UV RADIATION, DNA DAMAGE, MUTATIONS AND SKIN CANCER - Environmental UV Radiation: Impact on Ecosystems and Human Health and Predictive Models - page 241

radiation organisms at the earth's surface have acquired certain adaptive features: e.g.,
UV-absorbing surface layers, repair of damaged cells or replacing damaged or killed
cells entirely. Because of the high absorption in organic material, UV radiation does not
penetrate any deeper than the skin, and this organ clearly shows all of the mentioned
adaptive features. Despite these adaptations, solar UV radiation still affects human
health, but the full extent of these effects remain largely unknown. Any increase in
ambient UVB radiation due to loss of stratospheric ozone can therefore be expected to
have important public health impacts.
About DNA, genes and cancer
Basic cancer research has shown that cancer is a disease stemming from
disturbances in signaling pathways that control the cell cycle and differentiation. The
most persistent disturbance is introduced by synthesis of dysfunctional signaling
proteins or by a complete lack of synthesis of such proteins from miscoding or lost
genes. Two types of genes are directly relevant to carcinogenesis: the oncogene
(dominant) whose protein actively contributes to the cancerous progression, and the
tumor suppressor gene (recessive) whose protein should counter such an uncontroled
progression. A combination of such genes need to be affected in order for a cell to
become cancerous. Such altered genes are passed on to daughter cells, thus propagating
the problem of controlling cell growth. From the above it is immediately obvious that
the ubiquitous solar UV radiation can damage the DNA of genes in exposed skin cells.
Thus solar UV radiation poses a continuous threat to the genomic integrity of skin cells.
The fact that healthy humans do not readily develop skin cancer attests to an
impressively adequate adaptation of the human skin, it has several lines of defence
ranging from increasing UV absorption to protect germinative basal cells, to DNA
repair or removal of damages or transformed cells.
2. UV radiation, DNA damage, repair and mutation
UV absorption and DNA damage
Typical UV absorbing features in organic molecules are conjugated bonds:
alternating single and double bonds, absorbing generally radiation of wavelengths
between 200 and 250 nm, and in a ring between 250 and 300 nm (see reference 3).
(Feynman et al. 4 give an elegantly simplified, quantummechanical introductory analysis
of energy states of double bonds). Absorption maxima at longer wavelengths
(300 - 450 nm) are found in some molecules with three (e.g., riboflavin) or four rings
(e.g., porphyrines), and in long-chain repeats (e.g., carotenoids) of conjugated bonds.
The collective protein fraction from cells shows a maximum absorption around 280 nm,
whereas the DNA fraction shows a maximum around 260 nm. Major absorbers in the
protein fraction are the tryptophan and tyrosine amino acids. In the DNA all nucleic
acids are aromatic and contribute to the absorption maximum. DNA appears to
contribute appreciably to the total absorption of UVC (200 - 280nm) radiation by a cell.
Although absorption by DNA in the UVB around 300 nm is far less than in the UVC
(10 to 100 fold lower), sun exposure causes significant levels of DNA damage.