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Title
Evidence for peroxynitrite as an oxidative stress-inducing compound
of
aqueous cigarette smoke fractions.
Author
Muller T; Haussmann HJ; Schepers G
Address
INBIFO Institut f ur biologische Forschung GmBH' K oln' Germany.
Source
Carcinogenesis, 18(2):295-301 1997 Feb
Abstract
Previous studies have shown that exposure of Swiss 3T3 cells
to
mainstream cigarette smoke (CS) trapped in phosphate-buffered
saline
(smoke-bubbled PBS) resulted in the expression of stress response
genes' i.e. haem oxygenase and c-fos' partial inhibition of protein
phosphatases 1 and 2A' as well as partial depletion of the cellular
glutathione (GSH) pool. Using c-fos gene expression in Swiss
3T3 cells
as an indicator for a cellular response against oxidative stress'
the
following observations are consistent with peroxynitrite as an
active
principal formed by CS in aqueous solutions: (i) sustained c-fos
expression was obtained for smoke-bubbled PBS' peroxynitrite
itself and
a compound known to stoichiometrically release superoxide and
nitric
oxide (NO) (3-morpholino-sydnonimine' SIN-1); (ii) c-fos expression
in
cells exposed to aqueous smoke fractions was inhibited by either
the
superoxide-scavenging enzyme superoxide dismutase (SOD)' in combination
with catalase' or the NO-scavenger oxyhaemoglobin (HbO2); and
(iii)
activation of guanylate cyclase in rat lung cells was observed
only
when bubbling was performed with filtered smoke and with whole
smoke in
the presence of SOD/catalase. These results are consistent with
a rapid
NO-consuming reaction coupled with superoxide-generating properties
of
the particulate phase of CS. Moreover' (iv) the half-life of
the
c-fos-inducing activity in smoke-bubbled PBS was found to be
<1 h which
can be explained by a sustained peroxynitrite formation. Finally'
depletion of intracellular thiol levels by smoke-bubbled PBS
appears to
favour the activation of a redox-sensitive component of the
c-fos-inducing pathway.
Title
Modulation by glutathione of DNA strand breaks induced by
4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and its aldehyde
metabolites in rat hepatocytes.
Author
Demkowicz-Dobrzanski K; Castonguay A
Address
Laboratory of Cancer Etiology and Chemoprevention' School of
Pharmacy'
Laval University' Quebec City' Canada.
Source
Carcinogenesis, 13(8):1447-54 1992 Aug
Abstract
Activation of the tobacco carcinogen
4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) produced
methylating species and two aldehydes: formaldehyde and
4-oxo-4-(3-pyridyl)-butanal (OPB). We investigated the modulation
by
glutathione of single-strand breaks (SSB) generated by
N-methyl-N-nitrosourea (MNU) and the two aldehydes. Hepatocytes
were
simultaneously exposed to 0.2 mM MNU and to 0-2.00 mM formaldehyde
or
OPB for 4 h. Both aldehydes induced SSB in a dose-dependent manner.
Formaldehyde and OPB exerted a synergistic effect on the formation
of
DNA SSB by MNU. It is postulated that both aldehydes interfere
with DNA
repair processes and thus increase the genotoxic effect of DNA
methylating species. We investigated whether glutathione (GSH)
could
protect DNA from NNK-derived intermediates. Formaldehyde (2 mM)
and OPB
(2 mM) decreased intracellular GSH contents to 60 and 86% of
control
respectively. DL-Buthionine-[S'R -sulfoximine (BSO) treatment
reduced
the GSH contents of hepatocytes to 19% of control but did not
reduce
the content of cytochrome P450 nor the metabolism of NNK. The
frequency
of DNA SSB induced by NNK' formaldehyde or OPB was significantly
higher
in GSH-depleted hepatocytes. GSH repletion with GSH monoethyl
ester
returned NNK-induced SSB to its initial frequency. OPB but not
NNK nor
formaldehyde induced double-strand breaks. We conclude that OPB
and
formaldehyde inhibit the repair of DNA damage induced by methylating
species and that GSH reduces the level of DNA damage induced
by
NNK-derived reactive metabolites.
Title
The role of glutathione in the acute nephrotoxicity of sodium
dichromate.
Author
Na KJ; Jeong SY; Lim CH
Address
Korea Ginseng and tobacco Research Institute' TaeJon.
