EXPLOSIVES AS TOXIC ENVIRONMENTAL POLLUTANTS: THE LEVEL OF

CONTAMINATION, TOXICITY, AND ITS MECHANISMS

Narimantas nas*, Aura Nemeikait-nien**, Audron Marozien*,
Jonas arlauskas*,Valentina Vilutien**, Juozas Baublys**


* Institute of Biochemistry, Mokslinink 12, LT-08662 Vilnius, Lithuania
** The General Jonas emaitis Military Academy of Lithuania, ilo 5a, LT- 10322 Vilnius, Lithuania,
E-mail: ncenas@bchi.lt, hidrazon@bchi.lt,

ivk@lka.lt




Abstract. The survey of literature analyzes the levels of the environment contamination by explosives, and their
toxic effects to humans. It is possible to conclude that among modern explosives, pentaerythritol tetranitrate (PETN)
is the least toxic for humans. The impact of hexahydro-1,3,5-trinitro-1,3,5-triazine (RDX) on humans is unclear.
Since 2,4,6-trinitrotoluene (TNT) is the most widespread explosive, its toxicity (methemoglobinemia, cataract, liver
disorders) has been reported most intensively. The mechanisms of toxicity of TNT and other nitroaromatic
explosives involve flavoenzyme-catalyzed single- and/or two-electron reduction (redox cycling of free radicals
and/or formation of alkylating hydroxylamines), and the direct oxidation of oxyhemoglobin. In general, the toxicity
of nitroaromatic explosives increases with an increase with their electron-accepting potency. Thus, some explosives
of novel generation, e.g., 5-nitro-1,2,4-triazol-3-one (NTO), 5-nitro-1,2,4-triazol-3-amine may be less toxic to
humans and other mammalian species than TNT. The experimental data of the present work show that xanthine
oxidoreductase and cytochromes P-450 may be involved in the activation of nitroaromatic explosives in mammalian
cells. Besides, some amino- metabolites of TNT may be more efficient than expected methemoglobinemia-inducing
agents in erythrocytes.

Keywords: explosives, toxicity, mechanism, negative influence, impact, redox, methemoglobin, oxyhemoglobin.

1. Introduction.

Currently, the research project Analysis, evaluation
and modeling of the impact on the environment of
explosion products coming from explosive substances
and ammunition used in training areas during military
training is being carried out at the General Jonas
emaitis Military Academy of Lithuania, partly in
cooperation with the Institute of Biochemistry. The
explosives and ammunition can make a significant impact
on the environment, when they are exploded at training
areas during the military training. One of the objectives
of this work is to analyze the impact of explosion
products on the environment. This will enable us to
foresee the scope of the impact, measures for mitigating
the impact and possibilities of the long-term usage of the
training areas.
In this paper, we present the literature survey on the
environment contamination with explosives and their
residues, their toxicity, and diseases caused to humans. A
second part of the paper is devoted to the clarification of
some mechanistic aspects of toxicity of 2,4,6-
trinitrotoluene (TNT), its degradation products, and other
nitroaromatic explosives (Fig. 1) towards the mammalian
cells in vitro.


