The heat-shock response is a cellular defence mechanism against environment
al stresses that is evolutionarily conserved from bacteria to man. Numerous
reports demonstrate the beneficial effects of heat-shock protein induction
on cell survival under toxic or oxidative stress, e.g., in cardiac and cer
ebral ischemia or prior to organ transplantation. However, there is little
data on the effects of heat treatment on damage caused by UV irradiation. A
pplying three independent techniques, we have tested the influence of therm
al pretreatment of skin cells (1 h, 43 degrees C) on the initial extent of
UV-B induced DNA damage and its subsequent repair. For cultured human epide
rmal keratinocytes and dermal fibroblasts we can show reduced levels of nuc
leotide-excision-repair-associated DNA strand incision in the comet assay.
Moreover, immunostaining and how cytometric quantitation of thymidine dimer
s immediately and one day after irradiation, respectively, reveal that the
initial DNA damage is not (keratinocytes) or only moderately (fibroblasts)
lower in heat-shocked cells as compared to untreated controls. However, exc
ision repair of dimers is significantly attenuated during the first 24 h in
both cell types. Furthermore, using a modified host-cell reactivation assa
y, we are able to demonstrate that repair of UV-B-damaged plasmid DNA is lo
wer if the transfected cells are previously heat shocked. In summary, heat
treatment (1 h, 43 degrees C) inducing heat-shock proteins reduces nucleoti
de excision repair of UV-B-mediated DNA lesions in fibroblasts and keratino
cytes during the following 24 h. This is not necessarily caused by elevated
heat-shock protein levels themselves. Possibly the direct thermal damage o
f repair enzymes is more severe than the potential protective effects of he
at-shock proteins. (C)1999 Elsevier Science S.A. All rights reserved.