Protective Effects Of Garlic Oil Research Articles

Garlic oil supplementation blocks inflammatory pyroptosis-related acute lung injury by suppressing the NF-κB/NLRP3 signaling pathway via H2S generation.

Acute lung injury (ALI) is a major cause of acute respiratory failure with a high morbidity and mortality rate, and effective therapeutic strategies for ALI remain limited. Inflammatory response is considered crucial for the pathogenesis of ALI. Garlic, a globally used cooking spice, reportedly exhibits excellent anti-inflammatory bioactivity. However, protective effects of garlic against ALI have never been reported. This study aimed to investigate the protective effects of garlic oil (GO) supplementation on lipopolysaccharide (LPS)-induced ALI models. Hematoxylin and eosin staining, pathology scores, lung myeloperoxidase (MPO) activity measurement, lung wet/dry (W/D) ratio detection, and bronchoalveolar lavage fluid (BALF) analysis were performed to investigate ALI histopathology. Real-time polymerase chain reaction, western blotting, and enzyme-linked immunosorbent assay were conducted to evaluate the expression levels of inflammatory factors, nuclear factor-κB (NF-κB), NLRP3, pyroptosis-related proteins, and H2S-producing enzymes. GO attenuated LPS-induced pulmonary pathological changes, lung W/D ratio, MPO activity, and inflammatory cytokines in the lungs and BALF. Additionally, GO suppressed LPS-induced NF-κB activation, NLRP3 inflammasome expression, and inflammatory-related pyroptosis. Mechanistically, GO promoted increased H2S production in lung tissues by enhancing the conversion of GO-rich polysulfide compounds or by increasing the expression of H2S-producing enzymes in vivo. Inhibition of endogenous or exogenous H2S production reversed the protective effects of GO on ALI and eliminated the inhibitory effects of GO on NF-κB, NLRP3, and pyroptotic signaling pathways. Overall, these findings indicate that GO has a critical anti-inflammatory effect and protects against LPS-induced ALI by suppressing the NF-κB/NLRP3 signaling pathway via H2S generation.

Protective Effect of Garlic Oil Supplementation on Serum Sodium and Potassium Ions against Formaldehyde Induced Toxicity in Wistar Rats

The present experimental study was designed to investigate the protective effect of garlic oil against formaldehyde vapor induced toxicity on serum electrolytes namely sodium (Na+) and potassium (K+). Twenty four male rats were randomly divided into three groups (control set 1, experimental set 2 and experimental set 3). The control set 1 was fed with standard food without any exposure and garlic oil supplementation while experimental set 2 was exposed to 6 ppm formaldehyde vapors for one hour daily for 30 days and experimental set 3 was given garlic oil supplementation (1 ml/100 g b. wt.) after exposure to 6 ppm formaldehyde vapors for one hour daily for 30 days. A highly significant increase in serum sodium ion level and a highly significant decrease in serum potassium ion level was observed respectively after exposure to formaldehyde vapors (P<0.01), while a significant decrease in serum sodium ion level (P<0.05) and a highly significant increase in serum potassium ion level has been noticed respectively after supplementation of garlic oil in comparison to formaldehyde vapor exposed rats (P<0.01). Therefore, it is concluded that garlic oil has shown positive potential to detoxify the toxic effect of formaldehyde inhalation on serum electrolytes sodium Na+ and potassium K+.

