Protecting Workers from Ultraviolet Radiation - icnirp

Protecting Workers from Ultraviolet Radiation
A protein P53, encoded by P53 gene, is activated upon absorption of UVR and is intended to link
with nuclear DNA, blocking cell division to allow the DNA to be repaired before replication in
the early phase of cell division. Any mutation in the gene structure will result in inactive P53 and
so, in unregulated mitosis and skin cancers. “Signature mutations” occur at specific sites in the
gene and are specific for the agent responsible for the mutation i.e. UV-induced mutations,
which are found in most of the human skin cancers. If DNA damages are too numerous to be
repaired, a series of events will be followed by a specific type of cell death, i.e. apoptosis, which
follows UVR absorption in the skin where “sunburn cells” can be observed histologically.
Lipoperoxydation of membrane lipids will result in cell damages and cell membrane fractures
and cell death. A simple irradiation dose of UV near the MED will result in near 300,000 DNA
lesions per cell, most of them being repaired in a few hours. The same dose induces activation or
inactivation for 5,000 genes, which can be down or up-regulated. Dimers formations are strong
inducers of the neo-melanogenesis responsible for skin darkening. Also DNA damages and
repairs are able to induce cell divisions, which contribute to the thickening of the epidermis
(Bruls et al 1984). Both neomelanogenesis and skin thickening are responsible for skin
darkening, commonly called tanning.
Upon irradiation, several cytokines are liberated or activated or synthesized by keratinocytes.
They belong to several categories and responsible for local or systemic inflammatory reactions,
for vasodilatation, oedema, and fever.
3.2.1 Structure and physiology of the skin
The human tegument is constituted by three main layers: the epidermis, the dermis and the
subcutaneous tissue (Figure 3). Each layer has specific components of epithelial, mesothelial and
neural origin.
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