Oxidative impairment and histopathological alterations in kidney and brain of mice following subacute lambda-cyhalothrin exposure.

Autor: Pawar NN; 1 Division of Pharmacology and Toxicology, Indian Veterinary Research Institute, Izatnagar, India., Badgujar PC; 1 Division of Pharmacology and Toxicology, Indian Veterinary Research Institute, Izatnagar, India.; 2 Department of Food Science and Technology, Food Toxicology Section, National Institute of Food Technology Entrepreneurship and Management, Kundli, Sonipat, Haryana, India., Sharma LP; 1 Division of Pharmacology and Toxicology, Indian Veterinary Research Institute, Izatnagar, India., Telang AG; 3 Toxicology Laboratory, Centre for Animal Disease Research and Diagnosis, Indian Veterinary Research Institute, Izatnagar, India., Singh KP; 4 Pathology Laboratory, Centre for Animal Disease Research and Diagnosis, Indian Veterinary Research Institute, Izatnagar, India.
Jazyk: angličtina
Zdroj: Toxicology and industrial health [Toxicol Ind Health] 2017 Mar; Vol. 33 (3), pp. 277-286. Date of Electronic Publication: 2016 Jul 09.
DOI: 10.1177/0748233715627736
Abstrakt: Lambda cyhalothrin (LCT), a broad-spectrum type II (α-cyano) synthetic pyrethroid pesticide, is widely employed in various agricultural and animal husbandry practices for the control of pests. Acute and chronic exposure to LCT can elicit several adverse effects including oxidative stress. With the objective to investigate nephrotoxicity and neurotoxicity of LCT in mice, we evaluated oxidative stress parameters and histological changes in the kidney and brain of LCT exposed mice. Swiss albino mice were divided randomly into four groups ( n = 6 per group) as: (A) corn oil/vehicle control; (B) 0.5 mg/kg body weight (b.w.) LCT; (C) 1 mg/kg b.w. LCT; (D) 2 mg/kg b.w. LCT. Mice were treated orally for 28 days. LCT exposure significantly increased serum urea nitrogen, creatinine and urea levels. LCT exposure also increased lipid peroxidation, superoxide anion generation, nitrite level and decreased the level of reduced glutathione. The activities of superoxide dismutase, catalase and glutathione- S-transferase were depleted significantly in both kidney and brain. Histological examination revealed marked histopathological changes in the kidney and brain of mice that were more pronounced at high dose of LCT. Thus, results of the present study indicate that 28 days oral exposure of LCT causes oxidative damage to the kidney and brain of mice which in turn could be responsible for nephrotoxicity and neurotoxicity. Nevertheless, further detailed studies are required to prove these effects especially after long-term exposure.
Databáze: MEDLINE