A study of The Possible Protective Effects of Garlic Oil and Rosemary Extract Against Some Toxic effects of Acrylamid on Adult Male Albino Rats

Background:Acrylamide (AA) is a chemical compound that is typically formed in starchy food products during high-temperature cooking. Itis a known lethal neurotoxin and genotoxin. Aim: The study was designed to illustrate gait change, biochemical and histopathological alterations besides the genotoxicity of AA on the brain of rats and the possible protection of both garlic oil and rosemary extract when administrated in co-treatment. Materials M negative control, garlic oil group, rosemary extract group, AA group, AA+ garlic oil group, AA+ rosemary extract group. Rats were gavaged orally for six weeks. At the end of experimental period, the gait score of rats was evaluated then, blood samples and brains from the rats were obtained for biochemical, histological and cytogenetic evaluation. Results: AA exposed rats exhibited abnormal gait with significant decline in superoxide dismutase (SOD), catalase (CAT), acetylcholine esterase (AChE), deoxyribonucleic acid (DNA), ribonucleic acid (RNA) and protein contents and an increase malondialdehyde (MDA) with histopathological changes of the brain tissues. Either treatment with garlic oil or rosemary extract improves these changes. Conclusion: AA is toxic to the brain of rats. Garlic oil or rosemary extract can ameliorate this toxicity. Recommendation: Strict control of AA consumption is urgently needed. Key words: Acrylamide, garlic oil, rosemary extract, AChE, DNA, RNA.

Protective Effects of Garlic and Cinnamon Oils on Hepatocellular Carcinoma in Albino Rats.

Natural oils are traditional medicinal herbs, which have attracted interests for its potential anti-inflammatory and anticancer activities. The present work is aimed at evaluating the protective effect of garlic oil and cinnamon oil on diethylnitrosamine- (DENA-) and 2-acetylaminofluorene- (2-AAF-) induced p53 gene mutation and hepatocarcinogenesis in rats. Forty male albino rats were divided into 4 equal groups: control, hepatocellular carcinoma (HCC), garlic oil-HCC, and cinnamon oil-HCC. The HCC-induced group showed a significant decrease in the body mass and a significant elevation in the liver weight, alpha-fetoprotein (AFP), liver enzymes, hepatic malondialdehyde (MDA), and p53 protein expression levels as well as genetic mutations in intron 5 of p53 gene in the form of Single-Nucleotide Polymorphisms (SNPs) and insertions. In addition, the glutathione (GSH) level and superoxide dismutase (SOD) activities were increased. While HCC rats pretreated with garlic oil or cinnamon oil were significantly reversed, these destructive actions increased GSH and SOD levels. The HCC-induced group showed histopathological features of liver cancer including hypercellularity, nuclear hyperchromasia, mitotic figures, and preneoplastic foci. On the other hand, HCC rats pretreated with garlic oil or cinnamon oil revealed partial reversal of normal liver architecture. The present findings proposed that these natural oils have the ability to improve liver function, significantly reduced the liver toxicity and HCC development. However, further sophisticated studies are recommended before their use as conventional therapeutics for HCC treatment.

Protective effect of garlic oil on furan-induced damage in the pancreas of adult male rat

Objectives The aim of this study was to investigate the effect of furan on the pancreas of adult male rat and to evaluate the possible protective role of garlic oil (GO). Background Furan is carcinogenic in rats and mice and possibly carcinogenic to humans. Methods Sprague–Dawley rats were divided randomly into four main groups: control, GO (80 mg/kg/day), furan-treated (2 and 8 mg/kg/day), and protected group (furan and GO). All rats were treated orally by a gavage for 5 days per week for 8 weeks. At the end of the experiment, pancreases were subjected to biochemical (measurement of the level of glucose, amylase, lipase, and oxidative stress indices in pancreatic tissue), histological, and immunohistochemical analyses. Results Our results showed the toxic effects of furan on the pancreas in adult male albino rats. This was indicated by an increase in pancreatic (amylase and lipase levels) and lipid peroxidation biomarker (malondialdehyde), and a decrease in antioxidant enzymes, including catalase, superoxide dismutase, and glutathione. In addition, histopathological alterations were detected, including mononuclear cellular infiltration, congestion of blood vessels, and cytoplasmic vacuolation of the acinar cells. There were significant increases in the number of inflammatory cells and apoptotic expression, whereas cytochrome P450 2E1 expression was significantly decreased after the administration of furan. Furan-induced toxicity was ameliorated by the coadministration of GO. Conclusion The administration of furan-induced biochemical and histopathological changes in the pancreas of adult male albino rats. These changes were improved by the coadministration of GO.

