Selenomethionine alleviates T-2 toxin-induced articular chondrocyte ferroptosis via the system Xc−/GSH/GPX4 axis
T-2 toxin can induce bone and cartilage development disorder, and oxidative stress plays an important role in it. It is well known that selenomethionine (Se-Met) has antioxidative stress properties and promotes the repair of cartilage lesion, but it remains unclear whether Se-Met can relieve damaged...
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Elsevier
2025-01-01
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| Series: | Ecotoxicology and Environmental Safety |
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| Online Access: | http://www.sciencedirect.com/science/article/pii/S0147651324016452 |
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| author | Fang-fang Yu Juan Zuo Miao Wang Shui-yuan Yu Kang-ting Luo Tong-tong Sha Qian Li Zai-chao Dong Guo-yu Zhou Feng Zhang Xiong Guo Yue Ba Yan-jie Wang |
| author_facet | Fang-fang Yu Juan Zuo Miao Wang Shui-yuan Yu Kang-ting Luo Tong-tong Sha Qian Li Zai-chao Dong Guo-yu Zhou Feng Zhang Xiong Guo Yue Ba Yan-jie Wang |
| author_sort | Fang-fang Yu |
| collection | DOAJ |
| description | T-2 toxin can induce bone and cartilage development disorder, and oxidative stress plays an important role in it. It is well known that selenomethionine (Se-Met) has antioxidative stress properties and promotes the repair of cartilage lesion, but it remains unclear whether Se-Met can relieve damaged cartilage exposure to T-2 toxin. Here, the oxidative stress and ferroptosis of chondrocytes exposure to T-2 toxin were observed. Mechanistically, T-2 toxin increased ROS, lipid ROS, MDA and Fe2+ contents in chondrocytes, decreased GSH and GPX4 activity, and inhibited the system Xc−/GSH/GPX4 antioxidant axis. In addition, the mitochondria of chondrocytes shrunk and the mitochondrial crest decreased or disappeared. However, Fer-1 (Ferrostatin-1) inhibited ferroptosis induced by T-2 toxin in chondrocytes. The Se-Met alleviated lipid peroxidation, oxidative stress, and damaged mitochondrial in T-2 toxin-infected chondrocytes, enhanced antioxidant enzyme activity, and activated the system Xc−/GSH/GPX4 axis, thereby antagonizing ferroptosis of chondrocytes and alleviating articular cartilage damage. In conclusion, our findings highlight the essentiality of ferroptosis in chondrocyte caused by T-2 toxin, elucidate how Se-Met offers protection against this injury and provide research evidence for the drug treatment target of Kashin-Beck disease. |
| format | Article |
| id | doaj-art-6bc70aaef1e34ddba7acffdab1c22783 |
| institution | Kabale University |
| issn | 0147-6513 |
| language | English |
| publishDate | 2025-01-01 |
| publisher | Elsevier |
| record_format | Article |
| series | Ecotoxicology and Environmental Safety |
| spelling | doaj-art-6bc70aaef1e34ddba7acffdab1c227832025-02-12T05:29:49ZengElsevierEcotoxicology and Environmental Safety0147-65132025-01-01290117569Selenomethionine alleviates T-2 toxin-induced articular chondrocyte ferroptosis via the system Xc−/GSH/GPX4 axisFang-fang Yu0Juan Zuo1Miao Wang2Shui-yuan Yu3Kang-ting Luo4Tong-tong Sha5Qian Li6Zai-chao Dong7Guo-yu Zhou8Feng Zhang9Xiong Guo10Yue Ba11Yan-jie Wang12Department of Environmental Health, School of Public Health, Zhengzhou University, Zhengzhou, Henan 450001, PR ChinaDepartment of Environmental Health, School of Public Health, Zhengzhou University, Zhengzhou, Henan 450001, PR China; Department of Medical Technology, Zhengzhou Shuqing Medical College, Zhengzhou, Henan 450064, PR ChinaDepartment of Environmental Health, School of Public Health, Zhengzhou University, Zhengzhou, Henan 450001, PR ChinaDepartment of Environmental Health, School of Public Health, Zhengzhou University, Zhengzhou, Henan 450001, PR ChinaDepartment of Environmental Health, School of Public Health, Zhengzhou University, Zhengzhou, Henan 450001, PR ChinaDepartment of Environmental Health, School of