2. The importance of the problem (literature survey).

2.1. The contamination of the environment with
explosives and their residues.

Because of the military activities, the development of
military industry, tests of armaments in training areas and
the civil use of explosives, nitroaromatic and
nitroaliphatic explosives, their residues and degradation
products have contaminated large areas of soil and natural
water sources. At present, there are several hundred
locations in Germany alone that are dangerously
contaminated with explosives [1]. We think that this
problem is relevant to Lithuania as well (Pabrade, Rukla
and other training areas).
The most widely-spread explosive 2,4,6-
trinitrotoluene (TNT) (Fig. 1) has been used since 1902.
At the end of the 20th century, about 1,000 tons of it were
produced per year. The toxicity of TNT was noticed as
early as 1919 [2].
The harmless concentration of TNT in the soil and
natural water sources is < 30 mg/kg and < 0.14 mg/l,
respectively. However, the contamination of the territory
of training areas and explosive plants by TNT reaches
12-20 g/kg and 0.1 g/l [3, 4]. It is suggested that the
harmless TNT concentration in the drinking water that
the population of the neighboring areas are supposed to
use throughout their lives is 2 mkg/l [5]. TNT
biodegrades relatively slowly under natural conditions,
and some biodegradation products (hydroxylamines,
amines) are also toxic. It appeared that 96 % of the
explosive residue in the soil in historically-formed
training areas, are relatively coarse particles (> 3 mm in
diameter) [6]. This complicates the degradation of
explosives. Depending on the conditions, the ratio of
TNT and its degradation products monoamino-
dinitrotoluenes in the soil of training areas ranges from
1:0.07 to 1:0.4 (expressed in g/kg of the soil) [7]. In
ammunition plants and mining industry, employees come
into contact with TNT and its vapor. The recommended
concentrations in the air are 0.5-1.5 in the USA and 1
mg/m in China, however the actual air contamination is
greater [8].
It is suggested that a single standard tetryl
production line in the USA emits 16 kg of tetryl per 24
hours [9], however, there are no data about the possible
amount of tetryl residues in the soil and water.
The amount of hexahydro-1,3,5-trinitro-1,3,5-
triazine (RDX) and octahidro-1,3,5,7-tetranitro-1,3,5,7-
tetrazocine (HMX) (Fig. 1) in the soil of training areas
may reach 20-50 mg/kg [7], and in the run-off waters of
ammunition plants it exceeds 1.5 mg/l [10], reaching 12
mg/l in separate cases [11]. It is suggested that the
harmless concentration of RDX or HMX in the drinking
water that the population of the neighboring areas is
supposed to use throughout their lives, is 0.1 mg/l [12].
Explosives and their residues in the soil and water
are usually detected by means of high-pressure liquid
chromatography, sometimes in conjunction with the
mass-spectroscopy analysis (HPLC/ms) [9].
During recent years, attempts have been made to
detect explosive vapor in the air by using different
semiconductor sensors (electronic noses) [13] and its
residues in water and other biological liquids by using
immunosensors [14, 15].
In 2002 the data about the use of enzymatic
biosensor in TNT analysis was published [16].
Enterobacter cloacae PB2 nitroreductase is immobilized
on the surface of the electrode in the conductive polymer
matrix. The enzyme is electrocatalytically reduced by the
immobilized polymer component 4.4dialkylbipyridine
derivative, and reoxidized back by TNT added to the
medium. This results in an increase in the reduction
current. The linear part of the response is 60 M (13.6
mg/ml) of TNT. This would correspond to the dilution of
TNT-contaminated waters by several times.







