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Life Sciences 78 (200
Effect of bacoside A on brain antioxidant status
in cigarette smoke exposed rats
K. Anbarasi a, G. Vani a, K. Balakrishna b, C.SR Shyamala Devi c,*
a Department of Biochemistry, University of Madras, Guindy Campus, Chennai-600 025, Indiab Central Research Institute (Siddha), Chennai-600 106, India
c Department of Biochemistry, University of Madras, Guindy Campus, Chennai-600 025, India
Received 30 March 2005; accepted 11 July 2005
Abstract
Free radicals mediated oxidative stress has been implicated in the pathogenesis of smoking-related diseases and antioxidant nutrients are
reported to prevent the oxidative damage induced by smoking. Therefore, the present study was conducted to evaluate the antioxidant role of
bacoside A (triterpenoid saponin isolated from Bacopa monniera) against chronic cigarette smoking induced oxidative damage in rat brain. Adult
male albino rats were exposed to cigarette smoke for a period of 12 weeks and simultaneously administered with bacoside A (10 mg/kg b.w./day,
p.o.). Antioxidant status of the brain was assessed from the levels of reduced glutathione, vitamin C, vitamin E, and vitamin A and the activities of
superoxide dismutase, catalase, glutathione peroxidase and glutathione reductase. The levels of copper, iron, zinc and selenium in brain and serum
ceruloplasmin activity were also measured. Oxidative stress was evident from the diminished levels of both enzymatic and non-enzymatic
antioxidants. Alterations in the levels of trace elements with accumulation of copper and iron, and depletion of zinc and selenium were also
observed. Bacoside A administration improved the antioxidant status and maintained the levels of trace elements. These results suggest that
chronic cigarette smoke exposure enhances oxidative stress, thereby disturbing the tissue defense system and bacoside A protects the brain from
the oxidative damage through its antioxidant potential.
D 2005 Elsevier Inc. All rights reserved.
Keywords: Antioxidants; Bacoside A; Bacopa monniera; Cigarette smoking; Lipid peroxidation; Oxidative stress; Trace elements
Introduction
There is a preponderance of evidence showing a strong
association between cigarette smoking and alarming increase
in the mortality rate from smoking-related diseases such as
pulmonary diseases, cardio and cerebrovascular diseases,
cancers, and several others (US DHHS, 1989). The role of
free radicals in the pathogenesis of these diseases has been
well documented (Church and Pryor, 1985). Formation of
free radicals and reactive oxygen species (ROS) is a normal
consequence of a variety of biochemical reactions. However,
0024-3205/$ - see front matter D 2005 Elsevier Inc. All rights reserved.
doi:10.1016/j.lfs.2005.07.030
* Corresponding author. Old No. 62, New No. 66, Second main road, Gandhi
Nagar, Adyar, Chennai-600 020, India. Tel.: +91 44 2441 2575; fax: +91 44
2235 2494.
E-mail addresses: [email protected] (K. Anbarasi),
[email protected] (C.S.S. Devi).
these free radicals are capable of independent existence and
can cause oxidative damage to the tissues through lipid
peroxidation (Cross et al., 1987). The human body has an
inherent synergistic and multilevel defense mechanism,
which comprise of two major classes of cellular protection
against ROS (Muzakova et al., 2001). The enzymatic part is
represented by free radical scavenger enzymes namely
superoxide dismutase, catalase and glutathione peroxidase.
The non-enzymatic part includes a large number of natural
and synthetic antioxidant compounds (e.g. vitamins, thiols
etc.) that have the ability to inhibit oxidative stress by
scavenging the highly destructive free radical species. The
deleterious effects of the free radicals are kept under check
by a delicate balance between the rate of their production
and the rate of their elimination by these defense systems
(Halliwell, 1994). When there is an excessive addition of
free radicals from exogenous sources added to the endog-
enous production, the available tissue defense system
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K. Anbarasi et al. / Life Sciences 78 (2006) 1378–1384 1379
becomes overwhelmed resulting in oxidative damage to the
tissues.
A major exogenous source of free radicals is cigarette
smoke which is a heterogeneous aerosol consisting of more
than 4000 compounds including high concentrations of free
radicals, and reactive oxygen and nitrogen species (Stedman,
1968). The obligatory use of the body’s reserve of antioxidants
to detoxify the tremendous level of these free radicals in
smokers therefore results in severe antioxidant deficiency
status, thereby predisposing them to the development of life
threatening diseases. Further, this deficiency in smokers may
be enhanced by their generally lower intake of both supple-
mentary and dietary antioxidants (Zondervan et al., 1996).
