Food and Chemical Toxicology 47 (2009) 1945–1949
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Effects of water extracts of thyme (Thymus vulgaris) and ginger (Zingiber officinale Roscoe) on alcohol abuse Ali A. Shati a, Fahmy G. Elsaid a,b,* a b
Biological Science Department, Faculty of Science, King Khalid University, Abha, Saudi Arabia Zoology Department, Faculty of Science, Mansoura University, Egypt
a r t i c l e
i n f o
Article history: Received 25 March 2009 Accepted 11 May 2009
Keywords: Alcohol abuse Thyme Ginger Antioxidant enzymes Liver function Mice
a b s t r a c t Introduction: Alcohol abuse has many harmful effects on human body. This study aimed to investigate the role of water extracts of thyme (Thymus vulgaris) and ginger (Zingiber officinale Roscoe) as natural product extracts to detoxify the injuries of alcohol abuse on liver and brain of mice. Materials and methods: Alcohol at a dose of 1.25 ml/50 ml water was orally administered at the first day of treatment with continuously increase of 1.25 ml per day to the end of experiment (14 days, 0.1 ml/45 g /d). Mice also were orally administered with alcohol and water extracts of thyme and ginger in concentration of 500 mg /kg body weight for 2 weeks. Results: The results showed very highly significant increase in nitric oxide and malondialdehyde level in liver and brain and a very highly significant decrease in the total antioxidant capacity and glutathione peroxidase activity in alcoholic group. In addition, the liver function enzymes such as L-c-glutamyl transpeptidase and butyryl cholinesterase activities showed very highly significant increase in alcoholic group. In contrast, the water extracts of thyme and ginger showed significant amelioration on these changes both in liver and brain tissues. Conclusion: The water extracts of thyme and ginger has detoxifying and antioxidant effects. Therefore, it is recommended to use them to avoid alcohol toxicity. Ó 2009 Elsevier Ltd. All rights reserved.
1. Introduction 1.1. Alcohol abuse Alcohol is a widespread and potentially important risk factor for chronic diseases. Chronic abuse of alcohol usually results in progressive damage and organ failure mainly in the liver (Brunt and McGee, 1995). The association between chronic ethanol abuse and the development of cirrhosis is well documented (El-Serag, 2001). However, a single acute dose of ethanol results in oxidative stress in rat pancreas (Van-Gossum et al., 1996). Ethanol is rapidly oxidized to acetaldehyde and to acetate in a two-step process involving the enzymes alcohol dehydrogenase and aldehyde dehydrogenase. The liver alcohol dehydrogenase pathway is considered to be the primary pathway of ethanol metabolism (Crow and Hardman, 1989). However, other enzymes including catalase (CAT) have also been shown to contribute (Koechling and Amit, 1992). Both aldehyde dehydrogenase and catalase have been shown to be widely distributed in mammalian extrahepatic tissues, including
* Corresponding author. Address: Zoology Department, Faculty of Science, Mansoura University, Egypt. E-mail addresses:
[email protected] (A.A. Shati),
[email protected] (F.G. Elsaid). 0278-6915/$ - see front matter Ó 2009 Elsevier Ltd. All rights reserved. doi:10.1016/j.fct.2009.05.007
the brain (Zimatkin and Deitrich, 1995). Alcohol toxicity in the liver, is due primarily to acetaldehyde or metabolic changes of alcohol oxidation (Niemela et al., 1995). The formation of acetaldehyde is associated with an increase in reactive oxygen species formation, leading to the development of oxidative stress in the liver (Cederbaum, 1989). Acetaldehyde and malondialdehyde (MDA) were reported to react with plasma, red blood cells, and hepatic proteins, forming both stable and unstable condensation products, leading to the altered metabolism of circulating proteins. Free radicals or reactive oxygen species (such as a-hydroxy ethyl radical, superoxide radical, hydroxy radical, peroxy radical, and hydrogen peroxide) are implicated in ethanol-induced oxidative tissue injury (Ramakrishna Rao et al., 1996). Mechanisms of ethanol toxicity have been most extensively studied in the liver, and metabolism of ethanol by hepatocytes is widely thought to play a central role in the pathogenesis of alcoholic liver disease (Lieber, 1992). In the liver, ethanol is largely metabolized by oxidation, which may lead to cellular injury through the production of hydrogen or toxic metabolites such as acetaldehyde and acetate. It is predictable that prolonged exposure to ethanol would be associated with the overproduction of reactive oxygen species and reactive nitrogen species such as nitric oxide owing to the ability to amplify oxidative stress. Production of the ethanol-derived a-hydroxyethyl radical (CH3CH2OH) has also been
