plasma and brain ChE s in chicks. In vitro ChE inhibition, though it does not exclude interfering factors, could be useful for initial screening of the inhibitory actions of organophosphate insecticides in chickens.
A modified electrometric cholinesterase method has been described for use in ruminants exposed to organophosphate insecticides. The method was used to measure cholinesterase activities in the plasma and erythrocytes of sheep, goats and cattle treated with organophosphate insecticides under field conditions. The animals were treated topically to control ectoparasites with malathion (0.05%) or diazinon (0.06%). The treated animals did not suffer from adverse effects related to cholinesterase inhibition. However, 2 h after treatments, plasma and erythrocyte cholinesterase activities significantly decreased in sheep by 20% and 39% and in goats by 18% and 30%, respectively, when compared with respective untreated control values. Diazinon did not significantly affect plasma and erythrocyte cholinesterase activities in the cattle. The results suggest that the described electrometric method could be efficiently used for detecting cholinesterase inhibition in ruminants exposed to organophosphate insecticides.
Sulfur is one of the most reactive chemical elements, The EPA (environmental protection agency) has labeled elemental sulfur as generally safe. This study sheds light on the ability of sulfur to cause toxic biochemical effects by measuring biochemical changes in many parameters. The activity of alanine aminotransferase (ALT) and aspartate aminotransferase(AST), Glutathione (GSH) and Malondialdehyde (MDA) and glucose in blood plasma, brain, and liver of mice. Mice were orally dosed with sulfur at doses of 4 and 8 kg b.wt. which significantly decreased blood sugar level, ALT, and AST activity at 8 g/kg .in blood plasma after 4 and 1 day. On the other hand, administration of sulfur at doses of 1 and 4 g/kg b.wt, after 7 and 14 days of repeated treatment with it led to a significant decrease in the level of GSH in blood plasma and liver of mice with a significant increase in the level of GSH in the brain, while the 3doses of sulfur caused a significant increase of MDA level in blood plasma, brain, and liver of treated mice. The results of our follow-up testing also showed the biochemical effects of sulfur on both ALT and AST enzymes; it showed a slight increase in the level of both enzymes in blood plasma and a significant decrease in the level of brain GSH after 24 hrs of treatment. In contrast, the level of brain GSH significantly increased after 14 days of sulfur dosing, with a significant increase in the activity of both enzymes(ALT, AST) which indicates the persistence of the toxic effect on the liver. We conclude from this study the possibility and ability of sulfur to cause toxic biochemical effects in mice.
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