Veterinary medicine and science · 2026
Effects of Deltamethrin and Endosulfan on the Hepatic Markers and Neurobehavioural Alterations in Japanese Quail (Coturnix japonica).
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Malik Saba, Ahmad Shoaib, Naeem Muhammad, Bibi Iqra, Majid Muhammad Sakandar, Sadia Hafiza, Riaz Sheeba, Siddik Md Abu Bakkar
Аннотация
BACKGROUND: Deltamethrin (DLM), a synthetic pyrethroid, and endosulfan, an organochlorine pesticide, frequently co-occur in agricultural environments, yet their combined effects on hepatic function and behaviour in non-target avian species remain poorly understood.
OBJECTIVES: This study examined the toxic effects of combined DLM and endosulfan exposure on hepatic markers, lipid profile and neurobehaviour in Japanese quail (Coturnix japonica).
METHODS: Twelve adult quails were divided into three groups receiving: (1) control, (2) low-dose (0.1 mg/kg DLM + 0.15 mg/kg endosulfan) or (3) high-dose (0.4 mg/kg DLM + 0.5 mg/kg endosulfan) via daily oral gavage for 3 weeks. Body and organ weights, serum hepatic and lipid biomarkers and behavioural parameters were assessed.
RESULTS: The high-dose group showed a significant reduction in body weight compared with controls, while liver weight remained stable and kidney weights decreased in a dose-dependent manner. AST (aspartate aminotransferase) and ALP (alkaline phosphatase) were substantially increased in treated groups (p < 0.05), indicating hepatocellular damage. Lipid profiles showed significant elevations in LDL, VLDL and cholesterol (p < 0.05). Behavioural assessments demonstrated dose-dependent effects, including increased agonistic behaviour, reduced locomotor activity and dose-dependent onset of mucoid faeces (first recorded in Week 1 in the high-dose group and Week 2 in the low-dose group, with none observed in controls); foraging behaviour declined sharply in high-dose birds by Week 3.
CONCLUSIONS: Combined pesticide exposure induces measurable hepatotoxicity, metabolic disruption and neurobehavioural abnormalities in quail at the tested doses. These effects are consistent with DLM-mediated activation of Na+ channels and endosulfan-induced blockade of GABA_A receptors.
OBJECTIVES: This study examined the toxic effects of combined DLM and endosulfan exposure on hepatic markers, lipid profile and neurobehaviour in Japanese quail (Coturnix japonica).
METHODS: Twelve adult quails were divided into three groups receiving: (1) control, (2) low-dose (0.1 mg/kg DLM + 0.15 mg/kg endosulfan) or (3) high-dose (0.4 mg/kg DLM + 0.5 mg/kg endosulfan) via daily oral gavage for 3 weeks. Body and organ weights, serum hepatic and lipid biomarkers and behavioural parameters were assessed.
RESULTS: The high-dose group showed a significant reduction in body weight compared with controls, while liver weight remained stable and kidney weights decreased in a dose-dependent manner. AST (aspartate aminotransferase) and ALP (alkaline phosphatase) were substantially increased in treated groups (p < 0.05), indicating hepatocellular damage. Lipid profiles showed significant elevations in LDL, VLDL and cholesterol (p < 0.05). Behavioural assessments demonstrated dose-dependent effects, including increased agonistic behaviour, reduced locomotor activity and dose-dependent onset of mucoid faeces (first recorded in Week 1 in the high-dose group and Week 2 in the low-dose group, with none observed in controls); foraging behaviour declined sharply in high-dose birds by Week 3.
CONCLUSIONS: Combined pesticide exposure induces measurable hepatotoxicity, metabolic disruption and neurobehavioural abnormalities in quail at the tested doses. These effects are consistent with DLM-mediated activation of Na+ channels and endosulfan-induced blockade of GABA_A receptors.