Fig. 1. Formulae of modern explosives


2.2. Toxicity and diseases caused by the explosives in
humans

In discussing the toxicity of explosives and their
negative influence on humans, one may distinguish two
cases: first, the toxicity and explosives-induced diseases
of persons working with explosives and second, the
influence on the neighboring population.
Personnel working with explosives (producers of
explosives, military personnel, miners) are most often
diagnosed with methemoglobinemia, cataract, dermatitis,
liver malfunctions (including liver cirrhosis), and tumor
formation. Sometimes respiratory and digestive disorders
are observed. All these phenomena are observed when the
amount of TNT in the air is 1.5-0.5 mg/m. In separate
cases slight disorders (decrease in the amount of
hemoglobin and erythrocytes is observed already at 0.2
mg/m of TNT [17]. Therefore, it has long been
recommended to limit the permissible amount of TNT in
the air for an 8-hour shift to 0.5 mg/m.
TNT-induced methemoglobinemia (the formation of
methemoglobin, i.e., the oxidized hemoglobin that is
unable to bind oxygen) has been known since 1919 [2].
After the end of the contact with TNT, methemoglobin
remains in the blood for 2-5 days.Research carried out in
Israel indicated that the explosive plant employees of the
Mediterranean origin which characteristically had a lower
amount of antioxidant enzyme glucose-6-phosphate
dehydrogenase in their erythrocytes, frequently
experienced an acute hemolytic crisis even after a 2-4 day
contact with TNT [18, 19]. In several cases, decrease in
hemoglobin, increase in methemoglobin up to 1.5-8.6 %
of the total amount of hemoglobin, decrease in hematocrit
(erythrocyte concentration, v/v) to 17-24 % (normally
40-50 %), and an increase in the concentration of
reticulocytes, bilirubin, urobilinogen in urine were
observed.
Another mode of impact of explosives on
hemoglobin, the significance of which has not been fully
understood yet, but which can be used as a biomarker, is
the formation of covalent TNT adduct with hemoglobin
[20, 21]. After the precipitation and hydrolysis of
hemoglobin in blood samples, the concentration of mono-
aminodinitrotoluene is determined by HPLC/ms. The
authors point out that these adducts have not been
detected in the blood of the workers of a German
explosive plant, whereas in a Chinese plant they found
3.7-522 ng compound/g hemoglobin.
Among the employees aged 39.5 8.9 who came
into contact with TNT during the span of 6.8 4.7 years,
peripheral, both-sided, medium-complexity cataract
having no influence on the sharpness of the eyesight and
its scope was observed in 6 out of 12 cases [22]. In
China, among the 413 employees that had a contact with
TNT for longer than 3 years, 143 (34.6 %) cases of
cataract were found, and in a separate group that had a
contact with TNT for longer than 20 years the frequency
of cataract is 88.4 % [23]. A link between the
development of cataract and the concentration of TNT-
hemoglobin adduct in blood has been observed in the
explosive plants [20].
In comparing 61 employees of the explosive plant
that worked with organic nitrates with 56 employees of
the control group, 63 % of the former group (18 times
more than in the control group) were diagnosed with
asymptomatic light-form cataract [24].
Skin irritation is more frequent among miners that
come into contact with TNT than among the control
group [25]. Sometimes melanoderma is observed. To
avoid the latter antioxidant therapy is recommended [26].
Both TNT and tetryl cause dermatitis [27].
Several persons that had a long-term contact (about
35 years) with TNT were diagnosed with liver cirrhosis;
however, it is not clear whether TNT had been the
immediate cause of this disease [28]. Other authors did
not detect a direct link between liver cirrhosis and the
contact with TNT, claiming that the liability of persons
contacting with TNT to liver cirrhosis increased due to
alcohol abuse [29].
Mutagenic 4-aminodinitrotoluene is formed in the
organisms of workers of explosive plants. After a
working shift, 9.7 7.9 mg/l of aminodinitrotoluene (0.1-
44 mg/l, n = 219) is detected in the urine. In most cases,
this amount decreases during the weekend; however, in 8
out of 9 people traces of TNT metabolites are detected
even on the 17
th
day after work [30, 31]. It is interesting
to note that these amounts of aminodinitrotoluene (0.2-15
mg/l) can be determined by the simple colorimetric
method known since the World War II [32]. It is believed
that only 40 % of TNT that enters the human organism is
excreted as aminodinitrotoluene through the urine.
Among the employees contacting with nitroaromatic
explosives, cases of myelodysplastic syndrome (indicator
of the liability to myelocytic leukemia) are more frequent
[33]. In 1984-1997, among the 500 copper mine workers
of the former GDR (7-37 years of contact with
explosives) 6 cases of urinary tract tumors and 14 cases of
kidney tumors were registered. It is by 4.5 and 14.3 times
higher than the respective national average of the former
GDR [34]. The occurrence of urinary tract tumors
correlated with the intensity of the contact with nitro-
aromatic explosives, e.g. dinitrotoluene; however, the link
has not been detected in the case of kidney tumors. It is
also interesting to note, that some Chinese workers
contacting with TNT complained of the reproductive
disorders and/or impotence. They were diagnosed with
the decrease in sperm volume and quantity of mature
spermatozoa, also with different spermatozoan damage
[35, 8].
Concerning the negative effects of explosives on the
neighboring population, one may note that in the land of
Hesse (Germany), the morbidity with acute and chronic
leukemia in 1983-1989 was more frequent in one
Marburg community where the underground TNT plant
was operating during WWII, than in neighboring
communities. It was linked to the increased contamination
of soil and underground water with TNT and products of
its production [36]. The risk of chronic leukemia among
men but not among women in this locality exceeded the
national average by 10 times. Later research did not reject
this opinion by confirming that a small group of persons
living adjacent to the plant around 1940, actually
contracted leukemia much more often [37]. However, the
authors were unable to explain why leukemia morbidity
grew considerably around 1980.


