Therapeutic mechanism of nano-selenium in hexavalent chromium poisoning in laying hens

Abstract

As a widely recognized environmental pollutant, Cr (VI) (hexavalent chromium) is a toxin that triggers carcinogenesis in poultry, particularly through oxidative damage. A new selenium variant, nanoselenium, has shown promise in mitigating heavy metal-induced toxicity. While most research on Cr (VI) toxicity has focused on broilers, the effects on laying hens remain underexplored. This study investigated the therapeutic potential of nanoselenium in alleviating Cr (VI)-induced toxicity in laying hens both in vivo and in vitro. Specifically, the mechanisms underlying chromium-induced cardiac damage and the protective effects of nanoselenium were examined. In vivo, exposure to Cr (VI) led to significant oxidative damage, autophagy, and apoptosis in myocardial cells, which was mediated by dysregulation of the RAS/RAF/MEK/ERK and PI3K/AKT/mTOR signaling pathways and manifested as changes in reactive oxygen species (ROS) and matrix metalloproteinase (MMP) levels. Nanoselenium treatment effectively counteracted these effects, restoring pathway balance and reducing oxidative damage and mitochondrial dysfunction. Similarly, in vitro, nanoselenium reduces oxidative damage, and Cr (VI) initiates apoptosis in cardiac myocytes. These findings revealed that nanoselenium antagonizes chromium-induced cardiac toxicity in laying hens.

Keywords

Apoptosis / Autophagy / Chicken heart / Cr (VI) / Nanoselenium / Oxidative stress / PI3 K/AKT and RAS/RAF signaling pathways

Funding

Project of Technological Innovation Program of Hubei Province(2024BBB111)

National Natural Science Foundation of China(31972748)

Fundamental Research Funds for the Central Universities(2662020DKPY013)

Key Technologies Research and Development Program(2016YFD0501208)

RIGHTS & PERMISSIONS

The Author(s)