To start things off, let's look at the paper "Anatomical and Physiological Basis for Corneotrophic Care of the Skin"
'Amino acids. Some amino acids can be absorbed from the skin and may aid in tissue repair and regeneration. Altering cellular osmolality to a hyperosmotic state results in a decrease in ATP allied with oncosis and resultant necrosis. The following components discussed are ingredients in Olivamine.
Glycine (<100 d) protects ATP-depleted cells by low affinity interactions with multimeric channel protein, stabilization of which may otherwise lead to formation of pathological pores. Such porous defects in membranes of ATP-depleted cells have been characterized recently, showing definable exclusion limits for molecules of increasing sizes.23 Glycine provided during ATP depletion blocked the development of membranous pores completely. 24 The relationship between necrosis and an extracellular depletion of ATP makes its protection and restoration imperative during the pre lethal stages of necrosis or early necrosis.
l-Taurine (<200 d) can act as a direct antioxidant that scavenges or quenches oxygen-free radicals intracellularly to block ROS-mediated cell death. The beneficial effects of the ROS-scavenging capacity of l-taurine include attenuation of lipid peroxidation, reduction of membrane permeability, and inhibition of intracellular oxidation in different cells. 25 Apart from its effect on antioxidant defense, l-taurine also functions in osmoregulation and modulation of intracellular Ca 2+ concentration. Taurine prevents high glucose–induced apoptosis in endothelial cells through ROS inhibition and stabilization of intracellular calcium. 26
N-acetyl l-cysteine (NAC) is an antioxidant, particularly
working against hydrogen peroxide. The hypothesis that NAC-induced free-radical signaling delays G 0 /G 1 cell progression to S phase by regulating the cell cycle regulatory protein cyclin D 1 and the free radical–scavenging enzyme manganese superoxide dismutase (MnSOD) has been investigated. Treatment with NAC (<200 d) resulted in increased cellular glutathione levels, indicating a shift to a more reducing environment. This shift in cellular redox environment was associated with delayed progression from G 0 /G 1 to S. NAC treatment resulted in a decrease in cyclin D 1 and an increase in MnSOD protein levels. The absence of a NAC- induced G 1 arrest in fibroblasts overexpressing cyclin D 1 (or a nondegradable mutant of cyclin D 1 V T286A) indicates that cyclin D 1 regulates this delay in G 0 /G 1 to S progression. These results support the hypothesis that cellular redox environment regulates cellular proliferation via regulating cell cycle regulatory protein levels. 27 Furthermore, in the
authors’ opinion, the results also suggest that inclusion of NAC in skin care formulations might help in appropriate
wound healing by controlling proliferation and preventing scarring.'