1022-7954/02/3803- $27.00 © 2002
Russian Journal of Genetics, Vol. 38, No. 3, 2002, pp. 236–238. Translated from Genetika, Vol. 38, No. 3, 2002, pp. 306–309.
Original Russian Text Copyright © 2002 by Lvova, Zasukhina.
The adaptive response (AR) phenomenon has been
known for more than a decade; however, its mechanism
remains unknown. Most researchers believe that DNA
repair is involved in AR. This assumption is based on
various data. First, UV radiation has been shown to
induce repair DNA synthesis (RDS) during the AR .
It is logical to suggest that a cell population consists of
subpopulations with slow and rapid DNA repair. In this
case, slow-repair cells would be eliminated during the
AR. Second, it was demonstrated that 3-Aminobenza-
mide (3AB), an inhibitor of poly(ADP-ribose) poly-
merase, which is involved in DNA repair, inhibits the
AR. Third, many authors postulated that AR is con-
nected with DNA repair, because AR was absent in
repair-deﬁcient human cells. For example, AR was not
found in ataxia telangiectasia  and Down syndrome
. However, experiments with different types of
repair-deﬁcient cells may allow other relationships
between DNA repair and AR to be found.
Earlier, we obtained evidence that DNA repair pro-
cesses in the course of cell protection in repair-deﬁcient
diseases by means of AR are determined by indepen-
dent mechanisms [4, 5].
The purpose of this study was to determine similar-
ities and differences in induction of RDS during the
ARs induced by cadmium chloride (CdCl
quinoline-1-oxide (4NQO), and radiation in cells pre-
treated and not pretreated with garlic extract, which we
used as an antimutagen. Garlic extract is known to exert
a strong protective effect against
-radiation by means
of scavenging free radicals [6, 7].
We may assume that the antimutagenic effect of gar-
lic extract and cell protection during the AR have com-
mon pathways, as was the case with the AR to radiation
and interferon treatment in experiments earlier per-
formed in out laboratory .
The mutagenic effect of CdCl
is believed to be
related to generation of free radicals ; therefore,
radiation, whose biologic effect are also mediated by
free-radical processes, served as a positive control.
MATERIALS AND METHODS
We used the RD strain of human ﬁbroblasts. Their
protective activity was estimated based on the RDS rate.
The cells were treated with one of three mutagens:
M; treatment for 1 h),
-radiation (100 Gy),
M; treatment for 24 h). The cells were
irradiated using a GUPOS device (Vavilov Institute of
General Genetics, Russian Academy of Sciences). The
source of radiation was
Cs; the dose rate was
4.86 Gy/min. As a mutagen, a fresh water extract of
garlic was used. The extract was added at a concentra-
tion of 20 mg/ml to the culture medium one day before
irradiation (100 Gy) or treatment with 4NQO (10
When studying the AR, both 4NQO and CdCl
used at a concentration of 10
M. The solutions of the
mutagens were added simultaneously with garlic extract.
Four hours before irradiation of the cells at 100 Gy (the
damaging dose), they were exposed to
-radiation at a 1–
5 cGy (the adapting dose). The inhibitor of poly(ADP-
ribose) polymerase 3-aminobenzamide (3AB; Sigma)
was added at a concentration of 2 mM/mol 20 h before
cells were treated with mutagens at damaging doses.
RDS induced by 4NQO, CdCl
studied by the liquid-scintillation method. The RDS
Modification of Repair DNA Synthesis
in Mutagen-Treated Human Fibroblasts during Adaptive Response
and the Antimutagenic Effect of Garlic Extract
G. N. Lvova and G. D. Zasukhina
Vavilov Institute of General Genetics, Russian Academy of Sciences, Moscow, 119991 Russia;
fax: (095)132-89-59; e-mail: firstname.lastname@example.org
Received June 6, 2001
—Repair DNA synthesis (RDS) in human ﬁbroblasts during the adaptive responses (ARs) induced by
cadmium chloride (CdCl
-radiation, and 4-nitroquinoline-1-oxide (4NQO) was compared in cells pretreated
and not pretreated with garlic extract. The RDS was increased during the ARs induced CdCl
Garlic extract stimulated RDS in cells treated by the same mutagens. 3-Aminobenzamide (3AB), an inhibitor
of poly(ADP-ribose) polymerase, decreased the RDS rate in cells treated with CdCl
-irradiation but had
no signiﬁcant effect on cells treated with 4NQO. It was demonstrated that DNA repair was involved into cell
protection in different ways in the cases of antimutagen treatment and AR.