چکیده (انگلیسی):

Imidacloprid (IC) is a systemic insecticide related to the tobacco toxin nicotine. IC is a toxic
substance frequently used into combat insects, rodents and plants pests and other creatures
that can pose problems for agriculture. We, therefore, planned this study to assess risk
factors, biochemical and histological alterations associated with hepatotoxicity and nephrotoxicity.
Forty-eight adult male albino mice were divided into four groups of 12 animals
each. All the animals were given standard synthetic pellet diet. One group served as control,
and the other three were served as experimental groups. Decrease in the body weight of
the high dose group was observed at 15 mg/kg/day, and no mortality occurred during the
treatment period. High dose of imidacloprid caused a significant elevation of serum clinical
chemistry parameters, serum glutamic oxaloacetic transaminase (SGOT), serum glutamic
pyruvate kinase (SGPT), alkaline phosphatase (ALP) and total bilirubin (TBIL). Histology of
liver and kidney indicates hepatotoxicity and nephrotoxicity at a high dose of imidacloprid.
Based on the morphological, biochemical and histopathological analysis, it is evident
that imidacloprid induced toxicological effects at 15 mg/kg/day to mice. The results of the
present study demonstrate that IC had significant effects on body weight, liver functions
and kidney (p < 0.05) at a dose of 15 mg/kg body weight. IC treatment 5 and 10 mg/kg/day
may be considered as no observed adverse effect level (NOAEL) for mice. It was concluded
that IC can cause hepatotoxicity and nephrotoxicity at a dose much lower than the LD50
(131 mg/kg body weight) in mice.