Hydrogen sulfide (H2S), a common air pollutant and toxic gas, is detrimental to organisms and the environment. Exposure to highly concentrated H2S can induce oxidative stress and autophagy. However, the mechanism underlying the liver damage caused by H2S has not been identified. Lipopolysaccharide (LPS), the key component of endotoxin, can induce oxidative stress and autophagy. For this experiment, we used one-day-old chickens as model organisms to evaluate the effects of H2S combined with LPS on oxidative stress and autophagy. The four groups (control group, LPS group, H2S group and H2S-LPS group) were observed by electron microscopy, detected by oxidative stress kit, analyzed by quantitative real-time quantitative PCR, and analyzed by Western blot. We found that the activities of antioxidant enzymes (superoxide dismutase, antioxidant glutathione, catalase, and glutathione peroxidase) decreased in the H2S group compared to those in the control group; however, malondialdehyde levels in the H2S group increased. Molecular-level studies showed that the expression of genes associated with the PI3K/ AKT/ TOR pathways in the H2S group decreased, whereas the expression of other autophagy-related genes (Beclin1, ATG5 and the ratio of LC3-II/ LC3-I) increased compared to that in the control group. These findings suggest that H2S caused oxidative stress and induced autophagy through the PI3K/ AKT/ TOR pathway in chicken liver cells. Additionally, exposure to H2S aggravated LPS-induced oxidative stress and autophagy injury. Capsule: Aerial exposure to H2S can cause oxidative stress in chicken livers and induce autophagy through the PI3K/AKT/TOR pathway, and can aggravate LPS-induced oxidative stress and autophagy.

Selenium (Se) deficiency can seriously affect the small intestine of swine, and cause diarrhea in swine. However, the specific mechanism of Se deficiency-induced swine diarrhea has rarely been reported. Here, to explore the damage of Se deficiency on the calcium homeostasis and autophagy mechanism of swine, in vivo and in vitro models of swine intestinal Se deficiency were established. Twenty-four pure line castrated male Yorkshire pigs (45 d old, 12.50 ± 1.32 kg, 12 full-sibling pairs) were divided into 2 equal groups and fed Se-deficient diet (0.007 mg Se/kg) as the Se-deficiency group, or fed Se-adequate diet (0.3 mg Se/kg) as the control group for 16 weeks. The intestinal porcine enterocyte cell line (IPEC-J2) was divided into 2 groups, and cultured by Se-deficient medium as the Se-deficient group, or cultured by normal medium as the control group. Morphological observations showed that compared with the control group, intestinal cells in the Se-deficiency group were significantly damaged, and autophagosomes increased. Autophagy staining and cytoplasmic calcium staining results showed that in the Se-deficiency group, autophagy increased and calcium homeostasis was destroyed. According to the reactive oxygen species (ROS) staining results, the percentage of ROS in the Se-deficiency group was higher than that in the control group in the in vitro model. Compared with the control group, the protein and mRNA expressions of autophagy-calcium-related genes including Beclin 1, microtubule-associated proteins 1A (LC3-1), microtubule-associated proteins 1B (LC3-2), autophagy-related protein 5 (ATG5), autophagy-related protein 12 (ATG12), autophagy-related protein 16 (ATG16), mammalian target of rapamycin (mTOR), calmodulin-dependent protein kinase kinase β (CAMKK-β), adenosine 5′-monophosphate-activated protein kinase (AMPK), sarco(endo)plasmic reticulum Ca²⁺-ATPase (SERCA), and calpain in the Se-deficiency group were significantly increased which was consistent in vivo and in vitro (P < 0.05). Altogether, our results indicated that Se deficiency could destroy the calcium homeostasis of the swine small intestine to trigger cell autophagy and oxidative stress, which was helpful to explain the mechanism of Se deficiency-induced diarrhea in swine.

Zearalenone (ZEA) is the most common fungal toxin contaminating livestock and poultry feeding, especially in pigs, causing severe toxic effects and economic losses. However, the mechanism of ZEA damage to the intestine is unknown. We constructed an in vitro model of ZEA toxicity in a porcine small intestinal epithelial cell (IPEC-J2) line. ZEA causes severe oxidative stress in porcine small intestine cells, such as the production of ROS and a significant decrease in the levels of antioxidant enzymes GSH, CAT, SOD, and T-AOC. ZEA also caused apoptosis in porcine small intestine cells, resulting in a significant reduction in protein and/or mRNA expression of apoptosis-related pathway factors such as P53, caspase 3, caspase 9, Bax, and Cyt-c, which in turn caused a significant decrease in protein and/or mRNA expression of inflammatory-related factors such as IL-1β, IL-2, Cox-2, NF-κD, NLRP3, IL-6, and IL -18, which in turn caused a significant increase in protein and/or mRNA expression levels. The final results suggest that ZEA can cause a severe toxic response in porcine small intestine cells, with oxidative stress, apoptotic cell death and inflammatory damage.