Written by Angeline A. De Leon, Staff Writer. Peppermint oil, in doses of 15 and 40 mg/kg of body weight, protected against the hepato and renotoxicity from CCL4-induced oxidative stress as witnessed by a significant increase in the regenerative and reparative capabilities of both liver and kidneys of the participating rats.
The liver, an essential organ involved in the metabolism of fats, proteins, and carbohydrates and the purification and detoxification of blood, is particularly vulnerable to damage from free radicals (reactive oxygen species, ROSs). Evidence from experimental studies of liver disease highlights carbon tetrachloride (CCl4) as one of the primary environmental toxins associated with liver damage at the cellular level 1. CCl4 is a manufactured chemical, a colorless gas used in refrigerant fluids, pesticides, and certain dry-cleaning agents. Environmental reports identify CCl4 as a harmful contaminant associated with the production of free radicals, and since the early 2000’s, the supply and use of CCl4 have been largely restricted due to its toxic effects 2. Increasingly, research has turned to the use of natural antioxidants to bolster the body’s defense against free radical-mediated diseases. For example, oil of Mentha piperita L. (peppermint oil), an essential oil traditionally used for its anti-inflammatory, analgesic, and antiseptic properties, demonstrates clinical benefits for conditions ranging from ulcerative colitis to neuralgia 3. Research now confirms that the various pharmacological actions of peppermint oil stem from its high antioxidant activity and ability to protect against lipid peroxidation 4. For this reason, animal researchers in Tunisia aimed to examine whether the antioxidant activity of peppermint oil could provide protective benefits against CCl4-induced oxidative stress. In this trial, they compared the effects of peppermint oil to that of silymarin, a commonly used plant extract for liver and kidney health with proven hepatoprotective properties 5.
The controlled trial 6 involved a total of 70 male Wistar rats which were divided into seven groups and treated for one week. Group 1 (control) received saline orally for seven days and was injected with 1 ml/Kg BW (body weight) of a CCl4 solvent (olive oil) on the final day. Group 2 (control group for liver and kidney toxicity) received saline orally for seven days and was injected with 1 ml/Kg BW of a CCl4 and olive oil mixture. Group 3 was orally pretreated with 50 mg/kg BW of silymarin once every 24 hours. Groups 4, 5, 6, and 7 were orally pretreated with peppermint oil (5, 15, and 40 mg/kg BW, respectively) once every 24 hours. Following pretreatment with either silymarin or peppermint oil for one week, rats received an injection of 1 ml/kg BW of CCl4 on the 7th day and then sacrificed. In order to evaluate liver and kidney function, plasma levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), and gamma-glutamyl transpeptidase (GGT) were assessed. Additionally, antioxidant enzyme activities in liver and kidney tissue were evaluated by measuring catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx). Thiobarbituric acid reactive substances (TBARS, marker for free radical mediated lipid peroxidation) activity levels were also assessed.
While pretreatment with 5 mg/kg of peppermint oil failed to induce any significant changes in biochemical parameters, at doses of 15 and 40 mg/kg, peppermint oil was found to significantly reduce AST (15 mg/kg = 356.82 U/L, 40 mg/kg = 216.80 U/L), ALT (15 mg/kg = 147.35 U/L, 40 mg/kg = 97.82 U/L), ALP (15 mg/kg = 186.74 U/L, 40 mg/kg = 165.96 U/L), LDH (15 mg/kg = 34.16 U/L, 40 mg/kg = 31.64 U/L), and GGT levels (15 mg/kg = 4.06 U/L, 40 mg/kg = 3.51 U/L) (p < 0.05 for all), compared to the CCl4 group. Moreover, relative to CCl4, pretreatment with 40 mg/kg of peppermint oil was also associated with significant reduction in TBARS (p < 0.001), along with an increase in antioxidant enzymes SOD, CAT, and GPx (p < 0.01 for all) for both the liver and kidney.
Evidence substantiates the protective effects of peppermint oil against CCl4-induced oxidative damage in rodents, indicating that the essential oil significantly improves indicators of kidney and liver health. Results suggest that therapeutic effects may indeed be attributable to the free radical scavenging, antioxidant activities of peppermint oil. Given promising results in an animal model, future investigations confirming findings in human subjects would be valuable.
Source: Bellassoued K, Hsouna AB, Athmouni K, et al. Protective effects of Mentha piperita L. leaf essential oil against CCl4 induced hepatic oxidative damage and renal failure in rats. Lipids in Health and Disease. 2018; 17: 9. DOI: 10.1186/s12944-017-0645-9
© The Author(s). 2018 Open Access This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/)
Click here to read the full text study.
Posted July 20, 2018.
References:
- Wang C-Y, Ma F-L, Liu J-T, Tian J-W, Fu F-H. Protective effect of salvianic acid a on acute liver injury induced by carbon tetrachloride in rats. Biological and Pharmaceutical Bulletin. 2007;30(1):44-47.
- Abraham P, Wilfred G, Cathrine S. Oxidative damage to the lipids and proteins of the lungs, testis and kidney of rats during carbon tetrachloride intoxication. Clinica Chimica Acta. 1999;289(1-2):177-179.
- Cowan MM. Plant Products as Antimicrobial Agents. 1999.
- Lee C-P, Shih P-H, Hsu C-L, Yen G-C. Hepatoprotection of tea seed oil (Camellia oleifera Abel.) against CCl4-induced oxidative damage in rats. Food and Chemical Toxicology. 2007;45(6):888-895.
- Shahjahan M, Sabitha K, Jainu M, Devi CS. Effect of Solanum trilobatum against carbon tetrachloride induced hepatic damage in albino rats. Indian Journal of Medical Research. 2004;120(3):194.
- Bellassoued K, Hsouna AB, Athmouni K, et al. Protective effects of Mentha piperita L. leaf essential oil against CCl 4 induced hepatic oxidative damage and renal failure in rats. Lipids in health and disease. 2018;17(1):9.