When the normal level of antioxidant defense system is
insufficient for the eradication of excessive free radicals,
administration or supplementation of exogenous antioxidants
has a protective role to play (Rekha et al., 2001). Several
micronutrients and antioxidants of natural origin have been
experimentally proved as effective protective agents against
smoking induced oxidative stress (Sohn et al., 1993; Dilsiz et
al., 1999; Helen et al., 1999; Koul et al., 2001). In view of the
antioxidant property of Bacopa monniera (Tripathi et al.,
1996), the effect of bacoside A, which retains the biological
activity of Bacopa monniera, on the antioxidant defense
system in rat brain has been investigated (Anbarasi et al.,
2003).
Bacoside A is the dammarene type triterpenoid saponin
isolated from the plant Bacopa monniera, which is held in high
repute as a potent nerve tonic (Chopra et al., 1956). Bacopa
monniera Linn. is used in the indigenous systems of medicine
for the treatment of various nervous system ailments such as
insomnia, anxiety, epilepsy, hysteria etc. (Nadkarni, 1976).
Preclinical and clinical studies have shown that B. monniera
improves memory and mental function (Roodenrys et al., 2002;
Stough et al., 2001). The plant has been shown as a potent free
radical scavenger and antioxidant (Tripathi et al., 1996).
Besides it also exhibits vasodilatory (Channa et al., 2003),
calcium antagonistic (Dar and Channa, 1999) and muscle
relaxant (Dar and Channa, 1997) properties. Preliminary
studies indicated that bacosides, the major saponins are
responsible for the facilitatory and modulatory effects of B.
monniera (Singh et al., 1988).
Recently, we have demonstrated the protective effect of
bacoside A against smoking induced toxicity in rat brain
(Anbarasi et al., 2005a,b). The brain is exposed throughout the
life to oxidative stress and a number of diseases of the brain
have been hypothesized to involve free radical induced
oxidative damage either as a cause or as consequence of the
disease processes. This organ is highly susceptible to free
radical attack because it generates more of these toxicants per
gram of tissue than does any other organ and yet not
particularly enriched with protective antioxidants (Arivazhagan
et al., 2002). Hence, the present study was undertaken to assess
the neuroprotective role of bacoside A against oxidative stress
in the brain of rats exposed to cigarette smoke by measuring
the enzymatic and non-enzymatic antioxidants, and trace
elements.
Materials and methods
Chemicals and reagents
Reduced glutathione, epinephrine, NADPH, ascorbic acid
and a-tocopherol were obtained from Sigma Chemical
Company, St. Louis, MO, USA. All other chemicals and
reagents used were of reagent grade and highest purity, and
obtained from Himedia, Mumbai, India. Standard bacoside A
was purchased from Natural Remedies Private Limited,
Bangalore, India. Locally available brand of cigarette,
Scissors Standard (W.D & H.O. Wills), manufactured by
Hyderabad Deccan Cigarette Factory was used in the present
study.
Bacoside A
The plant Bacopa monniera was collected in and around
Chennai, India and authenticated by Dr. P. Brindha, Central
Research Institute (Siddha), Chennai, India. The dammarane
type triterpenoid saponin-bacoside A was isolated from the
plant by the standard procedure followed by Singh et al.
(1988). The purity of the isolated bacoside A was identified
by thin layer chromatography (TLC) and infrared (IR)
spectrum analysis using standard bacoside A (data not
shown). Aqueous suspension of bacoside A in 1% gum
acacia was given orally to the experimental animals at a
dosage of 10 mg/kg b.w./day for 12 weeks. Control animals
received a corresponding volume of the vehicle suspended in
normal saline.
Animals
Adult male albino rats of Wistar strain (120–200 g)
procured from Tamilnadu University of Veterinary and Animal
Sciences (TANUVAS), India were used for the present study.
The rats were provided with standard pelleted rat feed and
water ad libitum. They were acclimatized to the laboratory
conditions and maintained under 12 h light and dark cycles at
25T2 -C. The experiments were carried out in accordance with
the guidelines provided by the Institutional Animal Ethical
Committee (No. IAEC 01/037/04).
Experimental design
The animals were divided into four groups of 6 animals
each. Group I—control. Group II—rats exposed to cigarette
smoke. Group III—rats administered with bacoside A (10 mg/
kg b.w./day, p.o.). Group IV—rats exposed to cigarette smoke
and simultaneously administered with bacoside A. Group II
and Group IV rats were exposed to cigarette smoke for a
period of 12 weeks as described earlier (Anbarasi et al.,
2005c).
