Sir

In his News and Views article “Device physics: A bug-beating diode” (Nature 441, 299; 2006) describing the development of UVC-emitting diodes that promise to have major practical applications, Asif Khan states: “Earth's ozone layer completely blocks solar light of very low ultraviolet wavelengths. Biological organisms on Earth have therefore never developed a tolerance for this 'UVC' radiation, and artificially generated UVC light has become a useful tool in the treatment and destruction of bacteria, yeast, viruses and fungi.”

This statement is in error on many counts. Biological organisms existed on Earth before an oxygen atmosphere, approximately 2 billion years ago, and therefore before the protection afforded by the ozone layer. During this period, cells had ample time to experience UVC (260 nm wavelength). Evolutionary pressures led to the development of multiple repair and tolerance systems targeting UVC-induced cellular damage that are now found in all three biological kingdoms. (Early evidence for repair in bacteria is shown, for example, in R. F. Hill Biochim. Biophys. Acta 30, 636–637; 1958.) Loss of a UVC repair system in humans results in the UV-sensitive disease xeroderma pigmentosum, first described in 1968 (J. E. Cleaver Nature 218, 652; 196810.1038/218652a0).

Even after the appearance of the ozone layer, evolutionary pressure continued because of the similarity of the photochemistry of DNA exposed to UVC and to UVB (280–320 nm). Exposure to either wavelength results in similar photoproducts: covalent adducts between adjacent pyrimidines on the DNA strands (known as cyclobutane pyrimidine dimers and [6-4]-photoproducts). The difference between DNA damage at these wavelengths is mainly different relative proportions of photoproducts and different proportions of cytosine- and thymine-containing photoproducts.

Another misapprehension is that cells need exposure to a particular agent to develop resistance mechanisms to that agent. This fails to appreciate the versatility of most biological repair systems. DNA damage can involve a wide range of altered chemical structures, but is constrained by the structure of DNA itself. Repair systems consequently target specific structural alterations as well as general classes of lesions. The nucleotide excision repair system that repairs UVC damage excises a wide variety of DNA damage, even adducts formed by an agent such as cisplatin, which was unknown to biology before its human invention in recent years.

There is therefore ample evidence that repair and tolerance systems towards UVC have existed for long evolutionary periods and have great versatility. UVC light has become a useful tool in the treatment and destruction of bacteria, yeast, viruses and fungi because it is technically easy to generate high dose rates at a wavelength (254 nm) close to the absorption maximum of DNA with low-pressure mercury sources, not because cells lack tolerance or repair mechanisms.