Protective effects of garlic oil against 1,3-dichloro-2-propanol-induced hepatotoxicity: role of CYP2E1 and MAPKs

1,3-Dichloro-2-propanol (1,3-DCP) is a well-known food contaminant that can be detected during the production of a wide range of foods. We investigated whether garlic oil (GO) has protective effects against 1,3-DCP-induced hepatotixicy and oxidative damage in rats. GO significantly attenuated the 1,3-DCP-induced increase in serum aminotransferase activities. This effect was accompanied by attenuation of the histopahological alterations in liver caused by 1,3-DCP. In 1,3-DCP-treated rats, GO prevented formation of hepatic malondialdehyde and depletion of reduced glutathione content, and promoted hepatic antioxidant enzymes activities. 1,3-DCP caused apoptosis in the liver with increases phosphorylation of mitogen-activated protein kinases (MAPKs); GO significantly attenuated these alterations and suppressed the expression of hepatic cytochrome P450 2E1 (CYP2E1). These results suggest that the protective effects of GO against 1,3-DCP-induced hepatotoxicity involve the ability to induce antioxidant enzymes, block metabolic activation of 1,3-DCP by suppressing CYP2E1 expression, and induce antiapoptotic activity by inhibiting phosphorylation of MAPKs.

Beneficial effects of garlic (Allium sativum) oil in experimental corrosive esophageal burns effects of garlic oil in esophageal burns.

Corrosive esophageal burns, particularly common in developing countries, lead to different problems in different age groups. The ingestion of corrosive substances can cause such problems as stricture of the esophagus, to acute perforation, and even death. Because stricture formation is related to the severity of the initial injury, the prevention of stricture constitutes a main goal of treatment. The aim of this study was to investigate the protective and anti-inflammatory effects of garlic (Allium sativum) oil in corrosive esophageal burn. Twenty-eight rats were randomly divided into 4 equal groups: group 1 (sham), group 2 (control), group 3 (topical treatment), and group 4 (topical and systemic treatment). In groups 2, 3, and 4, corrosive esophageal burns were generated by applying sodium hydroxide to a 1.5-cm segment of the abdominal esophagus. Normal saline was applied to group 2, topical garlic oil to group 3, and topical and systemic garlic oil were used in group 4. The level of hydroxyproline was lower in the topical treatment groups than in the control group (p=0.023). There was difference in tumor necrosis factor alpha level between the systemic treatment groups and the control group (p=0.044). Treatment with garlic oil decreased stenosis index (SI) and histopathological damage score (HDS) in corrosive esophageal burn rats. The SI in the topical treatment group was significantly lower than that of the control group (p=0.016). The HDS was significantly lower in group 4 when compared with the control group (p=0.019). Garlic oil is an effective agent in promoting the regression of esophageal stenosis and tissue damage caused by corrosive burns. While the protective effect of garlic oil on tissue damage is more significant when applied topically, the anti-inflammatory effect is more pronounced when applied systemically. Therefore, we believe that the application of garlic oil in patients with corrosive esophageal burns can reduce complication rates.

Garlic Oil Suppressed Nitrosodiethylamine-Induced Hepatocarcinoma in Rats by Inhibiting PI3K-AKT-NF-κB Pathway.