Briefly, the rats were exposed to side stream cigarette smoke
in whole body smoke exposure chamber. Cigarette smoke was
exposed twice daily, the duration of each exposure was 3 h with
an interval of 10 min between each cigarette, using 8–10
Table 2
Levels of reduced glutathione (GSH), vitamin C, vitamin E, and vitamin A in
the brain of control and experimental animals
Parameters Group I Group II Group III Group IV
GSH 6.06T0.24 3.82T0.28* 6.50T0.35@ 5.92T0.20*
Vitamin C 1.56T0.15 0.61T0.10* 1.58T0.08NS 1.41T0.13*Vitamin E 5.21T0.30 3.30T0.32* 5.32T0.26NS 4.89T0.25*
Vitamin A 0.154T0.02 0.102T0.01* 0.157T0.02NS 0.146T0.02*
(Values are expressed as meanTSD, n =6).
Unit GSH: Amoles/mg protein.
Vitamins C, E, and A: mg/g wet tissue.
Statistical comparisons are made between Group I vs. Group II and Group III
Group II vs. Group IV.
*—p <0.001, @—p <0.05, NS—non significant.
K. Anbarasi et al. / Life Sciences 78 (2006) 1378–13841380
cigarettes per day. The same brand of locally available cigarette
was used throughout the experiment (Scissors Standard).
At the end of experimental period (12 weeks), the animals
were killed by cervical decapitation. Blood was collected and
serum separated by centrifugation. Brain tissue was excised
carefully and immediately washed in ice-cold saline. A 10%
(w/v) homogenate was prepared in 0.1 M Tris–HCl, pH 7.4
and used for biochemical studies.
Biochemical analysis
Superoxide dismutase was assayed by the method of Misra
and Fridovich (1972). One unit of the enzyme activity is
defined as the amount of enzyme required for the autooxida-
tion of epinephrine by 50% per minute. Catalase activity was
measured by following decomposition of H2O2 according to
the method of Beers and Sizer (1952). The activity of
glutathione peroxidase was assayed by measuring the amount
of GSH consumed in the reaction mixture by the method of
Rotruck et al. (1973). Glutathione reductase, which utilizes
NADPH to convert oxidized GSH to reduced form, was
assayed by the method of Stall et al. (1969). Protein was
estimated by the method of Lowry et al. (1951). Reduced
glutathione was measured according to the procedure of
Moron et al. (1979) using DTNB reagent. Vitamin C was
measured according to the method of Omaye et al. (1979)
using DTC reagent. Vitamin E was measured according to the
method of Quaife and Dju (1948) using dipyridyl reagent and
vitamin A was measured by the method of Otto et al. (1946).
Serum ceruloplasmin activity was assayed by following the
procedure as described by Ravin (1961). Copper, zinc and iron
was estimated using atomic absorption spectrophotometer
after digestion with nitric acid and perchloric acid and
selenium using coupled atomic emission spectrophotometer
and flurometer.
Statistical analysis
Results are expressed as meanTSD (n =6). Student’s t-test
was used for the statistical evaluation of the data obtained.
Table 1
Activities of superoxide dismutase (SOD), catalase (CAT), glutathione
peroxidase (GPx) and glutathione reductase (GR) in the brain of control and
experimental animals
Parameters Group I Group II Group III Group IV
SOD 2.84T0.13 1.17T0.20* 3.12T0.14# 2.70T0.15*
CAT 10.26T2.2 4.25T2.0* 13.52T1.20# 9.78T1.80*GPx 4.75T .022 2.19T0.34* 5.14T0.20# 4.42T0.32*
GR 0.81T0.03 0.58T0.02* 0.87T0.05# 0.78T0.03*
(Values are expressed as meanTSD, n =6).
Units: SOD: units/mg protein.
CAT: Amoles of H2O2 decomposed/min/mg protein.
GPx: Amoles of GSH oxidized/min/mg protein.
GR: Amoles of NADPH oxidized/min/mg protein.
Statistical comparisons are made between Group I vs. Group II and Group III;
Group II vs. Group IV.
*—p <0.001, #—p <0.01, NS—non significant.