Public Health, Zhengzhou University, Zhengzhou, Henan 450001, PR ChinaDepartment of Environmental Health, School of Public Health, Zhengzhou University, Zhengzhou, Henan 450001, PR ChinaDepartment of Environmental Health, School of Public Health, Zhengzhou University, Zhengzhou, Henan 450001, PR ChinaDepartment of Environmental Health, School of Public Health, Zhengzhou University, Zhengzhou, Henan 450001, PR ChinaInstitute of Endemic Diseases, School of Public Health of Health Science Center, Xi’an, Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi’an 710061, PR ChinaInstitute of Endemic Diseases, School of Public Health of Health Science Center, Xi’an, Jiaotong University, Key Laboratory of Trace Elements and Endemic Diseases, National Health and Family Planning Commission, Xi’an 710061, PR ChinaDepartment of Environmental Health, School of Public Health, Zhengzhou University, Zhengzhou, Henan 450001, PR ChinaDepartment of Environmental Health, School of Public Health, Zhengzhou University, Zhengzhou, Henan 450001, PR China; Correspondence to: School of Public Health, Zhengzhou University, 100 Kexue Avenue, Zhengzhou, Henan 450001, PR China.T-2 toxin can induce bone and cartilage development disorder, and oxidative stress plays an important role in it. It is well known that selenomethionine (Se-Met) has antioxidative stress properties and promotes the repair of cartilage lesion, but it remains unclear whether Se-Met can relieve damaged cartilage exposure to T-2 toxin. Here, the oxidative stress and ferroptosis of chondrocytes exposure to T-2 toxin were observed. Mechanistically, T-2 toxin increased ROS, lipid ROS, MDA and Fe2+ contents in chondrocytes, decreased GSH and GPX4 activity, and inhibited the system Xc−/GSH/GPX4 antioxidant axis. In addition, the mitochondria of chondrocytes shrunk and the mitochondrial crest decreased or disappeared. However, Fer-1 (Ferrostatin-1) inhibited ferroptosis induced by T-2 toxin in chondrocytes. The Se-Met alleviated lipid peroxidation, oxidative stress, and damaged mitochondrial in T-2 toxin-infected chondrocytes, enhanced antioxidant enzyme activity, and activated the system Xc−/GSH/GPX4 axis, thereby antagonizing ferroptosis of chondrocytes and alleviating articular cartilage damage. In conclusion, our findings highlight the essentiality of ferroptosis in chondrocyte caused by T-2 toxin, elucidate how Se-Met offers protection against this injury and provide research evidence for the drug treatment target of Kashin-Beck disease.http://www.sciencedirect.com/science/article/pii/S0147651324016452T-2 toxinSe-metFerroptosisDamaged cartilage |
| spellingShingle | Fang-fang Yu Juan Zuo Miao Wang Shui-yuan Yu Kang-ting Luo Tong-tong Sha Qian Li Zai-chao Dong Guo-yu Zhou Feng Zhang Xiong Guo Yue Ba Yan-jie Wang Selenomethionine alleviates T-2 toxin-induced articular chondrocyte ferroptosis via the system Xc−/GSH/GPX4 axis Ecotoxicology and Environmental Safety T-2 toxin Se-met Ferroptosis Damaged cartilage |
| title | Selenomethionine alleviates T-2 toxin-induced articular chondrocyte ferroptosis via the system Xc−/GSH/GPX4 axis |
| title_full | Selenomethionine alleviates T-2 toxin-induced articular chondrocyte ferroptosis via the system Xc−/GSH/GPX4 axis |
| title_fullStr | Selenomethionine alleviates T-2 toxin-induced articular chondrocyte ferroptosis via the system Xc−/GSH/GPX4 axis |
| title_full_unstemmed | Selenomethionine alleviates T-2 toxin-induced articular chondrocyte ferroptosis via the system Xc−/GSH/GPX4 axis |
| title_short | Selenomethionine alleviates T-2 toxin-induced articular chondrocyte ferroptosis via the system Xc−/GSH/GPX4 axis |
| title_sort | selenomethionine alleviates t 2 toxin induced articular chondrocyte ferroptosis via the system xc gsh gpx4 axis |
| topic | T-2 toxin Se-met Ferroptosis Damaged cartilage |
| url | http://www.sciencedirect.com/science/article/pii/S0147651324016452 |
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