Effect of selenium supplementation on aflatoxin B1-induced histopathological lesions and apoptosis in bursa of Fabricius in broilers

Chen, Kejie; Fang, Jing; Peng, Xi; Cui, Hengmin; Chen, Jin; Wang, Fengyuan; Chen, Zhengli; Zuo, Zhicai; Deng, Junliang; Lai, Weimin; Zhou, Yi

doi:10.1016/j.fct.2014.09.003

Cited by 59 publications

(47 citation statements)

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“…Even at low dietary concentrations, AFB1 can damage these immune tissues and suppress innate and adaptive immune responses [3,7,148]. AFB1 consumption during growth can lead to immune tissue atrophy, reducing relative weights of the bursa, spleen and thymus [120,122,134,139,[149][150][151][152]. Increases in relative spleen weight have also been observed during aflatoxicosis [117,120,[153][154][155][156].…”

Section: Immunotoxicitymentioning

confidence: 94%

“…In young chickens, tissue changes are concomitant to the development of histopathological lesions. AFB1 exposure causes visible congestion in the spleen and thymus, while nuclear debris accumulates in the thymus and bursa [139,149,150,156]. In AFB1-exposed chicks, vacuoles increase in the lymphoid follicles of the bursa and the white pulp of the spleen, especially the T-cell rich periarteriolar lymphoid sheaths [139,150,156].…”

Section: Immunotoxicitymentioning

confidence: 99%

“…This likely results from increased apoptosis of splenocytes, thymocytes and bursal B-cells as seen in young chickens during aflatoxicosis [139,149,156,169,170]. In the chicken, both CD4 + and CD8 + T lymphocytes in the spleen, thymus, peripheral blood, and even the ileum can be affected by AFB1 exposure [149,150,156,168,171,172].…”

Section: Immunotoxicitymentioning

confidence: 99%

“…AFB1 can induce circulating lymphocytopenia [34, 159,166,168] and cause lymphoid depletion in the bursa, spleen and thymus [34,134,139,149,150,159,166]. This likely results from increased apoptosis of splenocytes, thymocytes and bursal B-cells as seen in young chickens during aflatoxicosis [139,149,156,169,170].…”

Section: Immunotoxicitymentioning

confidence: 99%

“…In poultry, chronic AFB1 consumption is mutagenic and leads to remodeling of liver tissues. Hyperplasia of bile duct epithelial cells or oval cells develops first, followed by periportal fibrosis and nodular tissue regeneration [10,34,39,84,112,116,121,126,134,139].…”

Section: Hepatotoxicitymentioning

confidence: 99%

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Aflatoxicosis: Lessons from Toxicity and Responses to Aflatoxin B1 in Poultry

2015

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This review is a comprehensive introduction to the effects of poultry exposure to the toxic and carcinogenic mycotoxin aflatoxin B1 (AFB1). The relationship between AFB1 sensitivity and metabolism, major direct and indirect effects of AFB1, recent studies of gene expression and transcriptome responses to exposure, and mitigation strategies to reduce toxicity are discussed. Exposure to AFB1 primarily occurs by consumption of contaminated corn, grain or other feed components. Low levels of residual AFB1 in poultry feeds can cause reduction in growth, feed conversion, egg production, and compromised immune functions, resulting in significant economic costs to producers. Thus, AFB1 acts as a "force multiplier" synergizing the adverse effects of microbial pathogens and other agents, and factors detrimental to poultry health. Domestic turkeys (Meleagris gallopavo) are one of the most sensitive animals known to AFB1 due, in large part, to a combination of efficient hepatic bioactivation by cytochromes P450 1A5 and 3A37, and deficient hepatic glutathione-S-transferase (GST)-mediated detoxification. Because of their sensitivity, turkeys are a good model to investigate chemopreventive treatments and feed additives for their ability to reduce AFB1 toxicity. Transcriptome analysis (RNA-seq) of turkey poults (liver and spleen) has identified AFB1-induced gene expression changes in pathways of apoptosis, carcinogenesis, lipid regulation, antimicrobial activity, cytotoxicity and antigen presentation. Current research focuses on further identifying the molecular mechanisms OPEN ACCESSAgriculture 2015, 5 743 underlying AFB1 toxicity with the goal of reducing aflatoxicosis and improving poultry health.

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Section: Immunotoxicitymentioning

confidence: 94%

Section: Immunotoxicitymentioning

confidence: 99%

Section: Immunotoxicitymentioning

confidence: 99%

Section: Immunotoxicitymentioning

confidence: 99%

Section: Hepatotoxicitymentioning

confidence: 99%

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Aflatoxicosis: Lessons from Toxicity and Responses to Aflatoxin B1 in Poultry

2015

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Selenium mitigates methotrexate‐induced testicular injury: Insights from male NMRI mice model

