Immuno-pathological effects of experimentally inducedsodium selenite toxicity in broiler chickens

This is the authors' abstract. We don't add key points for this paper.

Selenium is an essential micronutrient for poultry, but excess intake causes acute and chronic toxicities. The present study was conducted to determine acute oral lethal dose 50 (ALD₅₀) of sodium selenite in broiler chickens and the associated gross, histopathological, and immunological alterations. A total of 300 day-old broiler chicks were used. Acute oral toxicity was assessed in 140 chicks by graded dosing, and the oral ALD₅₀ of sodium selenite was calculated as 21 mg/kg body weight (equivalent to 9.59 mg Se/kg), confirming its high toxicity. Chronic exposure was studied by administering sodium selenite at 15 ppm and 30 ppm in drinking water. Birds receiving 30 ppm showed marked anorexia, emaciation, nervous signs, and high mortality, while 15 ppm caused reduced weight gain without mortality. Gross lesions included emaciation, muscular pallor, hepatic haemorrhages, renal congestion, and lymphoid organ atrophy. Histopathology revealed lymphoid depletion, follicular necrosis, and degeneration of reticuloendothelial cells in lymphoid tissues. Immunologically, selenium-fed groups showed significant suppression of cell-mediated immunity, as evidenced by reduced delayed-type hypersensitivity response to phytohaemagglutinin, and diminished humoral response, reflected by lower antibody titres against Newcastle disease vaccine. These findings established sodium selenite as a potent immuno-toxicant in broiler chickens, with a narrow margin between requirement and toxicity. The study highlighted the risks of excessive selenium exposure in poultry production systems, particularly in selenium-endemic areas, due to its immunosuppressive potential.