Selenium alleviates cadmium-induced Golgi stress via HSPB7/GM130/CX-43 axis in the heart of sheep

Cadmium (Cd) is a hazardous pollutant and its widespread exposure causes subcellular damage leading to cardiotoxicity. Selenium (Se) possesses the capacity to antagonize Cd toxicity, alleviating the organ damage induced by Cd. However, the relationship between Se mitigation of Cd exposure-induced myocardial damage and the Golgi apparatus remains to be further elucidated. Thus, 48 sheep were divided into four groups and treated with 1 mg Cd kg^-1·BW or/and 0.34 mg Se kg^-1·BW for 50 days. Results showed that Cd exposure caused myocardial myogenic fiber breakage, widened Z-line blurred and swelled of the Golgi apparatus. Cd exposure downregulated the levels of MyoD, MyoG, MyHC, CX-43 and GM130, upregulated the levels of cTnT, FLNC, GOLPH2 and GOLPH3, as well as reduced the number of fluorescent co-localization sites between CX-43 and GM130. Besides, Cd has increased the levels of heat shock proteins (HSPs) and decreased the number of fluorescent colocalization points between HSPB7 and GM130. However, co-treatment with Se ameliorated the above factors alterations associated with Cd exposure. In summary, Se attenuated Cd-induced myocardial injury and Golgi stress in sheep via activation of the HSPB7/GM130/CX-43 axis.