Selenium Improves Bone Microenvironment-Related Hematopoiesis and Immunity in T-2 Toxin-Exposed Mice

Abstract

The T-2 toxin is one of the most frequent contaminants in the environment and agricultural production globally. It exerts a wide range of toxic effects. Selenium (Se), as an antioxidant, has the potential to be widely used to antagonize mycotoxin toxicity. To investigate the protective effects of Se on bone microenvironment (BM)-related hematopoiesis and immunity after T-2 toxin exposure, 36 male mice were treated with the T-2 toxin (1 mg/kg) and/or Se (0.2 mg/kg) by intragastric administration for 28 days. The results showed that Se alleviated T-2 toxin-induced cytopenia and splenic extramedullary hematopoiesis. Se also significantly relieved T-2 toxin-induced immunosuppression, as assessed by immune factors and lymphocytes. Furthermore, Se also attenuated oxidative stress and apoptosis and improved the BM in T-2 toxin-exposed mice. Therefore, Se improves BM-related hematopoiesis and immunity after T-2 toxin exposure. This study provides references for identifying the toxic mechanism and screening potential therapeutic drugs of the T-2 toxin.

Selenium supplementation effect of selenium-chelating peptide from sturgeon ( Acipenseridae ) heads and prevention of liver injury in selenium-deficient mice

“…In addition, the red and white pulp of the spleen in the normal control group appeared clear, displaying normal morphology with no structural abnormalities observed. 46 In contrast, sections of the spleen tissue from the model group revealed white pulp fusion, increased lymphocyte count, and irregular morphology, whereas those from the supplemented group presented no signicant structural abnormalities in the red or white pulp (Fig. 5D).…”

Selenium supplementation effect of selenium-chelating peptide from sturgeon ( Acipenseridae ) heads and prevention of liver injury in selenium-deficient mice

“…In addition, the red and white pulp of the spleen in the normal control group appeared clear, displaying normal morphology with no structural abnormalities observed. 46 In contrast, sections of the spleen tissue from the model group revealed white pulp fusion, increased lymphocyte count, and irregular morphology, whereas those from the supplemented group presented no signicant structural abnormalities in the red or white pulp (Fig. 5D).…”

Inhibition of Macrophage Pyroptosis─A New Therapeutic Strategy to Alleviate T-2 Toxin-Induced Subacute Liver Injury by Directly Competing with the Key Target

“…The results of a global survey (2008–2017) showed that the T-2 toxin detection rate in feed samples was about 19%, with a maximum concentration of 3051 μg/kg; T-2 toxin was also detected in drinking water and Chinese medicine samples . Moreover, T-2 toxin is stable in nature and difficult to completely remove from food and feed, which poses a serious threat to human and animal health . Also, T-2 toxin can cause liver DNA breakage, induce liver oxidative stress and apoptosis, ,, and induce the expression of liver inflammatory factors, leading to liver injury, which seriously endangers the health of animals and humans.…”

“…40 Moreover, T-2 toxin is stable in nature and difficult to completely remove from food and feed, which poses a serious threat to human and animal health. 41 Also, T-2 toxin can cause liver DNA breakage, 42 induce liver oxidative stress and apoptosis, 9,12,43 and induce the expression of liver inflammatory factors, leading to liver injury, 32 which seriously endangers the health of animals and humans. However, there is no effective antagonist to alleviate liver injury caused by T-2 toxin due to the lack of key targets and corresponding drugs for the liver injury.…”

Selenomethionine Antagonized microRNAs Involved in Apoptosis of Rat Articular Cartilage Induced by T-2 Toxin

“…Combined with the KEGG enrichment analysis results of the T-2 group vs. the control group, it was shown that the T-2 toxin could induce apoptosis, whereas SeMet indirectly antagonized apoptosis. Oxidative stress and apoptosis have been shown to occur in mice exposed to the T-2 toxin, and apoptosis was alleviated after treatment with Se [ 46 ]. Moreover, the apoptosis pathway was significantly enriched in the T-2 + SeMet group vs. the T-2 group, and the autophagy pathway appeared simultaneously.…”

Selenium supplementation effect of selenium-chelating peptide from sturgeon ( Acipenseridae ) heads and prevention of liver injury in selenium-deficient mice

“…In addition, the red and white pulp of the spleen in the normal control group appeared clear, displaying normal morphology with no structural abnormalities observed. 46 In contrast, sections of the spleen tissue from the model group revealed white pulp fusion, increased lymphocyte count, and irregular morphology, whereas those from the supplemented group presented no signicant structural abnormalities in the red or white pulp (Fig. 5D).…”