Table 3
Serum ceruloplasmin (CP) activity and the levels of copper (Cu), iron (Fe), zinc
(Zn), and selenium (Se) in the brain of control and experimental rats
Parameters Group I Group II Group III Group IV
CP 38.42T2.9 17.53T2.5* 39.50T3.0NS 35.25T3.2*Cu 13.2T3.2 24.5T2.8* 12.6T3.4NS 15.0T3.0*
Fe 268.12T15.6 358.33T12.1* 263.46T14.3NS 282.58T15.2*
Zn 0.89T0.02 0.57T0.01* 0.92T0.04NS 0.85T0.05*
Se 12.6T2.2 5.50T2.0* 12.8T3.2NS 11.8T2.5*
(Values are expressed as meanTSD, n =6).
Units: CP: units/mg protein.
Cu, Fe, Zn, Se: Ag/g wet tissue.
Statistical comparisons are made between Group I vs. Group II and Group III
Group II vs. Group IV.
*—p <0.001, NS—non significant.
;
Statistical comparisons are made between Group I vs. Group II
and Group III; Group II vs. Group IV.
Results
The activities of superoxide dismutase, catalase, glutathione
peroxidase, and glutathione reductase in brain of control and
experimental animals are summarized in Table 1. A significant
decrease (P <0.001) in the activities of the antioxidant
enzymes was observed in Group II rats exposed to cigarette
smoke compared to Group I rats. Group IV rats showed
increased (P <0.001) activities of these enzymes as compared
to Group II rats. Bacoside A per se administered Group III rats
showed a significant (P <0.01) increase in their activities as
compared to Group I rats which shows the enzymatic activation
of antioxidants by bacoside A.
Table 2 shows the levels of reduced glutathione, vitamin C,
vitamin E, vitamin A in the brain of control and experimental
animals. Group II rats exposed to cigarette smoke showed a
significant decrease (P <0.001) in the levels of glutathione and
vitamins C, E, and A when compared to control rats. A
significant increase (P <0.001) in the levels of the non-
enzymatic antioxidants was observed in Group IV rats when
compared to Group II rats. Group III rats administered with
bacoside A alone registered an increase (P <0.05) in GSH
levels with no significant changes in other parameters as
compared with Group I rats.
;
K. Anbarasi et al. / Life Sciences 78 (2006) 1378–1384 1381
Serum ceruloplasmin activity and the levels of copper, iron,
zinc, and selenium in the brain of control and experimental rats
are shown in Table 3. The activity of ceruloplasmin, and the
levels of zinc and selenium were significantly decreased
(P <0.001), while the levels of copper and iron were
significantly increased (P <0.001) in cigarette smoke exposed
to Group II rats compared to Group I rats. The levels of copper
and iron were significantly decreased (P <0.001) and the levels
of zinc, selenium and ceruloplasmin activity were significantly
increased (P <0.001) in Group IV rats compared to Group II
rats. No significant changes were observed in these parameters
in Group III rats compared to Group I rats.
Discussion
The brain is extremely vulnerable to oxidative stress, in part
because it is highly enriched with non-heme iron, which is
catalytically involved in the production of oxygen free radicals.
In addition, the brain contains a relatively high degree of
polyunsaturated fatty acids that are particularly good substrates
for peroxidation reactions (Halliwell and Gutteridge, 1985).
Cigarette smoke is a complex milieu possessing an array of free
radicals and ROS, namely hydroxyl, peroxyl, nitric oxide, and
superoxide radicals (Pryor, 1997). The sustained release of
reactive free radicals from the tar and gas phases of smoke
imposes an oxidant stress, promotes lipid peroxidation and
consequently perturbs the antioxidant defense system in the
blood and tissues of smokers (Pryor and Stone, 1993).
Modulation of antioxidant status by increased lipid peroxida-
tion during exposure to cigarette smoke has been reported in
various organs (Baskaran et al., 1999; Chitra et al., 2000;
Delibas et al., 2003). Our previous finding showed that
cigarette smoke exposure increased both basal and induced
lipid peroxidation in the rat brain (Anbarasi et al., 2005a).
Under an oxidative stress, the antioxidant enzyme levels are
increased, in order to cope with the tremendous increase in the
production of ROS (Gutteridge and Halliwell, 1994). Acute
exposure to cigarette smoke enhances the production of these
antioxidant enzymes as a result of adaptive response, which
consequently mitigate the damage caused by cigarette smoke
(Hilbert and Mohsenin, 1996). An increase in the activities the
antioxidant enzymes has been demonstrated upon exposure to
cigarette smoke for 4 weeks (Baskaran et al., 1999). However,
after prolonged exposure, the toxic effects of cigarette smoke
appear to override the adaptive mechanism of the body tissues,
as indicated by a decrement in the levels of these enzymes
(Hulea et al., 1995). Our results are in corroboration with the
above findings, showing decreased activities of superoxide
dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx)
and glutathione reductase (GR) in smoke exposed rat brain.