To explore the underlying mechanisms for the protective effects of garlic oil (GO) against nitrosodiethylamine (NDEA)-induced hepatocarcinoma, 60 male Wistar rats were randomized into 4 groups (n=15): control group, NDEA group, and two GO plus NDEA groups. The rats in GO plus NDEA groups were pretreated with GO (20 or 40 mg/kg) for 7 days. Then, all rats except those in control group were gavaged with NDEA for 20 weeks, and the rats in GO plus NDEA groups were continuously administered with GO. The results showed that GO co-treatment significantly suppressed the NDEA-induced increases of alpha fetal protein (AFP) level in serum, nuclear atypia in H&E staining, sirius red-positive areas and proliferating cell nuclear antigen (PCNA) expression. The molecular mechanisms exploration revealed that the protein levels of phosphatidylinositol 3 kinase (PI3K)-p85, PI3K-p110, total AKT, p-AKT (Ser473) and p-AKT (Thr308) in the liver of NDEA group rats were higher than those in control group rats. In addition, NDEA treatment induced IκB degradation and NF-κB p65 phosphorylation, and up-regulated the protein levels of downstream pro-inflammatory mediators. GO co-treatment significantly reversed all the above adverse effects induced by NDEA. These results suggested that the protective effects of GO against NDEA-induced hepatocarcinoma might be associated with the suppression of PI3K- AKT-NF-κB pathway.

Garlic Oil Attenuated Nitrosodiethylamine-Induced Hepatocarcinogenesis by Modulating the Metabolic Activation and Detoxification Enzymes

Nitrosodiethylamine (NDEA) is a potent carcinogen widely existing in the environment. Our previous study has demonstrated that garlic oil (GO) could prevent NDEA-induced hepatocarcinogenesis in rats, but the underlying mechanisms are not fully understood. It has been well documented that the metabolic activation may play important roles in NDEA-induced hepatocarcinogenesis. Therefore, we designed the current study to explore the potential mechanisms by investigating the changes of hepatic phase Ⅰ enzymes (including cytochrome P450 enzyme (CYP) 2E1, CYP1A2 and CYP1A1) and phase Ⅱ enzymes (including glutathione S transferases (GSTs) and UDP- Glucuronosyltransferases (UGTs)) by using enzymatic methods, real-time PCR, and western blotting analysis. We found that NDEA treatment resulted in significant decreases of the activities of CYP2E1, CYP1A2, GST alpha, GST mu, UGTs and increases of the activities of CYP1A1 and GST pi. Furthermore, the mRNA and protein levels of CYP2E1, CYP1A2, GST alpha, GST mu and UGT1A6 in the liver of NDEA-treated rats were significantly decreased compared with those of the control group rats, while the mRNA and protein levels of CYP1A1 and GST pi were dramatically increased. Interestingly, all these adverse effects induced by NDEA were simultaneously and significantly suppressed by GO co-treatment. These data suggest that the protective effects of GO against NDEA-induced hepatocarcinogenesis might be, at least partially, attributed to the modulation of phase I and phase II enzymes.

Protective Effects of Garlic Oil on Hepatocarcinoma Induced by N-Nitrosodiethylamine in Rats

To investigate the protective effects and the possible mechanisms of garlic oil (GO) against N-nitrosodiethylamine (NDEA)-induced hepatocarcinoma in rats, Wistar rats were gavaged with GO (20 or 40 mg/kg) for 1 week, and then were gavaged with GO and NDEA (10 mg/kg) for the next 20 weeks. The changes of morphology, histology, the biochemical indices of serum, and DNA oxidative damage of liver were examined to assess the protective effects. Lipid peroxidation (LPO), antioxidant defense system, and apoptosis-related proteins were measured to investigate potential mechanisms. At the end of the study (21 weeks), GO administration significantly inhibited the increase of the nodule incidence and average nodule number per nodule-bearing liver induced by NDEA, improved hepatocellular architecture, and dramatically inhibited NDEA-induced elevation of serum biochemical indices (alanine aminotransferase , aspartate aminotransferase, alkaline phosphatase and gamma-glutamyl transpeptidase) and hepatic 8-hydroxy-2'-deoxyguanosine (8-OHdG) levels in a dose-dependent manner. The mechanistic studies demonstrated that GO counteracted NDEA-induced oxidative stress in rats illustrated by the restoration of glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST) levels, and the reduction of the malondialdehyde (MDA) levels in liver. Furthermore, the mRNA and protein levels of Bcl-2, Bcl-xl, andβ-arrestin-2 were significantly decreased whereas those of Bax and caspase-3 were significantly increased. These data suggest that GO exhibited significant protection against NDEA-induced hepatocarcinogenesis, which might be related with the enhancement of the antioxidant activity and the induction of apoptosis.

