Based on the Sam50-MICOS-ATAD3-mtDNA axis: Exploring oligomeric proanthocyanidins to alleviate molybdenum and cadmium co-induced liver inflammation in sheep.

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Tác giả: Huabin Cao, Huifeng Chang, Huawei Chen, Jing Chen, Xueyan Dai, Feiyan Gao, Maokang Liu, Chenghong Xing, Fan Yang, Junhua Ye

Ngôn ngữ: eng

Ký hiệu phân loại: 594.38 *Pulmonata

Thông tin xuất bản: Netherlands : International journal of biological macromolecules , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 119006

Molybdenum (Mo) and cadmium (Cd), well-defined hazardous pollutants in the environment, exhibit potential toxic effects on liver tissues by inducing oxidative stress and inflammatory responses. This study aims to investigate the role of the Sam50-MICOS-ATAD3-mtDNA axis in mediating the inflammatory response in liver inflammation induced by co-exposure to Mo and Cd in sheep, as well as the protective effects of oligomeric proanthocyanidins (OPC). The findings indicated that co-exposure to Mo and Cd induced cellular degeneration, rupture of hepatic mitochondrial membranes and mitochondrial dysfunction that was accompanied by the levels of ATP, SDH and GSH-Px reduced in the sheep liver tissue. Furthermore, the co-exposure downregulated the expression levels of mitochondrial membrane proteins (Sam50, MICOS and ATAD3) and degree of co-localization between Sam50 and Mic60. In addition, co-exposure to Mo and Cd elicited an increase in mtDNA content and promoted the upregulation of inflammation-related factor levels, which resulted in an augmentation of TNF-α, CRP, and IL-18 contents. However, OPC alleviated the above changes induced by the combination of Mo and Cd. In conclusion, co-exposure to Mo and Cd decreases mtDNA stability by disrupting the Sam50-MICOS-ATAD3 axis, thereby inducing liver inflammation in sheep. Nevertheless, OPC could alleviate this damage.
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