Shahid Bahonar University of Kerman and Iranian Biotechnology Society Agricultural Biotechnology Journal 2228-6705 17 3 2025 08 23 The Histopathological and Immunohistochemical Effects of Lead Chloride on the cerebrum of Japanese Quail (Coturnix coturnix japonica) The Histopathological and Immunohistochemical Effects of Lead Chloride on the cerebrum of Japanese Quail (Coturnix coturnix japonica) 253 272 5007 10.22103/jab.2025.25556.1731 FA Maha I. Mohammed Department of Biology, College of Education for Pure Science, Mosul University, Mosul, Iraq 0009-0008-3928-8319 Ameer M. Taha Department of Biology, College of Education for Pure Science, Mosul University, Mosul, Iraq 0000-0003-0306-7545 Journal Article 2025 07 14 Objective<br />Lead toxicity is a major environmental health concern with well-documented neurotoxic effects across vertebrate species. The Japanese quail (Coturnix coturnix japonica) is a valuable avian model for studying heavy metal toxicity due to its sensitivity to environmental contaminants and relevance to wildlife and poultry health. This study investigates the histopathological effects of lead chloride (PbCl₂) on the quail cerebrum and evaluates immunohistochemical changes by measuring glial fibrillary acidic protein (GFAP) expression.<br /><br />Materials and methods<br />Thirty quails of both sexes were randomly divided into three groups of ten birds each. The control group received distilled water for 60 days. The first experimental group was administered PbCl₂ at 25 mg/kg body weight daily for 30 days, and the second experimental group received PbCl₂ at 50 mg/kg body weight daily for 30 days. Birds were euthanized at 15, 30, and 60 days from the start of the experiment for histopathological and immunohistochemical analysis.<br /><br />Results<br />Histological examination of the cerebrum revealed multiple lesions across all time points. Widespread congestion was observed in most cerebral cortex layers, particularly the inner pyramidal layer. Degeneration of glial and neuronal cells was noted in the outer granular layer, accompanied by glial cell clustering. Hypertrophy of pyramidal cells was observed in the outer pyramidal layer. Immunohistochemical analysis of GFAP expression in the first experimental group showed a strongly positive reaction (11-25 cells stained) at 15 days, a weakly positive reaction (1-3 cells stained) at 30 days, and a weakly positive reaction at 60 days. In the second experimental group, GFAP expression was very strongly positive (>25 cells stained) at 15 days, strongly positive (11-25 cells stained) at 30 days, and strongly positive at 60 days.<br /><br />Conclusions<br />Lead chloride exposure induces severe histopathological damage in the quail cerebrum, characterized by neuronal degeneration, glial activation, and inflammatory responses. Immunohistochemical and histopathological findings elucidate the cellular mechanisms of lead-induced neurotoxicity. These results enhance understanding of-heavy metal toxicity in avian species and support the use of Japanese quail as a sentinel species for environmental lead contamination studies. Objective<br />Lead toxicity is a major environmental health concern with well-documented neurotoxic effects across vertebrate species. The Japanese quail (Coturnix coturnix japonica) is a valuable avian model for studying heavy metal toxicity due to its sensitivity to environmental contaminants and relevance to wildlife and poultry health. This study investigates the histopathological effects of lead chloride (PbCl₂) on the quail cerebrum and evaluates immunohistochemical changes by measuring glial fibrillary acidic protein (GFAP) expression.<br /><br />Materials and methods<br />Thirty quails of both sexes were randomly divided into three groups of ten birds each. The control group received distilled water for 60 days. The first experimental group was administered PbCl₂ at 25 mg/kg body weight daily for 30 days, and the second experimental group received PbCl₂ at 50 mg/kg body weight daily for 30 days. Birds were euthanized at 15, 30, and 60 days from the start of the experiment for histopathological and immunohistochemical analysis.<br /><br />Results<br />Histological examination of the cerebrum revealed multiple lesions across all time points. Widespread congestion was observed in most cerebral cortex layers, particularly the inner pyramidal layer. Degeneration of glial and neuronal cells was noted in the outer granular layer, accompanied by glial cell clustering. Hypertrophy of pyramidal cells was observed in the outer pyramidal layer. Immunohistochemical analysis of GFAP expression in the first experimental group showed a strongly positive reaction (11-25 cells stained) at 15 days, a weakly positive reaction (1-3 cells stained) at 30 days, and a weakly positive reaction at 60 days. In the second experimental group, GFAP expression was very strongly positive (>25 cells stained) at 15 days, strongly positive (11-25 cells stained) at 30 days, and strongly positive at 60 days.<br /><br />Conclusions<br />Lead chloride exposure induces severe histopathological damage in the quail cerebrum, characterized by neuronal degeneration, glial activation, and inflammatory responses. Immunohistochemical and histopathological findings elucidate the cellular mechanisms of lead-induced neurotoxicity. These results enhance understanding of-heavy metal toxicity in avian species and support the use of Japanese quail as a sentinel species for environmental lead contamination studies. https://jab.uk.ac.ir/article_5007_351869bde8b9d6ad1e3090bd173f600d.pdf