SOD is the first enzyme in antioxidant defense that
scavenges superoxide radicals to form H2O2 and hence
diminishes the toxic effects of the radical. The quinone–
semiquinone radicals from the tar phase of cigarette smoke are
capable of reducing molecular oxygen to superoxide radicals
whose excessive generation inactivates this enzyme (Duthie
and Arthur, 1994). Hence, a decrease in SOD activity upon
smoke exposure could have resulted from its inactivation by tar
phase oxidants.
CAT is involved in the detoxification of high concentrations
of H2O2, whereas GPx is sensitive to lower concentration. The
brain contains less CAT levels and hence GPx has a major role
in quenching H2O2 and other peroxides which otherwise will
lead to the production of hydroxyl and peroxyl radicals in the
presence of iron (Bast and Barr, 1997; Gutteridge and
Halliwell, 1994). Inhibition of CAT activity in rat brain and
liver by cigarette smoke has been reported (Mendez-Alvarez et
al., 1998). The presence and production of the free radicals
from smoke lower this enzyme, leading to accumulation of
H2O2 and lipid hydroperoxides further worsening the damage
(Pryor, 1997). During acute smoke exposure, an increase in
CAT activity was observed by Baskaran et al. (1999). However,
a decrease in the activity of CAT in the present study suggests
the inability of host antioxidant defense to meet the oxidative
stress following chronic exposure to cigarette smoke.
An increase in GPx activity is expected when the activity of
CAT is not sufficient to cope with the oxidative stress. Absence
of an augmentation in GPx activity upon smoke exposure in
our study has been hypothesized to arise from a decrease in the
levels of GSH that is essential for the conjugation of lipid
peroxides. GR is an important enzyme for the maintenance of
intracellular concentration of reduced glutathione (Gutteridge
and Halliwell, 1994) and reduced availability of GSH could
have resulted in the reduction of activity of GR upon smoke
exposure.
Bacoside A administration increased the activities of SOD,
CAT, GPx and GR. Bhattacharya et al. (2000) reported
increased antioxidant enzymes in rat frontal cortex, striatum
and hippocampus upon administration of B. monniera .
Enhancement of these enzymes in liver and kidney by B.
monniera has been reported under different conditions (Sum-
athy et al., 2001; Rohini et al., 2004). Hence it is possible that
bacoside A might be involved in the activation of enzymic
antioxidants.
Reduced glutathione (GSH) serves as the brain’s primary
antioxidant defense against prooxidant stress and the level of
brain GSH was significantly lowered after exposure to cigarette
smoke. Smoking-induced depletion of GSH in kidney, lung and
liver has also been reported (Anand et al., 1996; Baskaran et
al., 1999). This depletion was directly associated with elevation
in brain lipid peroxidation which could be attributed to its
protection against ROS generated by smoke, besides its
consumption by the antioxidant enzymes GPx and GST
(Baskaran et al., 1999). Acetaldehyde, a major aldehyde from
the smoke has been shown to deplete the cells of their GSH by
conjugating with it, which further makes the cells more
vulnerable to peroxidative damage (Nadiger et al., 1987).
Hence, the decrease in GSH levels could possibly be related
to the inability of host tissue to synthesize GSH that is reflected
from decrease in vitamin C, E and A. GSH and these vitamins
are tightly linked to each other in a way that it helps to
replenish vitamin C which in turn regenerates vitamin E and A
(Rani and Panneerselvam, 2001). Ascorbate is the first strong
reductant in the aqueous phase that readily reacts with cigarette
K. Anbarasi et al. / Life Sciences 78 (2006) 1378–13841382
smoke oxidants and affords considerable protection to the cells
(Kallner et al., 1981). The lipid-soluble, membrane bound
vitamin E reacts with peroxyl radicals present in the smoke and
terminates lipid peroxidation (Brown et al., 1997) and vitamin
A effectively quenches singlet oxygen (Helen and Vijayammal,
1997).
However, smokers are constantly overexposed to free
radicals through inhalation of long-lived carbon- and oxygen-
centered radicals that subsequently deplete the plasma and
tissue stores of these micronutrients (Brown et al., 1997;
Pamuk et al., 1994). In vitro exposure of plasma to cigarette
smoke resulted in the destruction of tocopherols, carotenoids,
and retinol (Handelman et al., 1996). The present study also
revealed depletion in the levels of non-enzymatic antioxidants
such as vitamin C, E and A in the brain of rats exposed to
cigarette smoke.
