Selenium regulates Nrf2 signaling to prevent hepatotoxicity induced by hexavalent chromium in broilers

Wang, Jingqiu; Liu, Ci; Zhao, Yanbing; Wang, Jinglu; Li, Jianhui; Zheng, Minggang

doi:10.1016/j.psj.2022.102335

Cited by 5 publications

(3 citation statements)

References 58 publications

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“…Moreover, compared with the DON + 0.3 mg/kg Se group, piglets in the DON + 0.5 mg/kg Se group had up-regulated relative mRNA levels of Nrf2 , Gclm , SOD1 , and GPX1 in the livers. These findings are consistent with a study demonstrating that Se supplementation activated the Nrf2 signaling pathway to attenuate hepatotoxicity induced by hexavalent chromium [ 44 ]. Given these findings, the improved antioxidant capacity with 0.5 mg/kg Se supplementation can be attributed to the regulation of the hepatic Nrf2/Keap1 and its downstream antioxidant genes in piglets that were fed diets contaminated with DON.…”

Section: Discussionsupporting

confidence: 93%

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

Zhong,

Huang,

et al. 2024

Antioxidants

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This research evaluated the impacts of selenomethionine (Se-Met) on hepatic functions, oxidative stress, mitochondrial function, and apoptosis of piglets fed deoxynivalenol (DON)-contaminated diets. Twenty-four piglets were allocated four dietary treatments (n = 6) in a 28-day feeding trial. The four treatments included the control group, which received 0.3 mg/kg of Se (as Se-Met) without DON treatment, and the DON treatment groups received 0, 0.3, or 0.5 mg/kg Se as Se-Met. A dietary addition of 0.5 mg/kg Se improved liver pathology and reduced serum aspartate aminotransferase and lactate dehydrogenase levels in piglets fed DON-contaminated diets. Furthermore, 0.5 mg/kg Se mitigated the oxidative stress and apoptosis of piglets fed DON-contaminated diets, as indicated by the decreased reactive oxygen species level, and the down-regulated mRNA levels of NRF-1, Bax, and CASP9 in the liver. Importantly, 0.5 mg/kg Se enhanced the hepatic antioxidant capacity, as evidenced by increased hepatic total antioxidant capacity, catalase, glutathione peroxidase, and total superoxide dismutase activities, as well as the up-regulated mRNA levels of Nrf2, Gclm, NQO1, SOD1, and GPX1 in the liver. Moreover, 0.5 mg/kg Se down-regulated the p-JNK protein level in the liver of piglets fed DON-contaminated diets. Collectively, Se-Met supplementation mitigated liver dysfunction, oxidative injury, and apoptosis through enhancing antioxidant capacity and inhibiting the JNK MAPK pathway in piglets fed DON-contaminated diets.

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Section: Discussionsupporting

confidence: 93%

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

Zhong,

Huang,

et al. 2024

Antioxidants

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“…Zhao et al reported that 0.3 mg/mL Se-enriched soy protein effectively protected H 2 O 2 -exposed Caco-2 cells from oxidative stress by activating the Nrf2 pathway and elevating the activities of GPx and SOD [ 60 ]. Additionally, 0.3 mg/kg SY supplement in broiler diets was found to alleviate liver damage-stimulated oxidative stress by activating the Nrf2 pathway and downstream GPx and quinone oxidoreductase 1 (NQO1) [ 61 ]. Furthermore, 0.1 μM biogenic nano-selenium also effectively activated the Nrf2 pathway and elevated GPx activity in porcine jejunum epithelial cells [ 62 ].…”

Section: Resultsmentioning

confidence: 99%

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

Xie,

Xu,

Ding

et al. 2023

Antioxidants

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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.

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“…Given the importance of these results in clinical applications, the role of sodium selenite in the maintenance of rBM-MSCs stemness potential is highlighted. On the one hand, overexpression of Nrf2 not only improves the antioxidant capacity [ 103 ] and survival rate of rBM-MSCs but could also regulate the stemness potential. Nevertheless, to date, no studies confirmed the association between Nrf2 and MSCs stemness potential or the interaction between Nrf2 and the expression of stemness genes [ 97 ].…”

Section: Discussionmentioning

confidence: 99%

Sodium selenite preserves rBM-MSCs’ stemness, differentiation potential, and immunophenotype and protects them against oxidative stress via activation of the Nrf2 signaling pathway

Rahimi

Panahi

Lotfi

et al. 2023

BMC Complement Med Ther

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Background The physiological level of reactive oxygen species (ROS) is necessary for many cellular functions. However, during the in-vitro manipulations, cells face a high level of ROS, leading to reduced cell quality. Preventing this abnormal ROS level is a challenging task. Hence, here we evaluated the effect of sodium selenite supplementation on the antioxidant potential, stemness capacity, and differentiation of rat-derived Bone Marrow MSCs (rBM-MSCs) and planned to check our hypothesis on the molecular pathways and networks linked to sodium selenite’s antioxidant properties. Methods MTT assay was used to assess the rBM-MSCs cells’ viability following sodium selenite supplementation (concentrations of: 0.001, 0.01, 0.1, 1, 10 µM). The expression level of OCT-4, NANOG, and SIRT1 was explored using qPCR. The adipocyte differentiation capacity of MSCs was checked after Sodium Selenite treatment. The DCFH-DA assay was used to determine intracellular ROS levels. Sodium selenite-related expression of HIF-1α, GPX, SOD, TrxR, p-AKT, Nrf2, and p38 markers was determined using western blot. Significant findings were investigated by the String tool to picture the probable molecular network. Results Media supplemented with 0.1 µM sodium selenite helped to preserve rBM-MSCs multipotency and keep their surface markers presentation; this also reduced the ROS level and improved the rBM-MSCs’ antioxidant and stemness capacity. We observed enhanced viability and reduced senescence for rBM-MSCs. Moreover, sodium selenite helped in rBM-MSCs cytoprotection by regulating the expression of HIF-1 of AKT, Nrf2, SOD, GPX, and TrxR markers. Conclusions We showed that sodium selenite could help protect MSCs during in-vitro manipulations, probably via the Nrf2 pathway.

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Selenium regulates Nrf2 signaling to prevent hepatotoxicity induced by hexavalent chromium in broilers

Cited by 5 publications

References 58 publications

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

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

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

Sodium selenite preserves rBM-MSCs’ stemness, differentiation potential, and immunophenotype and protects them against oxidative stress via activation of the Nrf2 signaling pathway

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