[6] Release of GST-A1 as an indication of cellular necrosis [edit] Increases in serum and urinary GST-A1 have been found in association with hepatocyte and renal proximal tubular necrosis respectively, and have potential for monitoring injury to these tissues
That thought might sound reckless
Continuous exposure to any signaling molecule can lead to receptor downregulation, meaning the body responds less strongly over time
In order to be taken up by the liver it has to be degraded to amino acids. [I also wonder- since glutamate is elevated in metabolic disease, and a residue in the GSH tripeptide, might it be that providing glycine or serine to support synthesis could be preferred over glutathione
This duality is due to phenolic compounds, which may generate ROS in the presence of transition metals like copper (128)
However, there is a need to standardize parameter measurements (such as TEWL, collagen density, viscoelasticity, etc.) in randomized, placebo-controlled trials in designs that include estrogen-deficient skin in menopausal women with correlations to biomarkers examined in these clinical studies that assist patients and physicians as to how to evaluate, select, and provide the most effective treatments in the future