3. The mechanistic studies of toxicity of explosives

The mechanisms of toxicity of explosives were
assessed through the studies of laboratory animals, cell
cultures in vitro, and the relevant enzymatic reactions.
First, nitroaliphatic esters pentaerythritol tetranitrate
(PETN) and trinitroglycerol (TNG) (Fig. 1) were found to
be nontoxic to rats and mice [38]. Second, the
administration of RDX (Fig. 1) (30-300 mg/kg daily, 13
weeks) to rats caused hypotriglycidiremia, convulsions,
and death [39]. These symptoms were different from
those caused by TNT (methemoglobinemia, liver and
spleen damage). However, the latter symptoms were
similar to those induced in humans by chronic TNT
intoxication. The mechanisms underlying toxicity of
RDX and HMX remain undisclosed so far. However, the
toxicity of nitroaromatic explosives has been studied
more extensively ([40-42], and references cited therein).
Briefly, their toxicity may be manifested through several
mechanisms:
a) the redox cycling of free radicals of
nitroaromatics. Free radicals are formed in the single-
electron reduction of nitroaromatic compounds by
flavoenzymes dehydrogenases-electrontransferases, e.g.
liver NADPH: cytochrome P-450 reductase (EC 1.6.2.4):

Enzyme (reduced) + 2 TNT
Enzyme (oxidized) + 2 TNT

(1)

Subsequently, the radicals are reoxidized by oxygen:

TNT

+ O
2
TNT + O
2

(superoxide). (2)

Further, superoxide participates in Haber-Weiss reaction:

2 O
2

+ 2 H
+
+ Fe
2+
O
2
+ OH

+ Fe
3+
+ OH. (3)

The radical of hydroxyl (OH) is very active oxidant
that damages cell proteins, nucleic acids and
phospholipids.
b) the two-electron reduction of TNT to nitroso- and,
subsequently, to hydroxylamino-dinitrotoluenes under the
action of two electron-transferring flavoenzyme DT-
diaphorase (EC 1.6.99.2) in mammalian cells, or under
the action of oxygen-insensitive nitroreductases in
gastrointestinal tract bacteria ([41,43], and references
cited therein). The toxicity of aromatic hydroxylamines is
attributed to their reactions with DNA.
Our studies on the cytotoxicity of nitroaromatic
explosives towards bovine leukemia virus-transformed
lamb kidney fibroblasts (line FLK) [40-42] revealed that
their toxicity in general increases with an increase in their
electron-accepting potency, i..e., tetryl, pentryl >
tetranitrocarbazole > TNT, tetranitrobenzimidazolone >
4,6-dinitrobenzofuroxan (DNBF) > hydroxylamino- and
amino- metabolites of TNT > 5-nitro-1,2,4-triazol-3-one
(NTO), 5-nitro-1,2,4-triazol-3-amine (ANTA). These
data in general correlate with the studies on the toxicity
of several explosives in rats and in mice when given
perorally: teryl (LD
50
300 mg/kg [44]), TNT (LD
50
=
1300-600 mg/kg [45]), and NTO (LD
50
> 5 g/kg [46]).
The toxicity is partly prevented by the antioxidants N,N-
diphenyl-p-phenylene diamine and desferrioxamine, and
potentiated by the alkylating agent 1,3-bis-(2-
chloroethyl)-1-nitrosourea. These findings taken together
with a cytotoxicity increase with an increase in the
electron-accepting potency of explosives, show that the
cytotoxicity is caused mainly by the redox cycling
mechanism (reactions 1-3). However, the cytotoxicity of
amino- and hydroxylamino- metabolites of TNT was
higher than one may expect from their electron-accepting
properties. This points to the posibility of the additional
mechanisms of their toxicity. Besides, the protective
effects of the inhibitor of DT-diaphorase, dicumarol,
show that the formation of toxic hydroxylamine products
under the action of this enzyme is also partly responsible
for the cytotoxicity of nitroaromatic explosives.
In this work, we further clarified the mechanism of
cytotoxicity of TNT and its amino-metabolites towards
FLK cells, showing that their action is partly prevented by
the inhibitors of cytochromes P-450, -naphthoflavone
and izoniazide, and the inhibitor of xanthine
oxidoreductase (XOR, EC 1.1.3.22), allopurinol (Table
1).

