Selenomethionine Attenuated H2O2-Induced Oxidative Stress and Apoptosis by Nrf2 in Chicken Liver Cells

Abstract

Earlier studies have shown that selenomethionine (SM) supplements in broiler breeders had higher deposition in eggs, further reduced the mortality of chicken embryos, and exerted a stronger antioxidant ability in offspring than sodium selenite (SS). Since previous studies also confirmed that Se deposition in eggs was positively correlated with maternal supplementation, this study aimed to directly investigate the antioxidant activities and underlying mechanisms of SS and SM on the chicken hepatocellular carcinoma cell line (LMH). The cytotoxicity results showed that the safe concentration of SM was up to 1000 ng/mL, while SS was 100 ng/mL. In Se treatments, both SS and SM significantly elevated mRNA stability and the protein synthesis rate of glutathione peroxidase (GPx) and thioredoxin reductase (TrxR), two Se-containing antioxidant enzymes. Furthermore, SM exerted protective effects in the H2O2-induced oxidant stress model by reducing free radicals (including ROS, MDA, and NO) and elevating the activities of antioxidative enzymes, which performed better than SS. Furthermore, the results showed that cotreatment with SM significantly induced apoptosis induced by H2O2 on elevating the content of Bcl-2 and decreasing caspase-3. Moreover, investigations of the mechanism revealed that SM might exert antioxidant effects on H2O2-induced LMHs by activating the Nrf2 pathway and enhancing the activities of major antioxidant selenoenzymes downstream. These findings provide evidence for the effectiveness of SM on ameliorating H2O2-induced oxidative impairment and suggest SM has the potential to be used in the prevention or adjuvant treatment of oxidative-related impairment in poultry feeds.

Biogenic Selenium Nanoparticles Synthesized with Alginate Oligosaccharides Alleviate Heat Stress-Induced Oxidative Damage to Organs in Broilers through Activating Nrf2-Mediated Anti-Oxidation and Anti-Ferroptosis Pathways

“…Cao et al [75] and Sahin et al [76] found that HS resulted in a decline in mRNA expression level of Nrf2, SOD, GST, HO-1, etc. Conversely, previous studies showed that selenomethionine supplements enhanced the level of T-AOC and the ability of T-SOD in H 2 O 2 -induced liver damage model [77]. Wan et al [78] verified that selenomethionine could improve the glutathione system to enhance the antioxidant capacity of liver.…”

Selenomethionine Alleviates Deoxynivalenol-Induced Oxidative Injury in Porcine Intestinal Epithelial Cells Independent of MAPK Pathway Regulation

“…Inorganic selenium, particularly sodium selenite, constitutes the primary source, while organic selenium is predominantly derived from yeast selenium, with its principal form being selenomethionine (SeMet) [ 11 ]. Compared with sodium selenite, SeMet exerts a range of important advantages, including less toxicity and higher bioavailability [ 12 ]. SeMet could replace methionine to incorporate into protein synthesis or can be directly converted into selenocysteine through the trans-sulfuration pathway [ 12 ].…”

“…Compared with sodium selenite, SeMet exerts a range of important advantages, including less toxicity and higher bioavailability [ 12 ]. SeMet could replace methionine to incorporate into protein synthesis or can be directly converted into selenocysteine through the trans-sulfuration pathway [ 12 ]. Indeed, it is reported that SeMet supplementation enhanced the antioxidant capacity, immunity, and selenium deposition in pigs when compared to sodium selenite [ 13 , 14 , 15 ].…”

Selenomethionine Supplementation Mitigates Liver Dysfunction, Oxidative Injury and Apoptosis through Enhancing Antioxidant Capacity and Inhibiting JNK MAPK Pathway in Piglets Fed Deoxynivalenol-Contaminated Diets

“…Importantly, Se-Met was reported to mitigate oxidative stress induced by DON in the small intestinal epithelium of C57BL/6 mice [16]. Most recently, Se-Met has been demonstrated to exert protective effects for mitigating oxidative stress in poultry through the Nrf2 pathway [17][18][19]. Xie et al (2023), using an in vitro model of chicken liver cells, demonstrated that Se-Met mitigated hepatic oxidative stress caused by hydrogen peroxide challenge [17].…”

“…Most recently, Se-Met has been demonstrated to exert protective effects for mitigating oxidative stress in poultry through the Nrf2 pathway [17][18][19]. Xie et al (2023), using an in vitro model of chicken liver cells, demonstrated that Se-Met mitigated hepatic oxidative stress caused by hydrogen peroxide challenge [17]. Li et al (2024) also found that Se-Met effectively decreased oxidative injury associated with Nrf2 pathway regulation of laying hens challenged with lipopolysaccharide [18].…”