Source
Arch Toxicol, 66(9):646-51 1992
Abstract
Ascorbate treatment 30 min prior to sodium dichromate (20 or
30 mg/kg'
s.c.) shows higher potency than that of glutathione (GSH) in
protecting
against both the metabolic disturbance and nephrotoxicity induced
by
dichromate. However' ascorbate treatment after 2 h of dichromate
intoxication had no effect on dichromate-induced blood urea nitrogen
(BUN) elevation 3 days after intoxication. In contrast'
dichromate-induced glucosuria' which reached maximum levels at
3 days
after treatment' was significantly decreased by GSH or N-acetyl
cysteine (NAC) treatment' even if its administration was after
24 h of
dichromate intoxication. Pretreatment with GSH depletors such
as
diethyl maleate (DEM) and buthionine sulfoximine (BSO) had no
effect on
dichromate-induced nephrotoxicity. GSH levels in the liver and
kidney
were not affected at 3 h after dichromate treatment. However'
dichromate significantly increased tissue GSH levels with a marked
increase in liver per kidney GSH ratio at 24 h after treatment'
if food
was withheld subsequent to dichromate treatment' indicating that
GSH
biosynthesis resulted from the accelerated protein breakdown.
These
results suggest that GSH-mediated dichromate reduction is not
a
kinetically favorable pathway in vivo; however' GSH plays an
important
role in protection against dichromate-induced nephrotoxicity.
In
addition' the cellular metabolism of dichromate in the early
period
after treatment is important in the pathogenesis of its nephrotoxicity.
Title
Metabolic alterations produced by cigarette smoke in rat lung
and
liver' and their modulation by oral N-acetylcysteine.
Author
Bagnasco M; Bennicelli C; Camoirano A; Balansky RM; De Flora
S
Address
Institute of Hygiene and Preventive Medicine' University of Genoa'
Italy.
Source
Mutagenesis, 7(4):295-301 1992 Jul
Abstract
Male Sprague-Dawley rats were exposed whole-body to the mainstream
smoke produced by a commercial filter cigarette for 8 consecutive
days'
accounting for a cumulative exposure to the smoke of 75 cigarettes.
Liver and lung S12 fractions were used in the Salmonella mutagenicity
test in order to assess either the decrease of potency of a
direct-acting mutagen (sodium dichromate) or the metabolic activation
of promutagens' including cigarette smoke itself and its condensate'
benzo[a pyrene and its 7'8-diol' the aromatic amine 2-aminofluorene'
and the heterocyclic amine 3-amino-1-methyl-5H-pyrido(4'3)indole.
Moreover' individual biochemical parameters were measured in
the liver
and lung of the same rats and' in the case of cytochrome
P-450-dependent monooxygenases' also in the heart of untreated
or
Aroclor-treated rats. The monitored biochemical parameters included
aryl hydrocarbon (benzo[a pyrene) hydroxylase and ethoxyresorufin
deethylase in microsomal fractions' epoxide (benzo[a pyrene-4'5-oxide)
hydrolase in both microsomal and cytosolic fractions' glutathione
(GSH)
and GSH S-transferase in the cytosol. Exposure to cigarette smoke
resulted in a number of significant metabolic changes' as compared
to
sham-exposed rats. The most pronounced alterations consisted
in a
2.6-fold induction of aryl hydrocarbon hydroxylase in the lung
and
8-fold induction of ethoxyresorufin deethylase in the liver'
and in a
marked stimulation of the liver metabolic activation of all
promutagens. The last effect was inhibited by the oral administration
of the chemopreventive agent N-acetylcysteine. On the whole'
there was
a poor correlation between the monitored biochemical and mutagenicity
endpoints.(ABSTRACT TRUNCATED AT 250 WORDS)
Title
Cigarette smoke-induced alterations in the release of arachidonate
metabolites by pulmonary alveolar macrophage from selenium-fed
and
selenium-deficient rats.
Author
Gairola CG; Tai HH
Source
Biochem Pharmacol, 35(14):2423-8 1986 Jul 15
Abstract
Male weanling F-344 rats were maintained on selenium-supplemented
or
-deficient diets and were exposed to fresh cigarette smoke daily
for 28
weeks. The deficient status of animals was demonstrated by a
significant reduction in the pulmonary and hepatic glutathione
peroxidase (GSH-Px) activity of rats on selenium-deficient diet.