Table 1. The protective effects of -naphthoflavone (5.0 M),
izoniazide (1.0 mM), and allopurinol (100 M)
towards the toxicity of 2,4,6-trinitrotoluene (TNT, 25
M), 2-amino-4,6-dinitrotoluene (2-NH
2
-DNT, 450
M), and 4-amino-2,6-dinitrotoluene (4-NH
2
-DNT,
320 M) in FLK cells (n = 3, p < 0.02). The
cytotoxicity experiments were performed as described
in [40,41].

No. Compound Additions Cell viability
(%)
1 TNT None 45.23.5
2. TNT -Naphthoflavone 60.84.8
3. TNT Izoniazide 64.55.2
4. TNT Allopurinol 63.54.7
5. 2-NH
2
-DNT None 40.53.0
6. 2-NH
2
-DNT -Naphthoflavone 56.64.5
7. 2-NH
2
-DNT Izoniazide 60.15.0
8. 2-NH
2
-DNT Allopurinol 57.64.0
9. 4-NH
2
-DNT None 53.62.0
10. 4-NH
2
-DNT -Naphthoflavone 66.43.5
11. 4-NH
2
-DNT Izoniazide 62.03.0

The data of Table 1 confirm the suggestion that
cytochromes P-450 may perform N-hydroxylation of
NH
2
-DNTs, converting them into toxic hydroxylamines
[41,47]. The protective effects of -naphthoflavone and
izoniazide against the cytotoxicity of TNT indicate that a
fraction of TNT may be intracellularly reduced into NH
2
-
DNTs. This may take place in partly anaerobic cell
compartments with high concentration of reducing
flavoenzymes ([42], and references cited therein). The
data on the protective effects of allopurinol (Table 1)
show that XOR may be involved in the reductive
activation of TNT and other nitroaromatic compounds.
Because most flavoenzymes do not possess specific
inhibitors, this finding extends our understanding on the
involvement of individual flavoenzymes in the
bioreductive activation of nitroaromatic explosives.
Methemoglobinemia, i.e., methemoglobin (HbFe
3+
)
formation from oxyhemoglobin (HbFe
2+
O
2
) in human
blood erythrocytes is another important mechanism of
toxicity of nitroaromatic explosives ([48], and references
cited therein):

HbFe
2+
O
2
+ TNT Hb-Fe
3+
+ O
2

+ TNT

(4)

Using a number of compounds, we have concluded
that the rate constant of Hb-Fe
2+
-O
2
oxidation by
nitroaromatic explosives and the extent of Hb-Fe
3+

formation in intact erythrocytes in general increases with
an increase in their electron accepting potency [48]. In
this work, we extended these studies, using in particular
the amino- metabolites of TNT (Table 2).