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observed in the livers of mice and rats treated chronically with alcohol (Kono et al., 2000). Therefore oxidative stress is a central factor involved in alcohol-induced liver injury (Arteel, 2003). The pathogenesis of ethanol-induced gastric lesions is complex. These implications may be due to depletion of non-protein sulfhydryls concentration (Szabo et al., 1981), modulation of nitric oxide system (Whittle and Lopez-Belmonte, 1993), reduction of gastric mucosal blood flow (Holzer et al., 1991) and other factors such as the autonomic nervous system (Ko et al., 1994). Husain and Somani (1997) have shown that a single acute dose of ethanol significantly decreased CAT, GSH-reductase (GR), and GSH-peroxidase activity. NADPH is the electron donor cofactor in the glutathione reductase (GR, EC 1.6.4.2) catalyzed reaction to regenerate reduced glutathione (GSH), and it is also required in maintaining the H2O2 detoxifying enzyme, CAT in its active form. GSH is consumed in reactions that protect the cell by removing deleterious compounds and hydroperoxides, and is restored by enzymatic reduction of GSSG by GR. The last reaction requires an adequate supply of its cofactor NADPH (Filosa et al., 2003). It is well known that GSH regeneration depends on NADPH availability as well as on the NADPH/NADP+ ratio which in turn are regulated by GSH-Px activity (Dıaz-Flores et al., 2006).
2.3. Water extracts of T. vulgaris and Z. officinale Roscoe T. vulgaris and Z. officinale Roscoe were obtained from local supermarkets in Abha city, Saudi Arabia. Thirty gram of dried aerial material of thyme and rhizomes of ginger were infused each alone in 60 ml of distilled water for a day then, samples were filtered using filter paper and the two filtrates were stored at 20 °C for 3 days only (i.e., freshly prepared every 3 days). 2.4. Animal grouping Mice were divided into four groups (5 mice per group): 2.4.1. Control group Mice were supplied with normal laboratory diet for 14 days. 2.4.2. Alcohol group Mice were orally administered with 0.1 ml of alcohol/45 g/day for 14 days. 2.4.3. Group receiving thyme extract Mice were orally administered with alcohol and thyme extract in concentration of (500 mg/kg body weight) for 14 days. 2.4.4. Group receiving ginger extract Mice were orally administered with alcohol and ginger extract of (500 mg/kg body weight) for 14 days. 2.5. Methods
1.2. Natural product extracts The leaves of thyme (Thymus vulgaris) can be used fresh or dried as a spice. Essential oils extracted from fresh leaves and flowers can be used as aroma additives in food, pharmaceuticals and cosmetics (Javanmardi et al., 2002). Thyme also possesses various beneficial effects, e.g. antiseptic, carminative, antimicrobial and antioxidative properties (Baranauskiene et al., 2003). Ginger (Zingiber officinale Roscoe) has phenolic compounds such as shogaols, gingerols, sesquiterpenes, bisapolene, zingiberene, zingiberol, sesquiphellandrene and curcurmene. The active ingredients in ginger are thought to reside in its volatile oils, which comprise approximately 1–3% of its weight (Newall et al., 1996). Ginger’s active ingredients have a variety of physiologic effects. For example, the gingerols have analgesic, sedative, antipyretic and antibacterial effects in vitro and in animals (Mascolo et al., 1989). Although an intravenous bolus of gingerol had a half life of 7.23 min in rats (Ding et al., 1991), it is not clear how this relates to pharmacokinetics after oral administration in humans. In human aortic endothelial cells, zingerone demonstrated significant antioxidant effects on low density lipoproteins (Pearson et al., 1997; Zhou and Xu, 1992). In human erythrocyte membranes, ginger extracts inhibited lipid peroxidation by 72% (Sujatha and Srinivas, 1995). In addition, in rats fed with a high fat diet, supplementation with ginger provided significant antioxidant effects, raising tissue concentrations of superoxide dismutase and catalase and reduced gluatathione (Jeyakumar et al., 1999). So, this study is concerned with the role of water extracts of thyme and ginger to detoxify the injuries of alcohol abuse on liver and brain.