Garlic oil alleviated ethanol-induced fat accumulation via modulation of SREBP-1, PPAR-α, and CYP2E1

Garlic oil (GO) has been shown to partially attenuate ethanol-induced fatty liver, but the underlying mechanisms remain unclear. The current study was designed to evaluate the protective effects of GO against ethanol-induced steatosis in vitro and in vivo, and to explore potential mechanisms by investigating the sterol regulatory element binding protein-1c (SREBP-1c), peroxisome proliferators-activated receptor-α (PPAR-α), cytochrome P4502E1 (CYP2E1), and etc. In the in vitro study, human normal cell LO2 was exposed to 100mM ethanol in the presence or absence of GO for 24h. We found that ethanol increased the protein levels of n-SREBP-1c and CYP2E1, but decreased the protein levels of PPAR-α, which was significantly attenuated by GO co-treatment. In the in vivo study, male Kun-Ming mice were pretreated with single dose of GO (50–200mg/kg body weight) at 2h before ethanol (4.8g/kg body weight) exposure. The changes of n-SREBP-1c, PPAR-α and CYP2E1 were paralleled well to those of in vitro study. Furthermore, GO significantly reduced the protein levels of fatty acid synthase (FAS), and suppressed ethanol-induced hepatic mitochondrial dysfunction. These results suggested that GO had the potential to ameliorate alcoholic steatosis which might be related to its modulation on SREBP-1c, PPAR-α, and CYP2E1.

Protective effects of garlic oil on n-hexane-induced neurotoxicity in rats via inhibition of hepatic alcohol dehydrogenase activity

To study the protective effects of garlic oil (GO) on the peripheral nerve injuries induced by n-hexane. Male Wistar rats were randomly divided into four groups (10 rats in each group): the control, the n-hexane treatment (2000 mg/kg), the low dose GO, and the high dose GO groups. The rats in the low and high doses of GO groups were pretreated with GO (40 and 80 mg/kg) before exposure to n-hexane (2000 mg/ kg), while the animals of the n-hexane treatment group were given normal saline and then 2000 mg/ kg n-hexane. The rats were exposed to GO and n-hexane 6 times a week for 10 weeks. The gait scores and staying time on the rotating rod for all rats were detected every two weeks. The rats were sacrificed at the end of ten weeks, then the levels of alcohol dehydrogenase (ADH), maleic dialdehyde (MDA), reduced glutathione (GSH), glutathione peroxidase(GSH-Px), total antioxidation capacity(T-AOC) and the ability of inhibition of *OH in livers were examined. The gait scores increased significantly and the time staying on the rotating rod obviously decreased in rats of n-hexane treatment group, as compared with control group (P < 0.05 or P < 0.01). In the hepatic tissues of n-hexane group, the levels of MDA and ADH significantly increased, the activities of GSH-Px, T-AOC and the ability of inhibition of *OH obviously decreased, as compared to control group (P < 0.05 or P < 0.01). In 2 GO groups, the gait scores and the staying time on the rotating rod were significantly improved, the levels of MDA and ADH significantly decreased, the activities of GSH-Px, T-AOC and the ability of inhibition of *OH obviously increased, as compared with n-hexane group (P < 0.05 or P < 0.01 ). ADH could play an important role in the protective effects induced by garlic oil on the peripheral nerve injuries produced by n-hexane.

