Document Type : Research Paper
Authors
1
Assistant of the Department of Anesthesiology and Resuscitation, Сhildren's Anesthesiology and Resuscitation, Bukhara State Medical Institute, Bukhara, Uzbekistan
2
Docent, Head of the Department of Art Science, Karakalpak State University, Named after Berdak, Nukus, Republic of Karakalpakstan
3
Kimyo International University in Tashkent Shota Rustaveli Street 156, 100121, Тashkent, Uzbekistan
4
Assistant, Navoi State University of Mining and Technologies, Navoi, Uzbekistan
5
DSc, Professor of the Department of Pediatrics and Neonatology Faculty of Postgraduate Education of the Samarkand State Medical University, Samarkand, Uzbekistan
6
Associate professor, Tashkent State Technical University, Uzbekistan
7
Senior Teacher, Department of Pharmaceuticals and Chemistry, Faculty of Medicine, Alfraganus University, Tashkent, Uzbekistan
8
Assistant, Department of Engineering Graphics and Design Theory, Tashkent Institute of Irrigation and Agricultural Mechanization Engineers, National Research University, Tashkent, Uzbekistan
9
Associate Professor, Jizzakh State Pedagogical University, Jizzakh, Uzbekistan
10
Candidate of Medical Sciences, Associate Professor, Gulistan State University, Gulistan, Uzbekistan
10.22124/cjes.2025.8650
Abstract
Chlorpyrifos (CPF) is identified as a hepatotoxic agent that detrimentally influences various organ systems. This research examined Hesperidin's impacts and underlying mechanisms on the deterioration of liver and renal tissue function resulting from CPF exposure. A total of fifteen C57 mice were separated into three experimental groups: CPF, Control, and CPF+Hesperidin. The evaluation of serum SOD activity, alongside assessments of hepatic and renal function, was performed through enzyme level quantification and histopathological analysis. Post-CPF treatment, hepatic injury was marked by localized foci of coagulative necrosis, infiltration of inflammatory cells, and regenerative fibrosis. Conversely, the prescription of Hesperidin caused a noticeable decrease in the inflammation. The protective effects of Hesperidin may, at least partially, be attributed to its antioxidant and anti-inflammatory characteristics. Notably, BUN, SGOT, SGPT, and ALP concentrations were considerably diminished in the treatment cohort compared to the CPF. These findings suggest that CPF contributes to the manifestation of renal and hepatic lesions and underscore the importance of enzyme analysis in elucidating hepatotoxicity, which can be influenced by Hesperidin.
Keywords
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