Gholami,

Nemati,

Zarasvand

et al. 2024

Birth Defects Research

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Background and AimChemotherapy, particularly with methotrexate (MTX), often elicits testicular toxicity, leading to impaired spermatogenesis and hormone imbalances. This study aimed to investigate the potential protective effects of selenium (Se) against MTX‐induced testicular injury.Materials and MethodsMale mice were divided into control, MTX, Se, and MTX + Se groups. Histopathological examination involved the preparation of testicular tissue sections using the Johnsen's tubular biopsy score (JTBS) for spermatogenesis evaluation. Biochemical tests included the assessment of testosterone, malondialdehyde (MDA), luteinizing hormone (LH), and follicle‐stimulating hormone (FSH) levels. Real‐time quantitative polymerase chain reaction (RT‐qPCR) was employed to analyze the expression of caspase 3 (casp3), tumor protein 53 (p53), B‐cell lymphoma 2 (Bcl2), and Bcl2‐associated X protein (Bax) genes. Statistical analysis was performed using ANOVA and Tukey's tests (p < .05).ResultsHistopathological analysis revealed significant testicular damage in the MTX group, with decreased spermatogenesis and Leydig cell count, while Se administration mitigated these effects, preserving the structural integrity of the reproductive epithelium. Biochemical analysis demonstrated that MTX led to elevated malondialdehyde (MDA) levels and reduced testosterone, LH, and FSH levels, suggesting oxidative stress and Leydig cell dysfunction. Gene expression analysis indicated that MTX upregulated proapoptotic genes (casp3, p53, and bax) while downregulating the antiapoptotic Bcl2 gene. In contrast, Se treatment reversed these trends, highlighting its potential antiapoptotic properties.ConclusionOur findings underscore the potential of Se as a therapeutic agent to mitigate the reproductive toxicity associated with MTX‐induced testicular injury. Se exerts protective effects by regulating oxidative stress, preserving hormone balance, and modulating apoptotic pathways. These results suggest that Se supplementation could be a promising strategy to alleviate chemotherapy‐induced testicular damage and preserve male fertility.

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Selenium nanoparticles are more efficient than sodium selenite in reducing the toxicity of aflatoxin B₁ in Japanese quail

Khazraei

Tabeidian

Habibian

2021

Veterinary Medicine & Sci

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Background: Dietary selenium (Se), as an antioxidant element, plays a protective role in aflatoxin B 1 (AFB 1 ) toxicosis in poultry.Objectives: To compare the effects of sodium selenite (SS) and Se nanoparticles (SeNPs) against AFB 1 -induced toxicity on growth performance, carcass traits, immune response, antioxidant status and serum lipid concentrations in Japanese broiler quails.Methods: A total of 540 quails were divided into six treatments, each with six replicates and 15 birds per replicate at 24 days of age and reared for 21 days. Treatments included: (1) a basal diet without Se and AFB 1 (negative control; NC); (2) NC + 1.0 mg/kg AFB 1 (positive control; PC); (3) PC + 0.2 mg/kg Se as SS; (4) PC + 0.5 mg/kg Se as SS; (5) PC + 0.2 mg/kg Se as SeNPs; and (6) PC + 0.5 mg/kg Se as SeNPs.Results: Treatment with PC diet decreased feed intake and body weight gain and increased feed conversion ratio than the NC diet. The PC diet also atrophied the lymphoid organs and depressed antibody responses against Newcastle disease and avian influenza viruses and sheep red blood cell. Moreover, quails treated with PC diet appeared to have lower serum glutathione peroxidase and thioredoxin reductase activities and disturbed serum lipids than those receiving the NC diet. Dietary Se attenuated these detrimental effects, but failed to completely eliminate them. Additionally, SeNPs performed better than SS in improving thioredoxin reductase activity and antibody titer against sheep red blood cell.Conclusions: Diet supplementation with SeNPs to provide 0.5 mg/kg of Se is recommended to reduce the AFB 1 toxicosis in broiler quails.

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Effect of selenium supplementation on aflatoxin B1-induced histopathological lesions and apoptosis in bursa of Fabricius in broilers

Cited by 59 publications

References 44 publications

Aflatoxicosis: Lessons from Toxicity and Responses to Aflatoxin B1 in Poultry

Aflatoxicosis: Lessons from Toxicity and Responses to Aflatoxin B1 in Poultry

Selenium mitigates methotrexate‐induced testicular injury: Insights from male NMRI mice model

Selenium nanoparticles are more efficient than sodium selenite in reducing the toxicity of aflatoxin B₁ in Japanese quail

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Effect of selenium supplementation on aflatoxin B1-induced histopathological lesions and apoptosis in bursa of Fabricius in broilers

Cited by 59 publications

References 44 publications

Aflatoxicosis: Lessons from Toxicity and Responses to Aflatoxin B1 in Poultry

Aflatoxicosis: Lessons from Toxicity and Responses to Aflatoxin B1 in Poultry

Selenium mitigates methotrexate‐induced testicular injury: Insights from male NMRI mice model

Selenium nanoparticles are more efficient than sodium selenite in reducing the toxicity of aflatoxin B1 in Japanese quail

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Selenium nanoparticles are more efficient than sodium selenite in reducing the toxicity of aflatoxin B₁ in Japanese quail