Se is an essential trace element associated with animal growth and antioxidant and metabolic processes. However, whether Se, especially organic Se with higher bioavailability, can alleviate the adverse effects of low salinity stress on marine economic crustacean species has not been investigated. Accordingly, juvenile Pacific white shrimp (Litopenaeus vannamei) were reared in two culture conditions (low and standard salinity) fed diets supplemented with increasing levels of l-selenomethionine (0·41, 0·84 and 1·14 mg/kg Se) for 56 d, resulting in four treatments: 0·41 mg/kg under standard seawater (salinity 31) and 0·41, 0·84 and 1·14 mg/kg Se under low salinity (salinity 3). The diet containing 0·84 mg/kg Se significantly improved the survival and weight gain of shrimp under low salinity stress and enhanced the antioxidant capacity of the hepatopancreas. The increased numbers of B and R cells may be a passive change in hepatopancreas histology in the 1·14 mg/kg Se group. Transcriptomic analysis found that l-selenomethionine was involved in the regulatory pathways of energy metabolism, retinol metabolism and steroid hormones. In conclusion, dietary supplementation with 0·84 mg/kg Se (twice the recommended level) effectively alleviated the effects of low salinity stress on L. vannamei by regulating antioxidant capacity, hormone regulation and energy metabolism.

Ammonia has been reported to have a variety of toxicity to aquatic animals, farm animals and humans. However, its potential toxicity on the intestines remains unknown. L-selenomethionine is one of the important organic selenium sources. However, the mitigating effect of L-selenomethionine on ammonia exposure toxicity is still lacking. Therefore, in this study, the mechanism of toxic action of ammonia on intestinal tract and the detoxification effect of L-selenomethionine were examined. We evaluated the intestinal toxicity of ammonia and the alleviating effect of L-selenomethionine in an in vivo model, and then verified it in vitro model by a variety of cutting-edge experimental techniques. Our results showed that ammonia exposure causes oxidative stress, necroptosis, Th1/Th2 imbalance and inflammation in the intestinal tissue and the intestinal cells, and L-selenomethionine had a significant mitigation effect on the changes of these indexes induced by ammonia. In conclusion, ammonia exposure caused oxidative stress and Th1/Th2 imbalance in the porcine small intestine and IPEC-J2 cells, and that excessive ROS accumulation-mediated necroptosis targeted inflammatory responses, resulting in the destruction of tight connections of intestinal cells, thereby causing intestinal barrier dysfunction. L-selenomethionine could effectively reduce the intestinal injury caused by ammonia exposure and antagonize the toxic effect of ammonia.

Ammonia is a significant pollutant in the livestock houses and the atmospheric environment, and excessive ammonia would harm the health of livestock and breeders. Previous studies have shown that ammonia exposure could damage the tissue structure of the nervous system, but the molecular mechanism of ammonia-induced hypothalamus damage was still unclear. The purpose of this study was to determine the role of excessive ammonia in abnormal autophagy of pig hypothalamus and whether selenomethionine would have a mitigating effect on ammonia toxicity. Twenty-four 18-week pigs were randomly divided into four groups: the control group (C group), the selenium group (Se group), the ammonia + selenium group (A + Se group), and the ammonia group (A group). In our study, the expression levels of NF-κB, IL-1β, iNOS, TNF-α, IKK-α, p-IKK-α, Nrf2, ATG5, ATG 10, ATG 12, LC3 I/II, HSP60, HSP70, and HSP90 were increased after ammonia exposure; meanwhile, IFN-γ, IKB-α, p-IKB-α, Keap1, P62, mTOR, AKT, p-AKT, PI3K, SQSTM, and Beclin1 showed decreasing trends. The results indicated that excessive ammonia inhalation inhibited the AKT/mTOR pathway to acclerated autophagy through oxidative stress-mediated inflammation in the porcine hypothalamus. L-selenomethionine could alleviate hypothalamus injury induced by ammonia exposure.

Ammonia (NH3) is a common air pollutant, which poses a serious threat to farm animals. L-selenomethionine is organic selenium (Se), which can inhibit intracellular ROS generation, block ROS-dependent autophagy, promote mitochondrial energy metabolism, and enhance the body\'s immunity. Lung, as an important organ of the respiratory system, is highly susceptible to the toxic effects of NH3. However, there were few studies on the mechanism of toxic effects of NH3 on lung tissues. The aim of this study was to investigate the effect of NH3 on the lungs in pigs and the alleviating effect of L-selenomethionine. Twenty-four Large White*Duroc*Min pigs were randomly assigned to 4 groups: control group, NH3 group, Se group, and NH3 +Se group. The results showed that exposure to NH3 caused damage and inflammation in lung tissues and significantly increased blood NH3 concentration. NH3 induced changes of oxidative stress indexes (GSH, GSH-Px, SOD, MDA, Keap1, Nrf2, and HO-1) and expressions of energy metabolism related genes (HK1, HK2, PFK, PK, LDHA, and HIF-1α). Ultrastructure showed that mitochondrial damage and autophagosome increased significantly, and the expression levels of autophagy related genes (Beclin1, ATG5, ATG7, ATG10, and p62) changed. However, the addition of L-selenomethionine alleviated the above changes, but there was still a significant difference compared with the control group (P < 0.05). This finding can provide a new evidence for mitigation of NH3 toxicity.