Sham
and smoke treatment did not influence the GSH-Px activity in
either
diet group. Elevated levels of blood carboxyhemoglobin and pulmonary
aryl hydrocarbon hydroxylase activity in the smoke-exposed rats
of both
diet groups indicated effective inhalation of cigarette smoke
by
animals. Studies of the extracellular release of arachidonate
metabolites by pulmonary alveolar macrophages (PAMs) indicated
that
resting cells released small amounts of prostaglandin E2 (PGE2),
thromboxane B2 (TXB2) and leukotriene B4 (LTB4). Upon phagocytic
challenge by opsonized zymosan particles, the release of the
three
metabolites was substantially increased in all diet and treatment
groups. While the release of cyclooxygenase products, PGE2 and
TXB2,
remained unaffected by cigarette smoke, an inhibition of approximately
50% in the release of lipoxygenase product, LTB4, was observed
in cells
from selenium-fed animals. In selenium-deficient animals, cigarette
smoke almost completely inhibited (greater than 80%) the
zymosan-stimulated release of LTB4 by PAMs and additionally caused
about 50% reduction in TXB2 release. These results suggest a
specific
inhibition of lipoxygenase pathway by cigarette smoke in PAMs
of
selenium-fed rats and suggest that cigarette smoke may additionally
impair enzymes of the cyclooxygenase pathway in PAMs of
selenium-deficient animals.
Title
Hydroperoxide and cigarette smoke induced effects on lung mechanics
and
glutathione status in rat isolated perfused and ventilated lungs.
Author
Ryrfeldt A; Kröll F; Berggren M; Moldéus P
Address
Dept of Toxicology, Karolinska Institutet, Stockholm, Sweden.
Source
Life Sci, 42(15):1439-45 1988
Abstract
The effects of t-butylhydroperoxide (TBH) and cigarette smoke
on lung
mechanics (CDYN and RL) and glutathione status (GSH) were studied
using
an isolated perfused and ventilated rat lung preparation. TBH
(200,
400, 1000 microM) infused via the pulmonary circulation caused
a
dose-related bronchoconstriction. The lung GSH-levels were also
significantly reduced. Pretreatment of rats with diethylmaleate
(DEM)
potentiated the TBH elicited bronchoconstriction. DEM (1 mM)
infused
into the pulmonary circulation caused an almost complete depletion
of
GSH-content but no effects on lung mechanics were seen. Indomethacin
(2.8 and 28 microM) infusion attenuated TBH (400 microM) induced
bronchoconstriction. These findings suggest that the TBH induced
bronchoconstriction is at least partly mediated via arachidonic
acid
metabolites. When TBH was administered intratracheally, weak
and not
dose-related bronchoconstriction was observed even though doses
higher
than those given intravascularly were used. However, the GSH-content
of
the lungs was markedly decreased. Cigarette smoke caused weak
if any
effects on lung mechanics but significantly decreased lung GSH-content.
Title
Modulatory potential of smokeless tobacco on the garlic' mace
or black
mustard-altered hepatic detoxication system enzymes' sulfhydryl
content
and lipid peroxidation in murine system.
Author
Singh A; Singh SP
Address
School of Life Sciences' Jawaharlal Nehru University' New Delhi'
India.
Source
Cancer Lett, 118(1):109-14 1997 Sep 16
Abstract
The present study evaluates the potential of smokeless tobacco
to
modify the chemopreventive efficacy of minor dietary constituents'
including garlic' mace or black mustard' via modulating the competing
pathways of hepatic detoxication system and antioxidant defense
mechanism in murine system. Garlic (100 mg/kg b.w. per day) by
gavage
and mace (1% w/w) or black mustard (1% w/w) in diet induced a
significant increase in the levels of glutathione-S-transferase
(GST)'
acid-soluble sulfhydryl (-SH)' cytochrome b5 (Cyt.b5) and cytochrome
P-450 (Cyt.P-450) in murine liver. The hepatic levels of GST
and -SH
were significantly depressed whereas microsomal Cyt.b5' Cyt.P-450
and
MDA levels were elevated in groups treated with smokeless tobacco
(50
or 100 mg/kg b.w. per day). The data revealed the inhibitory
potential
of smokeless tobacco on garlic-induced hepatic GST/GSH system
besides
the significant augmentation by smokeless tobacco on garlic or
mace or
black mustard-induced microsomal cytochromes. The possible implications
of modulation in competing bioactivation and detoxication pathways
in
the process of chemical carcinogenesis are discussed.
