Chlorhexidine (CLX) is the most widely used antiseptic for wound and skin d
isinfection. Despite its potent bactericidal action, skin irritation is obs
erved when it is used topically. This study aimed to evaluate the mechanism
s underlying CLX-induced toxicity on human dermal fibroblasts with special
emphasis on factors that may mediate or counteract its undesirable effects.
Cells were exposed to CLX concentrations of 0.00005-0.025% for 3, 6, 8 or
24 h in the absence or presence of different concentrations of foetal calf
serum (FCS) (2, 5 and 10%). Depletion of cell ATP occurred, in a time- and
concentration-dependent manner, in all experimental conditions at [CLX] >0.
001%. At 24 h of CLX exposure time, the decrease in intracellular ATP was p
roduced from a 10-times lower CLX concentration (0.0001%). Concentrations g
reater than or equal to0.02% produced total loss of ATP. However, cell surv
ival was maintained after CLX treatment for 3 and 8 h and CLX concentration
s greater than or equal to0.005% were required to produce total cell death.
CLX exerted an inhibitory concentration-dependent effect on DNA synthesis
from concentrations as low as 0.0001%. Only FCS at 10% appeared to have a c
ytoprotective action against CLX-induced cytotoxicity. (C) 2001 Elsevier Sc
ience Ltd. All rights reserved.