Ammonia (NH3) is a hazardous substance to human and animal health. Selenium (Se) is an essential micronutrient with multiple health benefits. The present study aimed to verify whether and how Se supplementation has a protective role against NH3 mediated-nephrotoxicity in pigs. A Se-NH3 interaction model was established in pigs and the kidney samples were collected after a 30-day treatment period. The results showed that NH3 exposure inhibited the PI3K/AKT/mTOR pathway and enhanced the secretion of inflammatory cytokines to induce autophagy and inflammation. Se can regulate the PI3K/AKT/mTOR pathway and attenuate the secretion of inflammatory cytokines altered by NH3 to reduce autophagy and inflammation. In addition, Se co-treatment inhibited ROS production, elevated the activities of antioxidant systems, and increased the expression of 13 selenoproteins in pig kidneys caused by NH3 exposure. These results implied that L-selenomethionine can moderate NH3-induced nephrotoxicity in pigs. Our study gives new ideas for the specific mechanism of NH3 nephrotoxicity and provides a reference for comparative medicine and clinical medication.

Ammonia (NH3) is a harmful gas in livestock houses. So far, many researchers have demonstrated that NH3 is detrimental to animal and human organs. Selenium (Se) is one of the essential trace elements in the body and has a good antioxidant effect. However, there was little conclusive evidence that Se alleviated NH3 poisoning. To investigate the toxic mechanism of NH3 on pig spleen and the antagonistic effect of L-selenomethionine, a porcine NH3-poisoning model and an L-selenomethionine intervention model were established in this study. Our results showed that NH3 exposure increased the apoptosis rate, while L-selenomethionine supplementation alleviated the process of excessive apoptosis. Immunofluorescence staining, real-time quantitative polymerase chain reaction (qRT-PCR), and western blot results confirmed that exposure to NH3 changed the expression levels of interleukin family factors, apoptosis, death receptor, and oxidative stress factors. Our study further confirmed that excessive NH3 induced inflammatory response and mediated necroptosis leading to cell apoptosis by activating the Nrf2 signaling pathway. Excessive NH3 could mediate spleen injury through oxidative stress-induced mitochondrial dynamics disorder. L-Selenomethionine could alleviate inflammation and abnormal apoptosis by inhibiting the IL-17/TNF-α/FADD axis. Our study would pave the way for comparative medicine and environmental toxicology.

Selenium is an essential trace element for humans and other vertebrates, playing an important role in antioxidant defense, neurobiology and reproduction. However, the toxicity of excessive selenium has not been thoroughly evaluated, especially for the visual system of vertebrates. In this study, fertilized zebrafish embryos were treated with 0.5 µM L-selenomethionine to investigate how excessive selenium alters zebrafish eye development. Selenium-stressed zebrafish embryos showed microphthalmia and altered expression of genes required for retinal neurogenesis. Moreover, ectopic proliferation, disrupted mitochondrial morphology, elevated ROS-induced oxidative stress, apoptosis and ferroptosis were observed in selenium-stressed embryos. Two antioxidants-reduced glutathione (GSH) and N-acetylcysteine (NAC)-and the ferroptosis inhibitor ferrostatin (Fer-1) were unable to rescue selenium-induced eye defects, but the ferroptosis and apoptosis activator cisplatin (CDDP) was able to improve microphthalmia and the expression of retina-specific genes in selenium-stressed embryos. In summary, our results reveal that ferroptosis and apoptosis might play a key role in selenium-induced defects of embryonic eye development. The findings not only provide new insights into selenium-induced cellular damage and death, but also important implications for studying the association between excessive selenium and ocular diseases in the future.

L-Selenomethionine is one of the important organic selenium sources. The supplementation of L-selenomethionine in diets is significant to improve the health of pigs. Ammonia is a major pollutant in the atmosphere and piggery, posing a threat to human and animal health. Although ammonia exposure can damage the heart, the mechanism of cardiac toxicity by ammonia is still unknown. In this study, we investigated the mechanism of cardiac injury induced by ammonia exposure in pigs and the protective effect of L-selenomethionine on its cardiotoxicity. The results showed that the blood ammonia content of pig increased significantly in ammonia group, the expressions of energy metabolism-related genes (LDHA, PDK4, HK2, and CPTIB) and the oxidative stress indexes were significantly changed (P < 0.05), the AMPK/PPAR-γ/NF-κB signaling pathways were activated, the chromatin edge aggregation and nuclear pyknosis were observed in ultrastructure, the apoptotic cells were significantly increased (P < 0.05), and the mRNA and protein expressions of apoptosis-related genes (Bcl-2, Bax, Cyt-c, caspase-3, and caspase-9) were significantly affected (P < 0.05). The above changes were significantly alleviated in ammonia + L-selenomethionine group, but there were still significant differences compared with the C group (P < 0.05). Our results indicated that ammonia exposure could cause energy metabolism disorder and oxidative stress and induce apoptosis of cardiomyocytes through AMPK/PPAR-γ/NF-κB pathways, which could lead to cardiac injury and affect cardiac function. L-Selenomethionine could effectively alleviate the cardiac damage caused by ammonia and antagonize the cardiotoxicity of ammonia.

