1022-7954/05/4105- © 2005 Pleiades Publishing, Inc.
Russian Journal of Genetics, Vol. 41, No. 5, 2005, pp. 545–547. Translated from Genetika, Vol. 41, No. 5, 2005, pp. 676–679.
Original Russian Text Copyright © 2005 by Serebryanyi, Zoz, Morozova.
We have previously reported  experimental evi-
dence suggesting that plant antimutagenesis in general
and that caused by antioxidants in particular, is brought
about by an inducible system of stimulated repopula-
tion. Other mechanisms of antimutagenesis were pro-
posed, mostly for
, other animals, or pas-
saged cell cultures. Based on the available evidence,
De Flora  suggested the following ways of action of
antimutagens: they may (1) inhibit mutagen entry into
a cell; (2) they reduce the mutagen dose by inhibiting
its transformation into the directly acting mutagen;
(3) reduce the possibility of interaction with crucial
DNA sites; and (4) change the efﬁciency of DNA dam-
age repair. The latter variant is usually considered as the
The evidence reported in  completely excludes
the possibility that the effect of directly acting
mutagens is reduced by a repair mechanism, but in
these experiments, the antimutagen action preceded
that of the mutagen. Hence, a possibility remains that
an antimutagen might somehow inhibit the mutagen
entry into the cell or reduce the degree of DNA damage
and consequently the mutagen effect.
We have conducted a series of experiments, in
which the time of antimutagen introduction varied: the
wheat seedlings were treated by antimutagen both
before and after the action of mutagen N-nitroso N-
MATERIALS AND METHODS
The seeds of common winter wheat
, cultivar Moscovskaya 39 were used in this study.
Nitrosomethylurea (NMU) (CAS no. 684-93-5) and
thylaminomethyl)-benzamidazole) were synthesized in
the Institute of Biochemical Physics, Russian Academy
Pretreatment with antioxidant.
The seeds were ﬁrst
soaked for 12 h in either water or 0.0005% ambiol,
treated with 0.025% NMU solution for 12 h, and then
kept in water for 12 h. In control, the seeds were kept
for 36 h in water. After treatment, the seeds were germi-
nated at 24
C. The apical meristem of primary seedling
rootlets was analyzed for cell mitotic activity and the
frequency of aberrations in the ﬁrst mitosis anaphase
using a temporal ﬁxation 45, 48, and 51 h after begin-
ning of seed soaking .
Posttreatment with antioxidant.
Seeds were ﬁrst
soaked in water for 12 h, then treated with 0.025%
NMU for 12 h, and then with 0.0005% ambiol solution
for 12 h. In control, the seeds were kept in water for 36 h.
The following treatment was similar to that in the pre-
In each variant, at least ten rootlets were used. At
each ﬁxation term, at least 4000 and 200 cells were
examined to determine their mitotic activity and the
proportion of the aberrant cells, respectively.
Signiﬁcance of differences were estimated using
Student’s or Fisher’s
tests; the differences were con-
sidered signiﬁcant at
< 0.05. The correlation coefﬁ-
cients and parameters of linear regression were calcu-
lated and the corresponding lines plotted using Statis-
tica software package.
On Antimutagenesis Mechanism in Plants
A. M. Serebryanyi, N. N. Zoz, and I. S. Morozova
Emanuel Institute of Biochemical Physics, Russian Academy of Sciences, Moscow, 119991 Russia;
fax: (095)137-41-01; e-mail: email@example.com
Received July 15, 2004
—The effect of nitrosylmethylurea (NMU) on the mitotic index and the frequency of cells with aber-
rations, as well as the effects of pre- and posttreatment with antioxidant ambiol on the NMU effects were stud-
ied on seedlings of common winter wheat
cultivar Moskovskaya 39. Both pre- and posttreat-
ment with ambiol resulted in antimutagenic effect but after posttreatment, the effect was lower. Irrespective of
type of seedling treatment with ambiol and the time of their ﬁxation (45, 48, and 51 h), when mitotic index is
plotted versus frequency of cells with aberrations, all experimental points fall on the same regression line with
coefﬁcient of correlation of –0.82 (
< 0.001). This implies that the same mechanism underlies antimutagenic
effect irrespective of when the antimutagen was applied, before or after the knockout mutagen dose. This also
suggests that the antimutagenic effect is independent of the degree of the mutagen-induced damage, because by
the time of posttreatment, the volume of genome damage is already determined and the antimutagen fails to
change it. Finally, this suggests that irrespective of time of antimutagen treatment, the mutation frequency is
reduced by the mechanism of stimulated repopulation.