Title
Erythrocyte glutathione and urinary thioethers in smokers (published
erratum appears in Med Clin (Barc) 1991 Feb 9;96(5):38)
Author
Sinu]es B; Rueda P; S]aenz MA; Bernal ML; Alcal]a A
Address
Departamento de Farmacolog]ia' Facultad de Medicina' Universidad
de
Zaragoza.
Source
Med Clin (Barc), 95(19):725-7 1990 Dec 1
Abstract
The carcinogenic mechanism of smoking is related with the production
of
electrophilic reactants and their possible covalent binding with
DNA.
On the other hand' there are detoxifying mechanisms such as
glutathione-S-transferase' which results in mercaptopuric derivatives
that are excreted in the urine. The integrity of the erythrocyte
membrane is maintained by reduced glutathione among other factors.
In
the present study' the concentrations of erythrocyte reduced
glutathione (GSH) and urinary thioethers (UT) were measured in
a sample
of 81 subJects divided in two groups. Group I: 30 nonsmokers;
group II:
51 smokers' subdivided in group IIA (26 individuals smoking 10-20
cigarettes/day) and group IIB (25 individuals smoking more than
20
cigarettes/day). In the present study' the usefulness of GSH
and UT as
markers of collective internal contamination and of individual
risk
regarding tobacco exposure were evaluated. A higher concentration
of
GSH was found in smokers than in nonsmokers (F = 6.84' p less
than
0.02). Regarding VT elimination' a significant increase in these
parameters was found in association with the grade of smoking
(p less
than 0.05). They were higher in the subJects from the subgroup
IIB than
in the subgroup IIA (moderate smokers).
Title
Cigarette smoke oxidation of human plasma constituents.
Author
Cross CE; O`Neill CA; Reznick AZ; Hu ML; Marcocci L; Packer L;
Frei B
Address
Division of Pulmonary and Critical Care Medicine' University
of
California' Davis 95616.
Source
Ann N Y Acad Sci, 686():72-89; discussion 89-90 1993 May 28
Abstract
In vitro exposure of fresh human plasma to cigarette smoke (CS)
was
used as a model for reactions that could be occurring in CS-exposed
respiratory tract lining fluids (RTLFs) and lung parenchyma.
The
central focus of this model was to characterize the consumption
of
endogenous plasma antioxidants in relationship to the appearance
of
oxidized proteins and lipids as a consequence of exposure to
CS' or to
aldehydes present in CS. The amelioration of CS-induced protein
and
lipid oxidation in plasma by the addition of selective exogenous
antioxidants was also assessed. We found that: (i) exposure of
human
plasma to gas phase CS causes both lipid peroxidation and protein
oxidation' and endogenous ascorbic acid protects against lipid'
but not
protein' oxidation; (ii) whole CS causes protein oxidation' but
does
not induce lipid peroxidation; (iii) addition to plasma of aldehydes
known to be present in CS causes protein damage' but does not
induce
either lipid peroxidation or oxidation of ascorbic acid; and
(iv)
exogenously added dihydrolipoic acid (DHLA) preserves ascorbic
acid
levels in plasma exposed to the gas phase of CS' and protects'
to some
extent' against lipid peroxidation; DHLA also protects against
protein
oxidation' whereas added glutathione (GSH) only protects against
protein' but not lipid' oxidation.
Title
Probucol inhibits tobacco smoke-induced decrease in plasma
anti-elastase activity and ferroxidase activity in rats
Author
Kishi Y; Ishizaki T; Sasaki F; Takahashi H; Ameshima S; Nakai
T; Miyabo
S
Address
Department of Internal Medicine' Fukui Medical School' Japan.