2. Materials and methods 2.1. Experimental animals Male Albino mice (balb/c) weighing about 45 g were used in these experiments. The animals were kept under good ventilation, received balanced diet and water ad libitum throughout the study.
Glutamic-oxaloacetic transaminase (AST) and glutamic-pyruvic transaminase (ALT) activities were determined by the method of Reitman and Frankel (1957). L-c-Glutamyl transpeptidase and butyryl cholinesterase were estimated by the methods of Szasz (1969) and Knedel and Bottger (1967) respectively. Alkaline and acid phosphatase (total, prostatic and non-prostatic) activities were measured by the method of Belfield and Goldberg (1971) and Kind and King (1954). Bilirubin was measured by the method of Walter and Grade (1970). Nitric oxide assay was measured according to the method of Montogomery and Dymock (1961). The malondialdehyde was estimated by the method of Ohkawa et al. (1979). Glutathione peroxidase was measured by the method of (Paglia and Valentine, 1967). Total antioxidant capacity was estimated by the method of Koracevic et al. (2001).
3. Results Table 1 showed high significant increase in the level of AST, ALT, L-
c-glutamyl transpeptidase, butyryl cholinestrase, alkaline phos-
phatase, total acid phosphatase, non-prostatic acid phosphatase, bilirubin and prostatic acid phosphatase in alcoholic group. Thyme and ginger showed alleviation of the investigated parameters in alcohol and thyme group and alcohol and ginger group in comparison with alcohol administered group. Table 2 showed high significant increase in the nitric oxide level in alcohol group when compared with the control one. The amelioration of the nitric oxide level was observed in alcohol and thyme group and alcohol and ginger group. Table 3 showed very high significant decrease in the activity of glutathione peroxidase in alcohol group compared with the control group. Thyme and ginger water extracts showed significant increase in the activity of GPx in serum, liver and brain tissues. Table 4 showed significant decrease in serum, liver and brain total antioxidant capacities in alcohol group compared to the control one. In contrast, water extracts of thyme and ginger with alcohol showed non-significant changes in serum and significant changes in total antioxidant capacities in the investigated tissues when compared with the control group. Alcohol and thyme group and alcohol and ginger group showed a high significant increase in comparison with alcoholic group except in serum.
4. Discussion 2.2. Ethyl alcohol C2H5OH (99.9%) was diluted as 1.25 ml/50 ml distilled water in the first day of treatment, then the dose increased by 1.25 ml/day for 14 days. Each mouse was orally administered by 0.1 ml/45 g /d.