Ammonia (NH3) is a major pollutant in livestock houses and atmospheric environment. It has been demonstrated that NH3 can cause a series of damage to animals and human. However, toxicity evaluation of NH3 on farm animals was rarely reported, especially in the intestinal microflora. Therefore, in this study, twenty-four 125-day-old fattening pigs were randomly divided into 4 groups: control group, NH3 group (88.2 mg m-3 < NH3 concentration < 90.4 mg m-3), Se group (Se content: 0.5 mg kg-1), and NH3 + Se group (88.2 mg m-3 < NH3 concentration < 90.4 mg m-3, Se content: 0.5 mg kg-1), and the effects of NH3 and L-Selenomethionine on the microbiota composition in the jejunum and the levels of inflammatory markers in feces of fattening pigs were examined by 16S rDNA and ELISA, respectively. Our results showed that the content of Matrix metalloproteinase-9 (MMP-9), Myeloperoxidase (MPO), Lactoferrin (LTF) and Calprotectin in the ammonia group (A group) were significantly elevated compared to the control group, and the content of MMP-9, MPO, LTF and Calprotectin in the A + Se group were significantly reduced. A significant difference in microbiota composition in the phylum, class, family and genus levels was found in the A group and the NH3 + Se group. There was a negative correlation between Streptococcus and Calprotectin. Our results indicated that excessive NH3 inhalation could cause changes in inflammatory markers and beta diversity of intestinal microflora in fattening pigs. We found there was a positive correlation between MPO and Pseudomonas. In addition, we first proposed that L-Selenomethionine could improve the imbalance of microbial flora and the inflammatory injury caused by NH3. Changes in intestinal microflora and inflammatory markers can be used as important indicators to evaluate NH3 toxicity, and studying changes in intestinal microflora is also an important mechanism to reveal NH3 toxicity.

BACKGROUND: Studies in mammals proved dietary organic selenium (Se) being superior to inorganic Se regarding effects on growth performance, antioxidative status, immune response, and Se homeostasis. However, the picture of possible effects of different Se sources and - levels can be expanded. The present field study evaluated the effects on weight gain, hematological and selected biochemical variables as well as plasma concentrations of vitamin E (vitE), total Se and selenobiomolecules in piglets throughout the suckling period.
METHODS: Piglets were monitored from birth to 38 days of age (d). The mother sows\' diets were enriched with l-selenomethionine (SeMet-0.26 and -0.43 mg Se/kg feed) or sodium selenite (NaSe-0.40 and -0.60 mg Se/kg feed) from 1 month prior to farrowing until the end of lactation period. Piglets received pelleted feed supplemented with Se similarly to the sows\' diets from one week of age. Selenite at 0.40 mg Se/kg (NaSe-0.40) represents a common Se source and -level in pig feed and served as control diet.
RESULTS: From 24d, piglets in SeMet-groups had higher mean body weight (BW) compared with piglets from sows fed NaSe-0.40. Furthermore, from five-d and above, piglets from sows fed NaSe-0.60 had significantly higher BW than offspring from sows fed NaSe-0.40. Neonatal piglets in group SeMet-0.43 had significantly lower red blood cell counts (RBC), hemoglobin (Hgb) and hematocrit (Hct) concentrations compared with piglets from sows fed with NaSe-0.40. Neonatal and 5d-old piglets in group SeMet-0.26 showed higher gamma-glutamyl transferase activity than piglets in group NaSe-0.40. From five d and above, group NaSe-0.60 excelled with increased specific hematological variables culminating at age 38d with increased Hct, mean corpuscular volume (MCV), and MC hemoglobin (MCH) as well as increased activities of aspartate transaminase and lactate dehydrogenase compared with the other groups. Generally, offspring in the SeMet groups had higher total Se-concentrations in plasma than those from sows fed selenite, and showed a dose-response effect on plasma Se-concentrations. Furthermore, SeMet-fed piglets had higher plasma levels of the selenoproteins (Sel) glutathione peroxidase 3 (GPx3) and SelP as well as selenoalbumin. Plasma vitE levels were significantly negatively correlated with RBC throughout trial period.
CONCLUSIONS: Maternal supplementation with SeMet during gestation influenced hematology and clinical biochemistry in neonatal piglets in a different way than in offspring from sows receiving selenite enriched diets. Growth performance was positively influenced by both dietary Se source and Se level. Higher plasma levels of GPx3 observed in piglets receiving SeMet probably improved the protection against birth or growth related oxidative stress. These might prime the piglets for demanding situations as indicated by higher weight gain in offspring from sows fed with SeMet-supplemented diets. Our results on some enzyme activities might indicate that piglets fed NaSe-0.60 had to cope with increased levels of oxidative stress compared with those originating from sows fed SeMet or lower dietary levels of selenite. We assume that combining inorganic and organic Se sources in complete feed for breeding sows might be beneficial fro reproduction and the offspring\'s performance.