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Abstract As one of the mucosal lymphatic tissues, the gill is an important immune organ in fish. Water environmental pollutants enter fish body through the gill. Therefore, the gill is the initial site where pollutants produce toxic effects in water. Chlorpyrifos (CPF), a broad-spectrum organophosphate insecticide, is widely used for agricultural pests and causes river pollution. In the present study, we investigated histopathological effect, oxidative stress indexes (SOD, GSH, T-AOC, and MDA), and apoptosis-related genes (P53, PUMA, Bax, Bcl-2, Apaf-1, Caspase-9, and Caspase-3) in the gills of common carp exposed to CPF. The results indicated that CPF exposure decreased SOD, T-AOC, and GSH; increased MDA; decreased Bcl-2 mRNA expression; and increased P53, PUMA, Bax, Apaf-1, Caspase-9, and Caspase-3 mRNA expressions in common carp gills. Our results proved that CPF exposure caused oxidative stress and apoptosis in common carp gills; CPF exposure destroyed the structural integrity and affected the immune function through oxidative stress and apoptosis in common carp gills. These will provide evidence for the toxic effects of water environmental pollutants on immune function and structural integrity in fish gills. Graphical abstract Image 1 Highlights • CPF caused oxidative stress in common carp gills. • CPF caused apoptosis via P53-mitochondria-Caspase-3 pathway in common carp gills. • Oxidative stress was involved in CPF-caused apoptosis in carp gills. • CPF destroyed structural integrity and affected immune function in carp gills. [ABSTRACT FROM AUTHOR]

Ammonia (NH 3) emission is a common threat to farm animals. Selenium (Se) is known for its antioxidant property and can resist several stressors affecting farm animals. The aims of this study were (Ⅰ) to determine how excess NH 3 exert nephrotoxic effects in pigs and (Ⅱ) to investigate whether selenomethionine has an alleviative effect on NH 3 toxicity. Two diets supplemented with different doses of Se (0.22 mg/kg or 0.50 mg/kg) and two concentrations of NH 3 (< 5 mg/m3 or 89.8 mg/m3) were used in a 2 × 2 factorial design trial for a period of 30 days. The results showed that NH 3 exposure caused apoptosis and increased the number of apoptotic cells in pig kidneys. Further, the activities of antioxidant enzymes were decreased, and the transcriptional and translational levels of endoplasmic reticulum stress-related genes, Bcl-2 and Caspase family members were increased under NH 3 exposure. In addition, Wnt/β-catenin signaling pathway was suppressed after NH 3 treatment. Dietary supplement with selenomethionine appears to offer protection against NH 3 -induced kidney injury in pigs and the pathologic changes above were alleviated. Our findings provide additional insight into the mechanism of NH 3 toxicity in pigs while elucidating the role of Se as a potential antidote against NH 3 poisoning. [Display omitted] • Excess NH 3 induced apoptosis in pig kidneys. • ER stress, Bcl-2 and Caspase family members participated in apoptosis. • Selenomethionine had an alleviative effect on NH 3 toxicity. • Antioxidant and Wnt/β-catenin pathway linked with detoxification effect of Se. [ABSTRACT FROM AUTHOR]

Ammonia (NH 3) is considered as environmental pollutant and toxic agent for animals and humans including poultry. Previous reports demonstrated that NH 3 suppressed broilers immunity. However, the harmful effects of NH 3 on broilers bursa of fabricius (BF) is still unknown. Functionally, apoptosis is very important for many physiological processes including homeostasis of lymphocyte population. Therefore, the present study was aimed to investigate the underlying mechanisms of NH 3 toxicity in the broilers BF. Histological observation showed lymphocyte accumulation, cavities and increased interstitial cells in BF. Ultrastructural observation indicated mitochondrial vacuoles, deformation and disappearance of mitochondrial membranes. Oxidative stress markers (CAT, MDA, H 2 O 2 , GGT, GSH-Px and GSH) showed that NH 3 -induced oxidative stress in BF. Meanwhile, Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay revealed increased apoptotic cells. In addition, the mRNA and protein expression of dynamin-related protein 1 (Drp1), mitochondrial fission factor (Mff), mitofusin 1 and 2 (Mfn1 and Mfn2), optic atrophy 1 (Opa1) indicated imbalance between mitochondrial inner and outer membrane and results in mitochondrial dysfunction in broilers BF. The mRNA and protein expression of apoptosis-related genes including Caspase-3, Caspase-9, Caspase-8, Cytochrome-C (Cyt-C), p53, B-cell lymphoma 2 (Bcl-2) and Bcl-2 associated X protein (Bax) were significantly altered in broilers BF. Conclusively, these results displayed that excessive NH 3 causes BF damage and mitochondrial dysfunction through oxidative stress and apoptosis in BF and could affect immune function of BF. These findings provide possible therapeutic targets to prevent NH 3 induced toxicity in the BF of broilers. • The effects of ammonia (NH 3)-induced toxicity in broilers BF were investigated. • NH 3 -induced abnormal morphological and ultrastructural changes in the BF of broilers. • NH 3 inhalation causes a significant increase in oxidative stress and induced apoptosis. • The study provide possible therapeutic targets to prevent NH 3 -induced immune toxicity. [ABSTRACT FROM AUTHOR]