Protective effect of garlic oil against liver injury in experimental animals

Food derived antioxidants have a strong potential effect on the long term as chemopreventive agents in disease states involving oxidative stress, such as hepatitis. This study was done to clarify the potential effect of garlic oil in protecting the liver from lipopolysaccharide-induced hepatitis in D-galactosamine sensitized rats. Sixty male albino rats were used in the study. They were divided into four groups (15 rats in each) as follow: Group I (control group) received normal saline, group II (garlic group) received garlic oil orally, group III (DGa1N/LPS intoxicated) received normal saline orally for 15 days and then injected intraperitoneally by DGa1N/LPS for induction of hepatitis and group IV (garlic pretreated) received garlic oil (200 mg/kg body weight/day) for 15 days and then injected by DGa1N/LPS.DGaIN/LPS induced hepatic damage in rats manifested as significant increase in the mean levels of serum liver enzymes and production of oxidative stress manifested as significant increase in urinary F2- isoprostane (lipid peroxidation parameter), AOPP (protein oxidation parameter) and urinary 8-hydroxyguanosine (parameter of oxidative DNA damage). The damage of liver tissue is also confirmed by the histopathological examination. Pretreatment with garlic oil significantly ameliorated the toxic effect of DGa1N/LPS on the liver. Key words: Hepatitis, galactosamine, oxidative stress, garlic oil.

Garlic Oil and Vitamin E Prevent the Adverse Effects of Lead Acetate and Ethanol Separately as well as in Combination in the Drinking Water of Rats.

Daily feeding of drinking water containing lead acetate (160mg/l) or 10% alcohol by volume or a combination of both to rats for a month produced certain deleterious effects through oxidative stress. Both heavy metal lead and alcohol are capable of doing such damages. The deleterious alterations observed were in the parameters of blood, serum and tissues, viz; Hb, Pb, proteins, lipids, lipid per oxidation, Vitamins C and E levels and enzyme activities of AST, ALT, and catalase. Simultaneous feeding of either of the two antioxidants garlic oil (GO) and vitamin E at equal doses of 100mg/kg/day, to the rats counteracted the deleterious effects of the above two chemicals significantly. The maximum damage was brought about by feeding of drinking water containing both lead acetate and alcohol. The protective effects of GO and Vitamin E were not significantly different. The mechanism of actions of the Vitamin E and GO is probably due to their efficiency as detoxifying agents and antioxidants, to scavenging free radicals as well as an independent action of GO on the removal of lead salt as lead sulfide.

Protective effect of garlic oil given at different time against acute liver injury induced by CCl4

To observe and compare the protective effect of garlic oil against carbon tetrachloride (CCL)-induced acute liver injury. The experiments include 4 preventive groups and 2 therapeutic groups. In every preventive and therapeutic group, the mice were randomized into 6 groups with 15 each, including one negative control group, one solvent control group, one CCl4 model group and 3 garlic oil groups (25, 50, and 100 mg/kg body weight). Before given a single gavage of CCl4 (80 mg/kg), the mice were pretreated with garlic oil by gavage in preventive group 1 (30 days, once daily), preventive group 2 (5 days, once daily), preventive group 3 (ahead of 2 h, once), preventive group 4 (immediately, once) or the vehicle (corn oil, 10 ml/kg) in solvent control group. In therapeutic groups, the mice were gavaged garlic oil 2 h (once, in therapeutic 1) or for 5 days (once daily, in therapeutic 2) after administration CCl. After 24 h of the last administration, blood was collected and centrifuged at 2500 r/min at 4 degrees C for 10 min, and serum was removed to measure ALT and AST activities. The liver was dissected, weighed to calculate the liver coefficient (relative liver weight). At the same time, the liver samples were studied by histological examinations. Compared with negative group, the liver coefficient and the activities of ALT and AST in serum of model group were increased remarkably (P < 0.01). Compared with CCl model group, the liver coefficient and the activities of ALT and AST in serum were decreased significantly (P < 0.01) by garlic oil dose-dependently in each preventive group. Simultaneously, histological assessment showed that garlic oil effectively alleviated hepatocyte injuries induced by CCl4. Comparing the preventive effects of garlic oil in every group, it was better in preventive group 3 than others. However, all indexes and histological examinations in therapeutic group 1 did not show the difference with those of CCl4 model group. In therapeutic group 2, all indexes recovered after 5 d of CCl4 administration. Garlic oil can prevent acute liver injury induced by CCl4 and the effect is better in ahead of 2 h group than others.