Source
Nippon Kyobu Shikkan Gakkai Zasshi, 30(4):585-92 1992 Apr
Abstract
Elastolytic enzymes and active oxygen species derived from leukocytes
and alveolar macrophages during exposure to tobacco smoke' together
with active oxygen species directly derived from tobacco smoke'
are
thought to play a crucial role in the pathogenesis of pulmonary
emphysema by inactivating alpha 1 protease inhibitor (alpha 1
PI)' a
novel anti-elastase. We studied the inhibitory effect of probucol'
an
oral hypocholesterolemic agent' on tobacco smoke-induced decrease
in
plasma anti-elastase activity (EIA) and ferroxidase activity
(FA) in
conscious venous catheter instrumented rats. Rats exposed to
the smoke
of 5 cigarettes (nicotine 11 mg' tar 115 mg) in a plastic chamber
showed a prompt increase in plasma COHb to 17.9 +/- 2.7%' and
a prompt
decrease in plasma EIA by -17.9% (p less than 0.05) and FA by
-14.8% (p
less than 0.01)' which lasted for 6 hours after exposure. Rats
administered probucol (1% probucol in food) for 3 days showed
normal
cholesterol plasma levels' and rats administered probucol for
4 weeks
showed hypocholesterolemic plasma levels. EIA and FA were not
depressed
after smoking' and lipid peroxide product (TBA reactive substance)
in
lung tissue (p less than 0.05) and serum (p less than 0.1) showed
a
smaller increase in association with a smaller decrease in the
ratio of
lung tissue GSH/GSSG (p less than 0.01) compared with control
rats.
These results indicate that probucol' via its antioxidant action
rather
than its cholesterol lowering effect' has a protective effect
on lung
exposed to tobacco smoke in terms of protease-antiprotease balance
and
oxidant-antioxidant balance.
Title
The kinetic characteristics of the erythrocyte glutathione
S-transferase system as a function of sex and the tobacco habit
Author
Ort]in F; Giralt M; Cervell]o I; Nogu]es MR; Puerto AM; Argany
N;
Mallol J
Address
Unidad de Farmacolog]ia' Facultad de Medicina' Universidad Rovira
i
Virgili' Reus' Tarragona.
Source
Med Clin (Barc), 106(16):607-10 1996 Apr 27
Abstract
BACKGROUND: Erythrocytic glutathion S-transferase (GST) plays
an
important role as a protective mechanism against oxidative stress.
The
present study was conducted to evaluate the influence of both
smoking
habit and sex upon the kinetic characteristics of the enzyme.
SUBJECTS
AND METHODS: 176 healthy subJects (100 men and 76 women)' smokers
and
nonsmokers' were included. Enzyme parameters were calculated
in
erythrocytic haemolysates using 1-chloro-2'4-dinitrobenzene (CDNB)
and
glutathion (GSH) as substrates. Haemoglobin (Hb) was removed
by
affinity chromatography. In samples coming from 51 men and 42
women the
native haemolysate was subJected to thermal shock (52 degrees
C) and
the enzyme parameters were compared with those obtained in the
non-denatured samples. RESULTS: In non-denatured samples' Km
(mM) and
Vmax (mumol/min/g Hb) values for CDNB were significantly higher
(p <
0.001) in smokers than in non smokers' especially in women. Thus'
respectively for Km and Vmax (mean +/- standard deviation): for
men non
smokers' 1.43 +/- 0.54' 1.63 +/- 0.42 and smokers' 1.74 +/- 0.5'
1.8
+/- 0.69; for women' non smokers 1.42 +/- 0.56' 1.57 +/- 0.46
and
smokers' 2.05 +/- 0.59' 2.51 +/- 0.6. Thermal denaturation diminished
the enzyme activity in all cases and modified the Km values'
these
results were opposite to those obtained in the non-denatured
samples.
Thus' for Km and Vmax respectively: for men' smokers' 1.6 +/-
0.71 and
0.9 +/- 0.32 and non smokers' 1.4 +/- 0.66 and 0.53 +/- 0.29;
for
women' non smokers' 2.00 +/- 0.58' 1.13 +/- 0.29 and smokers
1.22 +/-
0.77' 0.52 +/- 0.23. The GSt content was similar in the four
groups
studied (3.75 +/- 1.15 mumol SH/g Hb). CONCLUSIONS: The greater
thermolability of GST activity and the increase in the Km values
observed in smokers' especially in women' should be considered
as
indicative of an increased risk for the erythrocytes against
oxidative
stress.
Title
Use of transgenic plants to study antioxidant defenses.
