Abstract
ERYTHEMA followed by scaling and increased pigmentation develops in human skin which has been exposed to moderate doses of ultraviolet radiation. Oedema, blistering and necrosis may occur after higher doses, and continued exposure to high intensity ultraviolet radiation may result in premature ageing and skin cancer; similar reactions occur in animal skin1–3. Biochemical and histochemical changes4–6 in irradiated skin have been difficult to correlate with these gross reactions. Decreased phospholipid in mouse skin after massive doses of ultraviolet radiation at −40° C7 and similar findings with lower doses in vivo8, together with reports of the formation of lipid peroxide in irradiated lipid9 and skin10, may be indicative of changes in membrane integrity. Although protein is considered the target for ultraviolet radiation haemolysis, increased permeability typically precedes colloid osmotic disruption of the plasma membrane11. Among the more complex membranous components of other tissue cells, lysosomes are the most susceptible to rupture by ultraviolet radiation12. There is also indirect evidence for lysosomal enzyme action in damage caused by this radiation to rat skin in organ culture13.
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