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10.1007/s00436-015-4759-6 54 MahmoudA

Clin Exp Immunol , 1986

Because SELENOF has a thioredoxin-like catalytic site, SELENOF is thought to either regulate UGGT activity or the redox state of UGGT substrates (32)

Cancer Symp 51:21, 1998

Accessed July 19, 2022

[43] revealed that initially, the increased hepatic lipid availability in obese individuals with NAFLD enhances hepatic mitochondrial competence, however, it eventually stimulates enhanced hepatic oxidative stress and therefore, decreases mitochondrial activity, promoting the development of NAFLD into NASH [44]