13 décembre 2009

Sun emits a large range of electromagnetic radiation. Among them are ultraviolet, of which only UVB and UVA portions pass through the stratospheric ozone layer.

The ultraviolet portion of the solar spectrum is at the origin of skin cancers. Two ranges are defined: UVB radiation is the most energetic (280-320 nm), while UVA is less powerful but at least 20 times more frequent. We have shown that, in spite of low absorption by the genome, UVA rays can induce mutagenic damage.


UVA rays are poorly absorbed by DNA, yet they induce mutations in cells and tumours. This mystery has long been explained by the indirect action of photo-sensitizers present in cells. These molecules absorb light energy and trigger oxidation reactions within DNA. This explains the abundance of antioxidants in many sun-protection products. However, several groups including ours have shown that UVA also leads to the formation of other DNA lesions. It is now clearly established that the major lesion arising from the formation of covalent bonds between adjacent bases, yields a “dimer”.


How are these dimers formed?  Are they formed directly through the few photons absorbed by DNA, or with help from endogenous sensitizers? In collaboration with a group at IRAMIS, we exposed pure DNA in solution to UVA. Result: the same dimers were produced, with the same reaction yield as for DNA inside cells! No need for additional help, to be harmful!  These experiments clearly show that low amounts of UVA energy absorbed by DNA are very efficient for inducing damage. These results further emphasize the need for efficient protection in the UVA range, and thus will help in the design of sunscreens.


Further reading: J. Cadet, et al., Photochemical and Photobiological Sciences 8 (2009) 903


Maj : 19/11/2014 (987)


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