The protective effects of garlic oil on acute ethanol‐induced oxidative stress in the liver of mice

AbstractBACKGROUND: Alcoholic liver disease is so serious that no effective therapies have been developed up to now. This study was conducted to elucidate the effects of garlic oil (GO) on acute ethanol‐induced liver injury. Male Kun‐Ming mice were orally administered GO (50, 100 or 200 mg kg−1) for 30 days and then ethanol (4.8 g kg−1). At 16 h after ethanol treatment the mice were sacrificed. Subsequent serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and triglyceride (TG) levels, hepatic malondialdehyde (MDA) and glutathione (GSH) levels and antioxidant enzyme activities were measured. Histopathological examination of mouse liver sections was performed by Sudan III staining.RESULTS: GO pretreatment significantly inhibited acute ethanol‐induced increase in ALT, AST, TG and MDA and decrease in GSH in a dose‐dependent manner. In the three GO groups the level of GSH increased by 10.3%, 15.8% (P &lt; 0.05) and 25.5% (P &lt; 0.01) respectively compared with that in the ethanol group. The activities of superoxide dismutase, catalase and glutathione reductase were increased markedly in the 200 mg kg−1 GO group (P &lt; 0.01). Histopathological examination showed fewer fat droplets in liver sections of GO‐pretreated mice.CONCLUSION: GO may have protective effects against acute ethanol‐induced liver injury through restoration of the GSH level and enhancement of the activities of antioxidant enzymes. Copyright © 2008 Society of Chemical Industry

Garlic oil ameliorates ferric nitrilotriacetate (Fe-NTA)-induced damage and tumor promotion: Implications for cancer prevention

Intraperitoneal injection of ferric nitrilotriacetate (Fe-NTA) to rats and mice results in iron-induced free radical injury and cancer in kidneys. This study was designed to investigate the effects of garlic oil on Fe-NTA-induced damage and tumor promotion. Pretreatment of rats with garlic oil at a dose regimen of 50–100 mg/kg body weight for a week significantly and dose dependently protected against Fe-NTA induced damage as well as tumor promotion. Garlic oil afforded protection against hepatic lipid peroxidation, generation of hydrogen peroxide, preserved glutathione levels and activities of antioxidant enzymes. A protection against Fe-NTA induced hepatic tumor promotion was also apparent as inhibition in the modulation of hepatic tumor markers viz., ornithine decarboxylase activity and DNA synthesis. These results clearly demonstrate the role of oxidative stress and its relation to tumor promotion and suggest protective effects of garlic oil against Fe-NTA induced hepatic toxicity and it can serve as potent chemopreventive agent to suppress oxidant-induced tissue injury and carcinogenesis.

Garlic Oil Enhances Hepatic and Blood Antioxidants During Hamster Buccal Pouch Carcinogenesis

We analyzed the protective effect of garlic oil on hepatic and blood lipid peroxidation and the antioxidant status during buccal pouch carcinogenesis induced by 7,12-dimethylbenz[a]anthracene (DMBA) in male Syrian hamsters. Enhanced lipid peroxidation in the liver and blood of tumor-bearing animals was accompanied by a significant decrease in antioxidant levels. Topical application of garlic oil effectively suppressed oral carcinomas, decreased lipid peroxidation, and enhanced antioxidant levels. Our results suggest that garlic oil may exert its chemopreventive effects by modulating lipid peroxidation and enhancing antioxidant status in the liver and blood.

