PAOLO GIACOMONI
Insight Analysis Consulting – Brownsboro, Alabama, United States

Abstract

The interaction of ultraviolet radiation with biological matter results in direct DNA damage and in indirect damage provoked by the production of Reactive Oxygen Species (ROS) catalyzed by photo-sensitizers.
Direct damage and indirect damage trigger a peroxidative cascade in the cytoskeleton and in membrane lipids, that can extend to thousands of molecular modifications per absorbed photon.
Superoxide and Singlet Oxygen are the main ROS that need to be tackled: this review describes some of the effects of Vitamin E on the molecular, biochemical, cellular and clinical consequences of exposure of cells and skin to UV radiation.

INTRODUCTION
Cell death induced by a variety of aggressors has been categorized as Necrosis or Apoptosis. Necrosis is a form of cell death that triggers an inflammatory response, and apoptosis is considered a form of programmed cell death, consequent to the loss of capability of producing ATP. Solar radiation has the capability of inducing both necrosis and apoptosis in irradiated cells.

About 5% of the solar energy reaching the earth is made of “ultraviolet” photons with wavelengths comprised between 290 nm and 400 nm. These wavelengths are labeled as UVA-1 (400 nm to 340 nm), UVA-2 (340 nm to 315 nm), UVB (315 nm to 290 nm). Shorter ultraviolet wavelengths (UVC) are filtered off by the Ozone layer.

UVB is absorbed by pure DNA. This makes it particularly interesting for its potential effects on living organisms, particularly on human skin.

Among the major biochemical and clinical effects of UV radiation, one finds DNA damage (1, 2), protein oxidation (3), lipid peroxidation (4, 5), erythema (6, 7, 8, 9, 10) pigmentation (11, 12) aging (13, 14), cancer (15, 16) and immune depression ...