Table 2. The rate constants of oxidation (k) of oxyhemoglobin
by nitroaromatic explosives and their metabolites in
lysed human erythrocytes (pH 7.0, 37
o
C), the amount
of methemoglobin (Hb-Fe
3+
) formed during 24 h
incubation of erythrocytes with 300 M of
corresponding compounds during 24 h at 37
o
C and
pH 7.0 (n = 3), and the single-electron reduction
potentials (E
1
7(calc.)
) of nitroaromatic explosives [49].
The experiments were performed as described in [48].
The concentration of Hb-Fe
3+
in control erythrocytes
was 0.40.1 %.

No. Compound k
(M
-1
s
-1
)
[Hb-Fe
3+
]
(%)
E
1
7(calc.)

(V)
1. Tetryl 8.90.5

42.51.2 -0.156
2. TNT 3.30.2

48.16.3 -0.254
3. TNT (100 M) 35.61.2
4. DNBF (100 M) 121.2 2.40.5 -0.258
5. 2-NH
2
-DNT 1.00.2 8.30.2 -0.423
6. 4-NH
2
-DNT 0.30.1 0.90.2 -0.453
7. 2,4-(NH
2
)
2
-NT 0.40.3 10.52.1 -0.467
8. ANTA 0.120.02 2.10.3 -0.466
9. NTO 0.1 1.20.3 -0.509

Our current results suggest that although an increase
in the electron-accepting potency of nitroaromatic
compounds (E
1
7(calc.)
, Table 2) in general increases Hb-
Fe
2+
-O
2
oxidation rate, it does correlate with the extent of
Hb-Fe
3+
formation in erythrocytes during long lasting
incubation. This discrepancy is most pronounced
comparing the efficiency of Hb-Fe
3+
formation by 2-NH
2
-
DNT, diamino- metabolite of TNT, 2,4-(NH
2
)
2
-NT, and
ANTA (Table 2). Possibly, the other reactions of amino-
metabolites of TNT in erythrocytes, e.g., their N-
hydroxylation by various redox forms of hemoglobin,
may substantially increase the extent of methemoglobin
formation under the chronic intoxication conditions [50].

5. Conclusions

The presented survey of literature reflects the most
important data about the contamination of the
environment with explosives, their negative influence on
personnel and the neighboring population. It is possible
to state that among modern explosives PETN is the least
toxic for humans. At present it is being tested as a
possible remedy for the ischemic disease (a substitute for
trinitroglycerol) [51].
The impact of RDX and HMX on humans is unclear,
as well as the mechanisms of their toxicity in other
mammalian species. Particular attention should be paid to
the results of long-term contact with RDX and HMX,
including the possible penetration of the vapor and
particles of these combinations into the organism through
the skin and the respiratory tract.
Since TNT is the most widespread explosive, its
toxicity has been investigated most thoroughly.
Particular attention should be paid to TNT-induced
cataract and damage to reproductive system. However,
the comparative data of German and Chinese explosive
plants indicate that the regulation of TNT amount in the
air might partly mitigate its toxic effects.
On the other hand, research carried out in TNT
contaminated location in Germany in reference to the
susceptibility to leukemia indicates that particular
attention should be paid to the acceleration of degradation
of TNT and related nitroaromatic explposives.
The mechanisms of toxicity of TNT and other
nitroaromatic explosives involve flavoenzyme-catalyzed
single- and two-electron reduction, and the direct
oxidation of oxyhemoglobin. In general, their action
increases with an increase with their electron-accepting
potency. Thus, some explosives of novel generation
(NTO, ANTA) may be less toxic to humans and other
mammalian species than TNT. The data of the present
work show that xanthine oxidoreductase and cytochromes
P-450 may be involved in the activation of explosives in
mammalian cells. Besides, some amino- metabolites of
TNT may be more efficient than expected
methemoglobinemia-inducing agents in erythrocytes.

Acknowledgements

This work was supported in part by the EC
Leonardo da Vinci Programme EUExcert and the
Agency for International Science and Technology
Development Programmes in Lithuania (COST Action
CM-0603).

