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Hepatoprotective Effect of N-acetyl Cysteine and/or β-Carotene on Monosodium
Glutamate-Induced Toxicity in Rats
Hazar Yaqub, Naira A. Abdel Baky, Hala A. Attia and Lila M. Faddah
Faculty of Pharmacy, Pharmacology department, King Saud University, Riyadh , KSA.
Introduction
Statistical Analysis
Data are presented as the mean ± S.D. For comparison of multiple data sets
one way analysis of variance (ANOVA) followed by Bonferroni multiple
comparison test swas used. Significance was accepted when p ≤ 0.05.
Results
Table (1): Activities of ALT, AST & ALP (U/L) and LDH (μmol/ml/min)
as well as albumin level (gm/dl) in serum of different normal and MSGtreated groups.
MSG - treated groups
Normal groups
CON
β-caro
NAC
β-caro
+
NAC
CON
β-caro
NAC
β-caro
+
NAC
ALT
65
±
4.83
77.83b
±
4.47
76.62b
±
2.92
71.6b
±
4.21
120.5a
±
13.17
85.13abc
±
4.40
75.5b
±
3.5
65b
±
3.14
AST
103.18
±
5.75
101.7b
±
6.78
100.1b
±
8.27
98.52b
±
7.69
153.8a
±
18.34
116.9b
±
5.26
112.3b
±
9.89
107.4b
±
5.18
LDH
68.85
±
7.55
54.34bc
±
8.78
51.96abc
±
5.21
40.5abc
±
2.54
118.5a
±
11.37
100.1abd
±
0.909
99.8abd
±
1.49
88.34abd
±
1.49
ALP
90.96
±
3.12
70.53bc
±
4.03
77.03bc
±
11.35
77.36bc
±
3.96
158.1a
±
24.4
96.45b
±
9.36
133.2abc
±
3.96
112.37bd
±
17.25
5.62
±
0.23
5.95b
±
0.28
5.1bc
±
0.39
5.13b
±
0.59
2.8a
±
0.34
5.93b
±
0.23
5.97b
±
0.44
6.4b
±
0.58
Albumin
Fig.(1): Effect of β carotene, NAC and their combination on hepatic
malondialdehyde (MDA), GSH and L-ascorbic acid levels. Fig 1 (a, b and
c, respectively) as well as serum nitrite levels Fig. 1 (d) in normal and
MSG-treated groups.
150
3
a
bcd
100
b
ab
50
b
(mol/gm tissue)
Aim of the work
In the present study, liver damage
induced by MSG was indicated from
significant increases in the activities of
ALT, AST, ALP LDH, and serum nitrite
concentrations as well as hepatic
malonaldehyde level and decreased serum
albumin level and hepatic contents of
L-ascorbic acid and GSH levels as
compared to normal control group.
oxidative stress and accumulation of free
radicals seems to be responsible for MSG
toxicity. NAC and β-carotene either alone
or in combination significantly restored the
normal antioxidant balance in liver cells.
Being a precursor of GSH, NAC provides
protection from toxic liver damage by
elevating intracellular GSH levels ( 9). As a
source of SH groups, NAC can enhance
glutathione-S-transferase activity, promote
detoxification, and act directly on reactive
oxidant radicals (10). In addition, βcarotene, like other antioxidants, protects
Hepatic GSH Content
N-acetyl-cysteine (NAC), is
one of a large group of exogenous
antioxidant drugs that may protect
against oxidative tissue injury. It
is considered as the drug of choice
in ameliorating hepatotoxicity due
to acetaminophen intoxication
(5).NAC has been shown to have
antimutagenic activity towards
various
genotoxic
agents.
(6).
Another natural antioxidant,
β-carotene protects the body
against free radicals, quench
singlet oxygen, and reduce
peroxyl radicals (7). β-carotene
also induces hepatic enzymes that
detoxify carcinogens (8).
Eighty adult male Wistar albino rats were divided into two major groups.