Ethanol-induced disturbances were more seriously advanced in the liver and brain. It might result from the fact that, the liver is the main site of ethanol biotransformation and at the same time, the
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A.A. Shati, F.G. Elsaid / Food and Chemical Toxicology 47 (2009) 1945–1949 Table 1 Serology of liver function in different mice groups. Liver function
Mice groups
AST ALT L-c-Glutamyl transpeptidase Butyryl cholinestrase Alkaline acid phosphatase Total acid phosphatase Non-prostatic acid phosphatase Prostatic acid phosphatase Bilirubin
Control
Alcohol
Alcohol and thyme
Alcohol and ginger
35.1 ± 1.6 40.8 ± 1.5 17.8 ± 2.9 1564.3 ± 356.1 42.6 ± 7.2 16.5 ± 1.1 14.5 ± 0.7 2.2 ± 0.6 3.4 ± 0.6
121.6 ± 6.3*** 133.0 ± 5.9*** 75.5 ± 12.2*** 5417.3 ± 1796.3*** 181.8 ± 24.7*** 27.8 ± 0.8*** 24.5 ± 0.5*** 3.3 ± 0.7** 11.9 ± 1.1***
71.6 ± 7.3***,a 96.6 ± 4.7***,a 62.4 ± 8.7***,c 1889.5 ± 72.6a 124.8 ± 15.3***,a 18.1 ± 1.3a 15.8 ± 1.4a 2.5 ± 0.4 5.5 ± 0.5**,a
58 ± 1.8***,a 75.2 ± 6.3***,a 45.6 ± 5.0***,a 2570.4 ± 101.2a 137.8 ± 18.1***,a 18.3 ± 2.6***,a 16.3 ± 2.3*,a 1.9 ± 0.6b 6.6 ± 1.1***,a
*
p 6 0.05, all different groups in comparison with the control group. p 6 0.01, all different groups in comparison with the control group. *** p 6 0.001, all different groups in comparison with the control group. a p 6 0.001, alcohol and thyme and alcohol and ginger groups in comparison with alcohol group. b p 6 0.01, alcohol and thyme and alcohol and ginger groups in comparison with alcohol group. c p 6 0.05, alcohol and thyme and alcohol and ginger groups in comparison with alcohol group. **
Table 2 Nitric oxide and malondialdehyde (MDA) level on different mice groups. Parameters
Mice groups Control
Serum (lmol/L) Liver (lmol/g) Brain (lmol/g) Liver MDA Brain MDA ** *** a
57.6 ± 15.4 23.7 ± 8.1 72.7 ± 2.5 123.8 ± 5.2 160.4 ± 9.6
Alcohol
Alcohol and thyme a
***
94.5 ± 6.1 158.3 ± 25.1*** 148.1 ± 8.6*** 178.6 ± 5.1** 217.5 ± 15.6***
68.1 ± 8.6 64.0 ± 4.7***,a 94.3 ± 3.3***,a 111.8 ± 1.1***,a 128.1 ± 1.9***,a
Alcohol and ginger 57.8 ± 4.6a 78.5 ± 6.3***,a 84.1 ± 6.4**,a 136.6 ± 6.3***,a 169.7 ± 7.7a
p 6 0.01, all different groups in comparison with the control group. p 6 0.001, all different groups in comparison with the control group. p 6 0.001, alcohol and thyme and alcohol and ginger groups in comparison with alcohol group.
Table 3 The effect of alcohol abuse on glutathione peroxidase activity on different mice groups. Tissues
Serum Liver Brain *** a b
Mice groups Control
Alcohol
Alcohol and thyme
Alcohol and ginger
550.6 ± 21.6 157.8 ± 26.9 200.7 ± 8.9
189.1 ± 7.5*** 90.5 ± 6.7*** 125.4 ± 7.6***
435.3 ± 71.8***,a 150.7 ± 23.6a 145.1 ± 7.1***,b
492.2 ± 51.8a 151.9 ± 2.7a 143.6 ± 24.0***,b
p 6 0.001, all different groups in comparison with the control group. p 6 0.001, alcohol and thyme and alcohol and ginger groups in comparison with alcohol group. p 6 0.05, alcohol and thyme and alcohol and ginger groups in comparison with alcohol group.
Table 4 The effect of alcohol abuse on total antioxidant capacity on different mice groups. Tissues
Serum Liver Brain * **
Mice groups Control
Alcohol
Alcohol and thymus
Alcohol and zingiber
1.33 ± 0.05 689 ± 3.6 687.4 ± 4.1
1.23 ± 0.08** 616.3 ± 12.1*** 671.4 ± 8.5*
1.33 ± 0.01b 703.3 ± 10.9*,a 708.4 ± 18.4**,a
1.32 ± 0.03b 720.9 ± 7.3***,a 687.3 ± 10.3c
p 6 0.05, all different groups in comparison with the control group. p 6 0.01, all different groups in comparison with the control group. p 6 0.001, all different groups in comparison with the control group. a p 6 0.001, alcohol and thyme and alcohol and ginger groups in comparison with alcohol group. b p 6 0.01, alcohol and thyme and alcohol and ginger groups in comparison with alcohol group. c p 6 0.05, alcohol and thyme and alcohol and ginger groups in comparison with alcohol group.