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SPROGMENYS KAIP TOKSIKI APLINKOS TARALAI: UTERTUMO LAIPSNIS, TOKSIKUMAS IR
JO MECHANIZMAI

N. nas, A. Nemeikait-nien, A. Marozien, J. arlauskas, V. Vilutien, J. Baublys

S a n t r a u k a

Literatros apvalgoje analizuojami aplinkos utertumo sprogmen likuiais laipsnis, ir j toksikumas monms. Galima teigti, kad
tarp iuolaikini sprogmen maiausiai toksikas yra pentaeritritolio tetranitratas (PETN). Heksahidro-1,3,5-trinitro-1,3,5-triazino
(RDX) poveikis monms nra aikus. Kadangi 2,4,6-trinitrotoluenas (TNT) yra labiausiai paplits sprogmuo, jo sukeliami toksiniai
efektai (methemoglobinemiia, katarakta, kepen sutrikimai) yra detaliauisiai aprayti. TNT ir kit nitroaromatini sprogmen
citotoksikumo mechanizmai yra flavinini ferment katalizuojama vien- ir/ar dvielektronin redukcija (laisvj radikal cikliniai
redoks procesai ir/ar alkilinani hidroksilamin susidarymas), ir tiesiogin oksihemoglobino oksidacija. Kaip taisykl,
nitroaromatini jungini toksikumas didja, didjant j elektronoakceptorinms savybms. Todl kai kurie naujos kartos
sprogmenys, pvz. 5-nitro-1,2,4-triazol-3-onas (NTO), 5-nitro-1,2,4-triazol-3-aminas gali bti maiau toksiki mogui ir kitiems
induoliams nei TNT. io darbo eksperimentiniai duomenys rodo, kad nitroaromatini sprogmen aktyvacijoje lstelje dalyvauja ir
ksantinoksidoreduktaz, bei citochromai P-450. Be to, paaikjo, kad kai kurie TNT amino metabolitai netiktai gali labai efektyviai
sukelti methemoglobino susidarym eritrocituose.

Raktiniai odiai: sprogstamosios mediagos, toksikumas, poveikio mechanizmas, methemoglobinas, oksihemoglobinas.

KAK T : ,


. , . -, . , . , . , .



(),
, . , (PETN)
. -1,3,5--1,3,5- (RDX) .
2,4,6- (TNT) ,
(, , ) . TNT
-
( ),
. ,
. , . 5--1,2,4--3- (NTO), 5-
-1,2,4--3- TNT. ,
P-450. ,
, - TNT
.



Narimantas nas
Biochemijos institutas, Ksenobiotik biochemijos skyrius, Mokslinink 12, LT-08662 Vilnius
Telefonas: (8 5) 272 90 42
El. patas: ncenas@bchi.lt


Aura Nemeikait-nien
Generolo Jono emaiio Lietuvos karo akademija, Taikomj moksl katedra, ilo 5a, LT- 10322 Vilnius
Telefonas: (8 5) 210 35 65
El. patas ceniene@imi.lt


Jonas arlauskas
Biochemijos institutas, Ksenobiotik biochemijos skyrius, Mokslinink 12, LT-08662 Vilnius
Telefonas: (8 5) 272 90 42
El. patas: hidrazon@bch.lt
EUExcert nacionalinis koordinatorius Lietuvai


Audron Marozien
Biochemijos institutas, Ksenobiotik biochemijos skyrius, Mokslinink 12, LT-08662 Vilnius
Telefonas: (8 5) 272 90 42
El. patas: hidrazon@bchi.lt


Valentina Vilutien
Generolo Jono emaiio Lietuvos karo akademija, Ininerins vadybos katedra, ilo 5a, LT- 10322 Vilnius
Telefonas: (8 5) 210 35 52
Faksas: (8 5) 212 73 18
El. patas: ivk@lka.lt
Atsakinga u korespondencij su urnalo redakcijos kolegija



Juozas Baublys
Generolo Jono emaiio Lietuvos karo akademija, Ininerins vadybos katedra, ilo 5a, LT- 10322 Vilnius
Telefonas: (8 5) 210 35 52
Faksas: (8 5) 212 73 18
El. patas: juozas.baublys@lka.lt