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Background: Numerous epidemiological and experimental researches indicate that in utero exposure to some environmental chemicals and prescribed drugs during pregnancy can mediate various embryonic abnormalities and complications via reactive oxygen species (ROS) generation, which damages cellular macromolecules. Objectives: The aim of the present study was to evaluate the sulfonamide-associated nephrotoxicity with possible underlying mechanisms in chicken embryo. Materials and Methods: In this experimental study, one hundred fertile eggs were obtained and divided into five groups: 1) control group (without injection), 2) group injected with 2 mg sulfadiazine, 3) group injected with 10 mg sulfadiazine, 4) group injected with 30 mg sulfadiazine and 5) group injected with 70 mg sulfadiazine. After hatching, the renal tissue from the newly hatched chick was harvested for histopathologic investigation and also measurement of oxidative stress parameters [the ferric reducing capacity assay, the glutathione content (GSH) and the situation of lipid peroxidation (LPO)] by spectrophotometer. Results: Histologic examination of the renal tissue revealed that sulfadiazine induces hydropic degeneration, tubular necrosis, glomerular and tubular atrophy, formation of hyaline cast, congestion, hemorrhage, interstitial nephritis and fibrosis. Conclusions: Result showed the dose-dependent administration of sulfadiazine significantly altered the histopathologic structure of renal tissues of chickens. Furthermore, the major histopathologic events in the course of sulfadiazine cytotoxicity are renal tubule epithelial cell necrosis, interstitial nephritis and fibrosis, formation of hyaline cast and congestion and hemorrhage, although sulfadiazine at dose 30 mg and 70 mg caused perturbation in antioxidant defense system by marked increase in LPO, and decrease in GSH.

Histopathological Evaluation of Dose Dependent Sulfadiazine-Associated Nephrotoxicity and Alteration on Oxidative Stress in Chicken Embryos