Author
Allen RD; Webb RP; Schake SA
Address
Department of Biological Sciences' Texas Tech University' Lubbock
79409' USA. brrda@ttu.edu
Source
Free Radic Biol Med, 23(3):473-9 1997
Abstract
The abundance of O2 and the highly energetic electron transfer
reactions associated with thylakoid membranes make chloroplasts
a maJor
source of reactive oxygen intermediates (ROI) in photosynthetic
tissues
of plants. Attempts to reduce oxidative damage in chloroplasts
have
included the manipulation of ROI-scavenging enzymes by gene transfer
technology. Much of this work has focused on chloroplast-localized
superoxide dismutase (SOD)' both chloroplast-targeted and cytosolic
ascorbate peroxidase (APX) and glutathione reductase (GR). Increased
activity of SOD in chloroplasts of transgenic tobacco plants
generally
leads to increased protection from membrane damage caused by
exposure
to methyl viologen (MV). In addition' overexpression of chloroplastic
Cu/Zn SOD can lead to increased protection from photooxidative
damage
caused by high light intensity and low temperatures. Transgenic
tobacco
plants that overexpress APX either in the cytosol or chloroplastic
compartments also show reduced damage following either MV exposure
or
photooxidative treatment and transgenic plants that express increased
levels of GR have elevated pools of ascorbate and GSH. Though
still
preliminary' these results clearly indicate that alterations
in the
expression of enzymes involved in ROI-scavenging can have significant
metabolic effects and provide the hope that this strategy can
be used
to develop crop plants with increased stress tolerance.
Title
Species difference in intestinal drug metabolising enzymes in
mouse'
rat and hamster and their inducibility by masheri' a pyrolysed
tobacco
product.
Author
Nair UJ; Ammigan N; Kulkarni JR; Bhide SV
Address
Carcinogenesis Division' Tata Memorial Centre' Bombay' India.
Source
Indian J Exp Biol, 29(3):256-8 1991 Mar
Abstract
Activities of several drug metabolising enzymes in the small
intestine
were investigated in Swiss mice' Sprague Dawley rats and Syrian
Golden
Hamsters fed 10% masheri' a pyrolysed tobacco product' in diet'
for 20
months. The basal levels of enzymes in proximal (PI)' medium
(MI) and
distal (DI) parts of the intestine in the three species were
similar.
However' the levels of cytochrome P-450' benzo(a) pyrene hydroxylase
(B(a)OH) and glutathione S-transferase (GST) were highest in
hamsters
followed by rat and mice. Upon treatment with masheri' significant
induction of cytochrome P-450 and B(a)PH was observed in PI and
DI of
all the three species. However' GSH and GST was depleted upon
masheri
treatment in all the three species again only in proximal and
distal
parts of the intestine. Thus increase in activating enzymes together
with depletion in GSH-GST system upon exposure could be an important
factor in the susceptibility of the small intestine to hazardous
xenobiotic exposure.
Title
Postnatal effect of smokeless tobacco on phytic acid or the butylated
hydroxyanisole-modulated hepatic detoxication system and antioxidant
defense mechanism in suckling neonates and lactating mice.
Author
Singh A; Singh SP
Address
Human Genetics Laboratory, School of Life Sciences, Jawaharlal
Nehru
University, New Delhi, India.
Source
Cancer Lett, 122(1-2):151-6 1998 Jan 9
Abstract
The present study evaluates the potential of smokeless tobacco
to
translactationally modify the chemopreventive efficacy of phytic
acid
and butylated hydroxyanisole (BHA) via modulation of the hepatic
xenobiotic detoxication system and antioxidant defense mechanism
in the
murine system. Phytic acid (1000 mg/kg b.w./day) by gavage while
BHA
(1% w/w) in diet induced a significant increase in the levels
of
glutathione-S-transferase (GST), acid soluble sulfhydryl (-SH),
cytochrome b5 (Cyt. b5) and cytochrome P-450 (Cyt. P-450) in
lactating
dams and suckling pups. The hepatic levels of GST and -SH were
significantly depressed whereas microsomal Cyt. b5, Cyt. P-450
and MDA
levels were elevated in groups treated with smokeless tobacco
(50 or
100 mg/kg b.w./day). The data reveals the inhibitory potential
of
smokeless tobacco on phytic acid-induced GST/GSH system efficiency
besides the significant augmentation by smokeless tobacco on
phytic
acid or BHA-induced microsomal phase I enzymes. The direct or
translactational modulation in the levels of xenobiotic detoxication
system enzymes suggests the potential of smokeless tobacco to
modify
the chemopreventive efficacy of phytic acid or BHA. |
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