***
main site of free radicals formation (Jurczuk et al., 2004). The high increase of nitric oxide and MDA level in alcohol mice group compared with the control one may be explained by the preceding
view. The high increase of malondialdehyde in alcohol group in both liver and brain tissues reflex the oxidative stress associated with the abuse of alcohol. An immediate product of ethanol metab-
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olism is acetaldehyde and unlike ethanol, this is a highly reactive and extremely cytotoxic compound (Holownia et al., 1999) which is involved in a number of non-enzymatic modifications of proteins, including formation of semialdehydes with consequent protein modification and inhibition of their biological functions (Morgan et al., 2002). The protection system depends mainly on GSH concentration by the activities of GSH related enzymes, such as glutathione reductase and GSH-Px (Wintrobe et al., 1975). GSH is the principle intracellular antioxidant in most mammalian cells, participates in the removal of H2O2 and toxic end product of lipid peroxidation known as lipid peroxides (Rizzardini et al., 2003). It was also reported by Lieber (2002) that chronic ethanol consumption depletes the body’s natural antioxidant supply such as GSH this may explain the decrease in the total antioxidant capacity in alcohol mice group compared with the control one. Husain and Somani (1997) showed that a single acute dose of ethanol significantly decreased GSH-PX activity in rats. As described in Table 3 there was a very highly significant decrease in the liver and brain GSH-Px activity in alcohol mice group. These results also coincide with Ali and A1-Swayeh (1997) who reported that ethanol decreased the level of GSH in rats and suggested that this decrease may be attributed to excess generation of reactive oxygen species by ethanol consumption that plays a major role in ethanol-induced oxidative stress (Lecomte et al., 1994). Oxidative stress in the cells or tissues refers to enhanced generation of reactive oxygen species and/or depletion in antioxidant defense system. ROS generated in the tissues are efficiently scavenged by enzymatic antioxidant system such as GSH-Px and glutathione reductase as well as non enzymatic antioxidants such as glutathione, vitamin A, C, and E (Schlorff et al., 1999). Husain and Somani (1997) have also reported that endogenous glutathione can react directly with ROS, protects thiol groups in proteins from oxidation and serves as substrate for GSH-Px and glutathione-s-transferase. These implications of alcohol abuse induced the deviation in liver functions as described in Table 1 especially the highly significant increase of AST, ALT, L-c-glutamyl transpeptidase and butyryl cholinesterase activities. Fortunately, the alleviation in most investigated biochemical parameters in alcohol and thyme group and alcohol and ginger group presented in the present work could be attributed to the antioxidant properties of thyme and ginger. Phenolic compounds such as shogaols and gingerols, zingiberene, zingiberol, curcurmene, zingerone, geraniol and neral in zingiber and thymol in thyme have antioxidative properties (Pearson et al., 1997; Baranauskiene et al., 2003). These components may be concerned in alleviation the reduction of the antioxidant capacity and glutathione peroxidase in liver and brain tissues in alcohol treated mice groups. This also reflects the decrease in nitric oxide and MDA level in alcohol and thyme group and alcohol and ginger group when compared with alcohol group. 5. Conclusion Ethanol abuse can cause harmful effects to some body organs such as liver and brain because it induces the production of reactive oxygen species that attack fats and proteins and rapidly enter cell membrane causing damage of the membrane and organelles. Water extract of natural products such as thyme and ginger have phenolic antioxidant compounds that may play part in protecting the body against the hazard effects caused by alcohol abuse. Conflict of interest statement The authors declare that there are no conflicts of interest.
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