& Stacpoole, P
Early intervention significantly improves outcomes and can prevent irreversible nerve damage
GSH has long been implicated as a major antioxidant and redox regulator that functions to mitigate and alleviate this oxidative damage ( However, the preceding sections of this paper establish that GSH is not merely a passive antioxidant, but an immune regulator and modulator with actions dependent upon the pathophysiologic context (Ghezzi, 2011) GSH acts to regulate the thresholds necessary for immunologic activation through redox-sensitive signal transduction pathways, influences antigen presentation and the development/differentiation of immune cells, and modulates the production of cytokines
Follow-up: serial DEXA/body comp at 3-6-12 months, inflammatory biomarkers, kidney/liver panels, hormone levels, any adverse events
Mar 2011;2(1):37-44
Upon stimulation by cytokines such as Tumor Necrosis Factor-alpha (TNF-) or Interleukin-1 (IL-1), endothelial cells undergo significant changes, including the de novo synthesis and cell surface expression of adhesion molecules like E-selectin, ICAM-1, and VCAM-1 [1] [2]