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Collectively, these data might indicate that the diminished ROS buffering of GSH-deficient cells leads to an increased activation of the mTOR pathway which could drive to the MZB-like properties of Gclc -deficient FoB
Pilot human studies describe measurable alterations in adipose-related metabolic markers without direct stimulation of systemic growth hormone levels
In addition, MPO generated by neutrophils during inflammation may result in irreversible protein and lipid alterations and increased levels of oxidized low-density lipoprotein, thereby promoting atherogenesis [87]
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