Skin stress response system

TCA applied for cosmetic treatment of photo-damaged skin has caused transient upregulation of certain genes, suggesting that it activates the skin stress response system (SSRS) and that the biological effects of propiomelanocortin are responsible for TCA-induced epidermal activation [295]. 

Kimura A, Kanazawa N, Li H-J, Yonel N, Yamamoto Y, Furukawa F. Influence of trichloroacetic add peeling on the skin stress response system. J Dermatol. 2010 37 1-8. 

Figure 19.17 The biochemistiy and physiology responsible for penile erection. Sexual activity itself begins with a state of arousal that leads to erection. Arousal results in part from stimulation of the sense organs. The hypothalamus coordinates the sensations and activates the autonomic nervous system. Sensory nerves from the skin of the penis and other erogenous zones stimulate the parasympathetic system. This activates nitric oxide synthase and the resultant nitric oxide, via cyclic GMP, causes vasodilation of the arterioles. This increases blood flow through the corpora cavernosa which then expands producing an erection. Pheromones secreted by the female can stimulate the odour detecting system in the nasal cavity of the male (Chapter 12 and see above). Stress, however, activates the sympathetic system releases cyclic AMP which can result in vasoconstriction of the arterioles. Other factors that can interfere with an erection are physical fatigue and alcohol.

On moist skin or mucous membranes, SO2 is converted to sulfurous acid, a direct irritant. This mechanism accounts for its ability to cause inflammation, burning sensation, and tissue damage (described below) in the eyes, throat, nose, and other respiratory tissues experiencing direct contact. Bronchoconstric-tion and other related effects may be mediated by release of leukotrienes, prostaglandins, or other inflammatory factors. How SO2 causes any of the other systemic and clastogenic effects reported below is unclear. Some evidence suggests that free radicals and oxidative stress may play a role, and that metabolites of SO2 (sulfites) may be responsible for clastogenicity. 

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