Ammonia is a major harmful gas in the environment of livestock and poultry. Studies have shown that excessive
ammonia inhalation has adverse effects in pig heart. However, the mechanism of
ammonia-induced
cardiac toxicity in pigs has not been reported. L-
selenomethionine is a kind of organic
selenium (Se) which is easily absorbed by the body. Therefore, in this study, twenty-four 125-day-old pigs were randomly divided into 4 groups: C (control) group, A (
ammonia) group, Se group (Se content: 0.5 mg kg-1), and A (
ammonia) + Se group. The mechanism of
ammonia-induced
cardiotoxicity and the alleviating effect of L-
selenomethionine were examined. The results in the A group showed as follows: a large number of myocardial fiber
edema and cytoplasmic bleakness were observed in the heart; a large number of mitochondrial autophagy were observed;
ATP content,
ATPase activities and hematological parameters decreased significantly; Endoplasmic reticulum stress (ERS) markers (
GRP78, IRE1α, ATF4, ATF6, and CHOP) were significantly induced in the
mRNA and
protein levels; PI3K/AKT/mTOR signaling pathway was activated; and autophagy key genes and
proteins (
Beclin-1, LC3, ATG3, and ATG5) were significantly up-regulated. The results of comparison between the A + Se group and the A group were as follows: the degree of
edema of cardiac muscle fiber in the A + Se group was somewhat relieved; the level of mitochondrial autophagy decreased;
ATP content and
ATPase activities increased significantly; the
mRNA and
protein levels of ERS markers were significantly down-regulated; the expression level of PI3K/AKT/mTOR signaling pathway was decreased; and the
mRNA and
protein levels of key autophagy genes were decreased. However, the changes of these indexes in the A + Se group were still significantly different from those in the C group. Our results indicated that L-
selenomethionine supplementation inhibited
ammonia-induced cardiac autophagy by activating the PI3K/AKT/mTOR signaling pathway, which confirmed that L-
selenomethionine could alleviate the cardiac injury caused by excessive
ammonia inhalation to a certain extent. This study aims to enrich the toxicological mechanism of
ammonia and provide valuable reference for future intervention of
ammonia toxicity.