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As the primary organ responsible for steroid metabolism, the liver is particularly susceptible to the toxic effects of 17--alkylated oral anabolicandrogenic steroids, such as stanozolol and methyltestosterone ( Mechanistic studies suggest that anabolicandrogenic steroids impair mitochondrial -oxidation and deplete intracellular glutathione stores, resulting in lipid peroxidation and activation of apoptotic signalling pathways

This process can be antagonized by methylation inhibitors silencing DNMT3a and SEPT9 overexpression, thereby reducing liver fibrosis, including upregulation of apoptosis-related proteins in myofibroblasts, and reduction of TGF-1-induced expression of -SMA and COL1A1

[DOI] [PubMed] [Google Scholar] 72.Ju J., Li X.-M., Zhao X.-M., Li F.-H., Wang S.-C., Wang K., Li R.-F., Zhou L.-Y., Liang L., Wang Y., et al

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