Inhibition of Macrophage Pyroptosis─A New Therapeutic Strategy to Alleviate T-2 Toxin-Induced Subacute Liver Injury by Directly Competing with the Key Target

“…The results of a global survey (2008–2017) showed that the T-2 toxin detection rate in feed samples was about 19%, with a maximum concentration of 3051 μg/kg; T-2 toxin was also detected in drinking water and Chinese medicine samples . Moreover, T-2 toxin is stable in nature and difficult to completely remove from food and feed, which poses a serious threat to human and animal health . Also, T-2 toxin can cause liver DNA breakage, induce liver oxidative stress and apoptosis, ,, and induce the expression of liver inflammatory factors, leading to liver injury, which seriously endangers the health of animals and humans.…”

“…40 Moreover, T-2 toxin is stable in nature and difficult to completely remove from food and feed, which poses a serious threat to human and animal health. 41 Also, T-2 toxin can cause liver DNA breakage, 42 induce liver oxidative stress and apoptosis, 9,12,43 and induce the expression of liver inflammatory factors, leading to liver injury, 32 which seriously endangers the health of animals and humans. However, there is no effective antagonist to alleviate liver injury caused by T-2 toxin due to the lack of key targets and corresponding drugs for the liver injury.…”

Selenomethionine Antagonized microRNAs Involved in Apoptosis of Rat Articular Cartilage Induced by T-2 Toxin

“…Combined with the KEGG enrichment analysis results of the T-2 group vs. the control group, it was shown that the T-2 toxin could induce apoptosis, whereas SeMet indirectly antagonized apoptosis. Oxidative stress and apoptosis have been shown to occur in mice exposed to the T-2 toxin, and apoptosis was alleviated after treatment with Se [ 46 ]. Moreover, the apoptosis pathway was significantly enriched in the T-2 + SeMet group vs. the T-2 group, and the autophagy pathway appeared simultaneously.…”

Selenium supplementation effect of selenium-chelating peptide from sturgeon ( Acipenseridae ) heads and prevention of liver injury in selenium-deficient mice

“…In addition, the red and white pulp of the spleen in the normal control group appeared clear, displaying normal morphology with no structural abnormalities observed. 46 In contrast, sections of the spleen tissue from the model group revealed white pulp fusion, increased lymphocyte count, and irregular morphology, whereas those from the supplemented group presented no signicant structural abnormalities in the red or white pulp (Fig. 5D).…”

Inhibition of Macrophage Pyroptosis─A New Therapeutic Strategy to Alleviate T-2 Toxin-Induced Subacute Liver Injury by Directly Competing with the Key Target

“…The results of a global survey (2008–2017) showed that the T-2 toxin detection rate in feed samples was about 19%, with a maximum concentration of 3051 μg/kg; T-2 toxin was also detected in drinking water and Chinese medicine samples . Moreover, T-2 toxin is stable in nature and difficult to completely remove from food and feed, which poses a serious threat to human and animal health . Also, T-2 toxin can cause liver DNA breakage, induce liver oxidative stress and apoptosis, ,, and induce the expression of liver inflammatory factors, leading to liver injury, which seriously endangers the health of animals and humans.…”

“…40 Moreover, T-2 toxin is stable in nature and difficult to completely remove from food and feed, which poses a serious threat to human and animal health. 41 Also, T-2 toxin can cause liver DNA breakage, 42 induce liver oxidative stress and apoptosis, 9,12,43 and induce the expression of liver inflammatory factors, leading to liver injury, 32 which seriously endangers the health of animals and humans. However, there is no effective antagonist to alleviate liver injury caused by T-2 toxin due to the lack of key targets and corresponding drugs for the liver injury.…”

Selenomethionine Antagonized microRNAs Involved in Apoptosis of Rat Articular Cartilage Induced by T-2 Toxin

“…Combined with the KEGG enrichment analysis results of the T-2 group vs. the control group, it was shown that the T-2 toxin could induce apoptosis, whereas SeMet indirectly antagonized apoptosis. Oxidative stress and apoptosis have been shown to occur in mice exposed to the T-2 toxin, and apoptosis was alleviated after treatment with Se [ 46 ]. Moreover, the apoptosis pathway was significantly enriched in the T-2 + SeMet group vs. the T-2 group, and the autophagy pathway appeared simultaneously.…”