Several mechanisms are likely to be involved in the solar radiation-me
diated modifications of cellular DNA. Direct excitation of DNA bases b
y the UVB component (290-320 nm) of solar light gives rise, mostly thr
ough oxygen independent reactions, to the formation of dimeric pyrimid
ine lesions including cyclobutadipyrimidines, pyrimidine (6-4) pyrimid
one photoproducts and related valence Dewar isomers, In addition, phot
oexcitation of cytosine and guanine may lead to the formation in relat
ively minor yields of 6-hydroxy-5,6-dihydrocytosine and 8-oxo-7,8-dihy
droguanine, respectively, A second mechanism that requires the partici
pation of endogenous photosensitizers together with oxygen is at the o
rigin of most of the DNA damage generated by the UVA (320-400 nm) and
visible light, Singlet oxygen, which arises from a type II mechanism,
is likely to be mostly involved in the formation of 8-oxo-7,8-dihydrog
uanine that was observed within both isolated and cellular DNA. Howeve
r, it may be expected that the latter oxidized purine lesion together
with DNA strand breaks and pyrimidine base oxidation products are also
generated with a lower efficiency through Fenton type reactions. A mo
re definitive assessment of these mechanisms would require further stu
dies aimed at the identification and quantification of the different D
NA photolesions including both dimeric pyrimidine photoproducts and ph
otooxidized lesions.