Administration of bacoside A increased glutathione levels in
the brain. Hepatoprotective and nephroprotective effect of B.
monniera following increased GSH levels have been reported
(Sumathy et al., 2001; Rohini et al., 2004). Similarly, an
increase in GSH levels against smoking induced depletion in
the brain indicates neuroprotective role of bacoside A. Baco-
side A has been shown to quench superoxide radicals, more
effectively than ascorbic acid (Pawar et al., 2001) and
effectively scavenge the hydroxyl, peroxyl and nitric oxide
radicals (Russo et al., 2003a,b). This could also be the reason
for the maintenance of the antioxidant vitamins which
otherwise would be spared in scavenging these radicals from
smoke.
Transition metal complexes are known to play a major role
in free radical biology and cigarette tar contains large amounts
of metals, complexed to some components of tar such as o-
diphenols (Cross et al., 1987). The observed increase in the
levels of copper and iron in the brain could be due to the
mobilization of iron from ferritin and copper from copper-
binding protein induced by cigarette smoke exposure, which
accelerate the oxidant injury through the formation of hydroxyl
radicals via Haber-Weiss/Fenton reaction (Lapenna et al.,
1995). Also cigarette smoke exposure resulted in decreased
serum ceruloplasmin activity. Ceruloplasmin is a copper
binding protein which functions as a ferroxidase that oxidizes
iron to Fe3+ and thereby prevents accumulation of free iron. A
decrease in serum ceruloplasmin activity has been reported in
smokers (Pacht and Davis, 1988). This may in part reflect the
increased levels of free iron and copper upon cigarette smoke
exposure. It is quite likely that soluble iron and copper are
highly toxic to brain. Damaged brain tissue undergoes rapid
lipid peroxidation, presumably because metals released by cell
disruption are not safely sequestered (Floyd, 1990).
The question remains whether this might have contributed
to the manifestation of brain damage or it was a consequence of
brain damage. B. monniera has been shown to chelate the
transition metals, inhibit formation of free radicals, and
terminate lipid peroxidation at the initiation level itself
(Tripathi et al., 1996). Thus, bacoside A could have protected
the brain from cigarette smoke-induced rise in copper and iron
as a metal chelator.
The levels of trace elements like zinc and selenium in
brain were decreased upon exposure to cigarette smoke. Zinc,
the cofactor for the enzyme SOD has been shown to protect
the brain during ischemia or hypoglycemia (Choi, 1989).
Selenium functions as an important nutrient of the brain and
being a component of GPx, it plays a major role in
preventing free radical mediated cell damage (Bou-Resli et
al., 2002). Cadmium, the heavy metal from tobacco,
decreased the bioavailability of selenium and zinc and hence
depletes the antioxidant status (Preston, 1991). Zinc and
selenium therapy has been found to be effective during
cigarette smoking (Al-Bader et al., 1999; Dilsiz et al., 1999).
However, alterations in mineral metabolism are secondary to
chronic diseases associated with long-term smoking. Admin-
istration of bacoside A restored the levels of zinc and
selenium, and the activity of ceruloplasmin in cigarette
smoke exposed rat brain, probably by preventing cadmium
mediated toxicity.
Conclusion
The above findings show that chronic cigarette smoking
induces an oxidative stress on the brain by augmenting lipid
peroxidation and diminishing both enzymatic and non-enzy-
matic antioxidant status. Bacoside A ameliorates cigarette
smoking induced peroxidative changes probably through its
free radical scavenging, anti-lipid peroxidative and antioxidant
activities in the brain tissue. Thus, the results of our
investigation suggest that bacoside A can be a potent
antioxidant in the brain, an organ highly prone to oxidative
stress against chronic smoking induced toxicity and hence may
have useful properties as a natural antioxidant supplement,
capable of preventing brain damage caused by oxidative stress.
However, further studies pertaining to the precise mechanism
of action of Bacoside A are warranted.
Acknowledgements
The financial assistance provided to Ms. K. Anbarasi (Grant
No: 9/115(593)/2003, EMR-I, dt 06.05.2003) and Dr. G. Vani
(Grant No: 9/115(511)/2000, EMR-I, dt 20.04.2000) by the
Council of Scientific and Industrial Research (CSIR), New
Delhi is gratefully acknowledged.
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