4.5 Article

Effect of Different Selenium Supplementation Levels on Oxidative Stress, Cytokines, and Immunotoxicity in Chicken Thymus

Journal

BIOLOGICAL TRACE ELEMENT RESEARCH
Volume 172, Issue 2, Pages 488-495

Publisher

SPRINGERNATURE
DOI: 10.1007/s12011-015-0598-7

Keywords

Chicken; Selenium; Cytokine; Oxidative stress; Immunotoxicity

Funding

  1. Southwest University of Science and Technology [15zx7121]
  2. Mianyang Science and Technology Project [14 N043]

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This study assessed the effects of different selenium (Se) supplementation levels on oxidative stress, cytokines, and immunotoxicity in chicken thymus. A total of 180 laying hens (1 day old; Mianyang, China) were randomly divided into 4 groups (n=45). The chickens were maintained either on a basic diet (control group) containing 0.2 mg/kg Se, a low-supplemented diet containing 5 mg/kg Se, a medium-supplemented diet containing 10 mg/kg Se, or a high-supplemented diet containing 15 mg/kg Se for 15, 30, and 45 days, respectively. Over the entire experimental period, serum and thymus samples were collected and used for the detection of the experimental index. The results indicated that the antioxidative enzyme activities and messenger RNA (mRNA) levels of antioxidative enzymes, IFN-gamma and IL-2 in the thymus, and the content of IFN-gamma and IL-2 in the serum of excessive-Se-treated chickens at all time points (except for the 5 mg/kg Se supplement group at 15 days) were significantly decreased (P<0.05) compared to the corresponding control groups. Interestingly, a significantly increase (P<0.05) in the content of IFN-gamma was observed in the serum and thymus in the 5 mg/kg Se supplement group at 15 and 30 days compared to the corresponding control groups. In histopathological examination, the thymus tissue from excessive-Se-treated chickens revealed different degrees of cortex drop, incrassation of the medulla, and degeneration of the reticular cells. These results suggested that the excessive Se could result in a decrease in immunity, an increase in oxidative damage, and a series of clinical pathology changes, such as cortex drop, incrassation of the medulla, and degeneration of the reticular cells.

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