Acute Toxic Effects of levamisole and Ivermectin in Mice

The study's objectives were to investigate the acute toxicity and related biochemical effects of levamisole and ivermectin in mice. The 24 h oral median lethal dose (LD50) of levamisole was determined by the up-and-down method and was 155.5 mg/ kg of body weight. The treated mice showed signs of acute poisoning represented by excessive grooming, lacrimation, piloerection, straub tail, tachycardia, bulged eyes, tremor, convulsion and finally death within 24 h of treatment. The approximate lethal dose (ALD) of levamisole was 368 mg/kg, and the mice showed signs of poisoning similar to the previous signs of poisoning within 24 h of treatment. The 24 h oral LD50 of ivermectin was 115.2 mg/kg and the mice showed acute signs of poisoning, represented by excessive grooming, lacrimation, closed eyelids, piloerection, tachycardia, rapid respiration, depression, flat body appearance, paralysis and finally death within 24 h of treatment, while the approximate lethal dose of ivermectin was 121 mg/kg and also with the presence of severe poisoning signs as mentioned before. Non-lethal toxic doses of levamisole at 100 and 150 mg/kg and ivermectin at 75 and 100 mg/kg led to significant blood biochemical changes after 24 h of treatment, represented by a significant increase in the activity of the enzymes alkaline phosphatase (ALP), lactate dehydrogenase (LDH), glutamate dehydrogenase (GDH), and a significantly increased total bilirubin concentration in the blood plasma of mice. These results proved the presence of acute toxicity and biochemical effects of both anthelmintics levamisole and ivermectin even though they have wide safety margins

Metoclopramide protection of diazinon-induced toxicosis in chickens

The efficacy of metoclopramide for preventing organophosphate insecticide-induced (diazinon) toxicosis was evaluated in 7~14 days old chicks. Injection of metoclopramide at 25 mg/kg, s.c. 15 min before diazinon increased the oral 24 h median lethal dose of the insecticide in the chicks by 80%. Metoclopramide alone inhibited the in vitro and in vivo plasma and whole brain cholinesterase activities of the chicks. Metoclopramide pretreatment at 100 mg/kg, s.c. reduced the extent of cholinesterase inhibition that was caused by diazinon (10 mg/kg, p.o.) in the plasma and whole brain by 24% and 7%, respectively. Diazinon at 10 mg/kg, p.o. produced signs of cholinergic toxicosis in the chicks, and these signs included salivation, lacrimation, gasping and convulsions within 2 h, and the 2-h and 24-h lethalities were 88 and 100%, respectively. Metoclopramide at the dose rates of 12.5, 25, 50, 100 and 200 mg/kg, s.c. given 15 min before diazinon (10 mg/kg, p.o.) variably decreased the occurrence of toxic manifestations in the chicks. The highest dose of metoclopramide (200 mg/kg, s.c.) reduced the 2-h and 24-h lethality of diazinon to 75% each and it reduced the overall toxicity score of diazinon by 32%. The data suggest that metoclopramide pretreatment only partially protected chicks against the acute toxicity of diazinon