Group I was consisted of four healthy normal subgroups; normal control ,
NAC, β-carotene (20 and 10 mg/kg , i.p. Three times/week for three weeks
,respectively) and combination of NAC and β-carotene-treated group (Gs1, 2,
3 and 4, respectively). On the other hand, group II comprised of four MSG (4
mg/g body wt i.p. Three times/week for 3 weeks )-treated groups; MSG
control, NAC, β-carotene (20 and 10 mg/kg i.p. one hour before MSG
injection ,respectively) and combination of NAC and β-carotene-treated
groups (Gs 5, 6,7 and 8, respectively). Animals were sacrificed 24 hour
following last dose adminstration. Liver function tests, MDA, GSH, Vit. C
and nitric oxide (NO) levels were determined.
(nmol/gm tissue)
Liver as the most metabolic
organ in the body; is higly liable
to toxicity due to various agents.
Actually, MSG has been reported
to increase the activities of serum
aspartate aminotransferase (AST),
and alanine aminotransferase
(ALT) enzymes (3). Moreover,
MSG causes membrane damage
by initiating free radical and
increasing lipid hydroperoxide
concentration. It also increases
hepatic calcium and ascorbic acid
and decreases both superoxid
dismutase (SOD) activity and
reduced glutathione (GSH) level
in hepatic tissue (4).
Discussion &Conclusions
Hepatic Malonaldehyde
Monosodium
glutamate
(MSG), is commonly used as a
flavor enhancer especially in
Chinese, Thainese and Japanese
foods (1).However, MSG produce
many
symptoms
such
as
numbness, flushing, sweating,
dizziness and headaches. In
addition, ingestion of MSG has
been alleged to cause or
exacerbate numerous conditions,
including asthma, urticaria, atopic
dermatitis, ventricular arrhythmia,
neuropathy
and
abdominal
discomfort (2).
Material & Methods
2
bc
bc
1
a
levels.
0
0
Fig. (1a)
Fig. (1b)
100
10
bc
a
a
75
(mol/Litere)
ab
b
20
Serum Nitrite Concentration
30
Hepatic L-Ascorbic Acid
(g/gm tissue)
The purpose of this study is to
evaluate the expected role of
NAC &β-carotene and the
possible synergistic effect of
their
co-administration
to
counteract the hazardous effects
of intraperitoneal injection of
MSG. This will be achieved
through
monitoring
liver
function tests, oxidative status;
malondialdehyde (MDA), GSH,
Vit. Cand nitric oxide (NO)
bc
50
b
b
25
0
0
Fig. (1c)
Fig.(1d)
Data are expressed as M ± SD
a: Significance from control , b: Significance from MSG group
c: Significance from MSG +COMP group
Control
MSG
MSG+ CAR
MSG+ NAC
MSG+COMB
the body against free
radicals, quench singlet oxygen, and
reduce
peroxyl
radicals
(7).Simultaneous supplementation
of NAC or/and β-carotene with
MSG significantly decreased NO
serum levels. This may be due to
that, β-carotene helps to strengthen
immune system (11), and also NAC
enhances inflammatory and immune
response (12). In conclusion, The
use
of
naturally
occurring
antioxidants like NAC and βcarotene is potentiated with their
synergetic
combination
in
ameliorating the hazardous effects
of MSG. This combination may
have a promising prophylactic
or/and therapeutic effects in
inflammatory liver diseases.
References
1-Ikeda, K. 1912; 38: 147.
2-Geha R.S., J. Nutr., 2000; 130,
1032S.
3-Onyema O.O., Indian J. Biochem.
Biophys. 2006; 43(1):20.
4-Farombi E.O. ,et al., Hum. Exp.
Toxicol. 2006 ;25 (5):251.
5-Prescott L.F., et al., Br. Med. J.
1979; 2: 1097.
6-Wilpart M, et al., Cancer Lett.
1986 ; 31(3):319.
7-Wang X.D., and Russell R.M. ,
Nutr. Rev. 1999; 57:263.
8-Edes T.E., et al., J. Nutr. 1989;
119:796.
9-Singh P, et al., Mol Cell Biochem.
2003; 243(1-2):139.
10-De Vries N. and De Flora S. , J.
Cell Biochem. 1993; 17F:S270.
11-Chew B.P. and Park J.S., J. Nutr.
2004; 134(1):257S.
12-Aihara M, et al., J. pathology,
2000; 67(6): 662.