PSIV-B-22 - Comparative effects of nanoparticle-selenium, selenium-enriched yeast and sodium selenite antagonize cadmium-induced cardiotoxicity in chicken (Gallus gallus) via modulating AHR/CAR/PXR/Nrf2 pathways

Thursday, July 15, 2021

1:45 PM – 2:45 PM EST

Location: Kentucky International Convention Center, Poster Hall/North Lobby

Presenting Author(s)

Jing Ge

Graduate student
1Northeast Agricultural University, College of Veterinary Medicine, Harbin, China 2Department of Animal Science, Division of Agriculture, University of Arkansas, Fayetteville, AR 72701, United States
Fayetteville, Arkansas, United States

Author(s)

Yan Huang, PhD

Assistant Professor
University of Arkansas
Fayetteville, Arkansas, United States
JL

Jinlong Li

Northeast Agricultural University
Harbin, Heilongjiang, China (People's Republic)

Selenium (Se), a nutritionally essential mineral for human and animals, has a significant antagonistic effect on heavy metal cadmium (Cd) biotoxicity. Still, the impact of different Se source on alleviating Cd toxicity has received only limited attention. Therefore, the purpose of the current study was to assess the mitigation level of Cd-induced cardiotoxicity by different sources such as nanoparticles of selenium (Nano-Se), selenium-rich yeast (SY) and sodium selenite (SS). Two hundred of male, 1-day old Hy-Line Variety White chickens were randomly, equally divided into five groups (n = 25). These chicken groups were assigned to (1) basal diet (Con), (2) 140 mg/kg CdCl[2] of basal diet Cd (Cd), (3) 1 mg/kg Nano-Se plus 140 mg/kg CdCl[2] of basal diet (Nano-Se + Cd), (4) 3 mg/kg selenium-enriched yeast plus 140 mg/kg CdCl[2] of basal diet (SY + Cd group), and (5) 3 mg/kg sodium selenite plus 140 mg/kg CdCl[2] of basal diet (SS+ Cd group). The results evidenced that presence of Cd
led to a significant increase in biochemical parameters such as lactate dehydrogenase (LDH) and creatine kinase (CK), as well as histopathological lesions in the heart of chickens. Cd exposure also resulted in more extensive effects on phase I metabolism enzymes and transcript CYP isoforms, elevated the levels of MDA and H[2]O[2] and depressed total superoxide dismutase (T-SOD), Cu-Zn SOD, total antioxidant capacity (T-AOC) and catalase (CAT) activities. The expression of nuclear receptors (NRs), AHR, CAR and PXR was declined, down-regulated Nrf2 and its downstream targets in the Cd-treat group. Notably, Se sources application alleviated Cd toxicity by triggering AHR/CAR/PXR/Nrf2 signaling pathway to promote restoring antioxidant defense system and phase I metabolism enzymes system. However, when compared the effectiveness of antagonism, the Nano-Se was superior in relieving Cd-induced cardiotoxicity via AHR/CAR/PXR/Nrf2 pathway activation than other Se- sources.