Protective Effects of Garlic Oil against Liver Damage Induced by Combined Administration of Ethanol and Carbon Tetrachloride in Rats

Herbs are known to play a vital role in the management of various liver diseases. Garlic oil (GO) contains numerous organosulfur compounds with potential hepatoprotective effects. The present work was planned to evaluate the possible preventive role of GO on biochemical and histopathological alterations induced by combined administration of ethanol (EOH) and carbon tetrachloride (CCl4) in rat liver. Two dose levels of GO (5 or 10 mg/kg/day) were administered orally to rats for 7 consecutive days with EOH + CCl4-induced liver damage. Activity of GO against liver damage was compared with that of silymarin (25 mg/kg/day, p.o. for 7 consecutive days). Biochemical parameters including serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyl transpeptidase (γ–GT), alkaline phophatase (ALP) and bilirubin were estimated to assess the liver function. In addition, the level of total proteins, triglycerides, total cholesterol, glutathione (GSH), and thiobarbituric acid reactive substances (TBARS), in liver tissues were estimated. Liver damage was evidenced by an increase in the activity/level of AST, ALT, γ-GT, ALP and bilirubin in sera of rats after the combined administration of EOH and CCl4 compared to normal animals. Pretreatment of rats with GO reduced the EOH + CCl4-induced elevated levels of the above indices. Similarly, GO significantly prevented the decline in total proteins and the increase in triglycerides and total cholesterol resulted after EOH + CCl4 administration in rat liver homogenates. In addition, GO pretreatment restored liver GSH levels decreased due to EOH + CCl4 administration. The elevation in liver TBARS level due to EOH + CCl4 administration was also prevented by pretreatment with both low and high doses of GO. Histopathological examination indicated that GO exhibited an obvious preventive effect against the centrilobular necrosis and nodule formation induced by EOH + CCl4 administration. In conclusion, GO exerts hepatoprotective actions against EOH + CCl4-induced toxicity in rats.

Protective Effects of Garlic Oil against Liver Damage Induced by Combined Administration of Ethanol and Carbon Tetrachloride in Rats

Herbs are known to play a vital role in the management of various liver diseases. Garlic oil (GO) contains numerous organosulfur compounds with potential hepatoprotective effects. The present work was planned to evaluate the possible preventive role of GO on biochemical and histopathological alterations induced by combined administration of ethanol (EOH) and carbon tetrachloride (CCl4) in rat liver. Two dose levels of GO (5 or 10 mg/kg/day) were administered orally to rats for 7 consecutive days with EOH + CCl4-induced liver damage. Activity of GO against liver damage was compared with that of silymarin (25 mg/kg/day, p.o. for 7 consecutive days). Biochemical parameters including serum aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyl transpeptidase (γ–GT), alkaline phophatase (ALP) and bilirubin were estimated to assess the liver function. In addition, the level of total proteins, triglycerides, total cholesterol, glutathione (GSH), and thiobarbituric acid reactive substances (TBARS), in liver tissues were estimated. Liver damage was evidenced by an increase in the activity/level of AST, ALT, γ-GT, ALP and bilirubin in sera of rats after the combined administration of EOH and CCl4 compared to normal animals. Pretreatment of rats with GO reduced the EOH + CCl4-induced elevated levels of the above indices. Similarly, GO significantly prevented the decline in total proteins and the increase in triglycerides and total cholesterol resulted after EOH + CCl4 administration in rat liver homogenates. In addition, GO pretreatment restored liver GSH levels decreased due to EOH + CCl4 administration. The elevation in liver TBARS level due to EOH + CCl4 administration was also prevented by pretreatment with both low and high doses of GO. Histopathological examination indicated that GO exhibited an obvious preventive effect against the centrilobular necrosis and nodule formation induced by EOH + CCl4 administration. In conclusion, GO exerts hepatoprotective actions against EOH + CCl4-induced toxicity in rats.