Repeat, SHs play a critical role in cell survival following irradiation 18 October 2004
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Eleni Papadopulos-Eleopulos,
Biophysicist
Department of Medical Physics, Royal Perth Hospital, Western Australia, 6001,
Valendar F Turner, John Papadimitriou, Barry Page, David Causer, Helman Alfonso, Sam Mhlongo, Todd Miller, Christian Fiala

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Re: Repeat, SHs play a critical role in cell survival following irradiation

Repeat, SHs play a critical role in cell survival following irradiation

In his rapid response 30 September 2004 Nicholas Bennett wrote: "In reply to their question regarding UV irradiation and covalent modification, I can see that a brief bit of physics may help. UV irradiation includes 260nm, the wavelength at which maximal absorption occurs for DNA (in fact many "quantitative" techniques for DNA use 260nm densitometry). The energy is sufficient to promote bond breakage and subsequent reformation. The major injury is linkage of adjacent thymidines: this acts as a bump in the road for DNA polymerase and RNA polymerase. There are proteins that can detect or repair these defects, and inherited mutations will lead to UV-related tumour syndromes (e.g. xeroderma pigmentosum). P53 indeed, the granddaddy of tumour-suppressor genes, detect thymidine dimers and initiates excision repair mechanisms (or apoptosis, depending on the level of damage). SH groups may well be involved in cellular signalling cascades, but that's not quite the same thing as saying that a general oxidative state will result in a specific decline of a SUBSET OF ONE CELL LINE, which practically is what the Perth Group are trying to convince us of. Far more likely is a virus that not only infects that particular cell line, but induces lytic cell death, cell cycle arrest and signalling dysfunction, and increases immune activation and apoptosis while preventing replacement. It all seems so simple, when put like that."

In our rapid responses: "More on radiation and oxidation", 17 September and "Cell death radiation and oxidation", 7 September, we:

(i) asked Nicholas Bennett to tell us what is the mechanism by which UV radiation causes "covalent modification of the DNA strand";

(ii) claimed that protein SHs are critically involved in cellular survival following irradiation, and gave two references to back our claim. Nicholas Bennett did not give us a mechanism by which UV radiation causes "covalent modification of the DNA strand". Neither did he make any comments regarding the evidence in the two references, on the relationship between protein SHs and cell survival. Instead, he gave us a long irrelevant story (what does he mean by a "subset of ONE CELL LINE"?), and a lesson in physics (or so he thinks - two of the Perth Group's members are physicists with special interest in radiobiology including UV).

Competing interests: None declared