Effect of abhrak bhasma and silicon dioxide on hepatic and renal glutathione status in rats: hepatoprotection testing against single dose carbon tetrachloride induced hepatotoxicity
Background: Glutathione (GSH) is an important intracellular antioxidant. Intrahepatic GSH levels are depleted in liver diseases.
Objectives: In present study, effect of abhrak bhasma (an Ayurvedic drug) and silicon dioxide (SiO2) on hepatic and renal GSH status against CCl4 intoxicated male albino rats were investigated.
Methods: Single dose of CCl4 (3.0ml/kg body wt, sc) was used to induce hepatotoxicity. Graded doses (10, 20, 30 and 40mg/ kg body wt) of abhrak bhasma and SiO2 were concurrently given with CCl4. Hepatic and renal GSH content was studied after 24 hrs.
Results: Results showed that rats exposed to CCl4 exhibited decreased GSH in liver. It was counteracted and maintained to normal levels by the treatment of abhrak bhasma (minimum protective dose-10mg). SiO2 treatments did not affect GSH activity in liver significantly. Single dose of CCl4 had not influenced GSH content in kidney alone or with any of the doses of abhrak bhasma or SiO2.
Conclusion: CCl4 single dose depletes GSH content significantly in liver but not in kidney. These results suggest that single dose treatment of abhrak bhasma (10mg onwards) protects GSH content and thus manages CCl4 induced free radical generation scavenging them.
Keywords: Abhrak Bhasma, Antioxidant, Glutathione, Hepatotoxicity, Silicon Dioxide.
Burk RF, Lane JM & Patel K (1984), Relationship of oxygen and glutathione in protection against carbon tetrachloride-induced hepatic microsomal lipid peroxidation and covalent binding in the rat. Rationale for the use of hyperbaric oxygen to treat carbon tetrachloride ingestion. J Clin Invest. 74(6), 1996-2001. http://dx.doi.org/10.1172/JCI111621.
Deneke S (2000), Thiol-based antioxidants. Curr. Top. Cell Reg. 36, 151. http://dx.doi.org/10.1016/S0070-2137 (01)80007-8.
Edward AL & Celia JR (1998), Xenobiotic Metabolizing En-zymes of the Kidney" Toxicologic Pathology 26(1), 18-25. http://dx.doi.org/10.1177/019262339802600102.
Grunert RR & Phillips P H (1951), Determination of glutathione. Arch Biochem, 30(2), 217-225.
Kaplowitz N, Aw TY, Simon FR & Stolz A (1986), Drug in-duced hepatotoxicity. Ann Intern Med; 104, 826-39. http://dx.doi.org/10.7326/0003-4819-104-6-826.
Ljubuncic P, Tanne Z & Bomzon A (2000), Evidence of a sys-temic phenomenon for oxidative stress in cholestatic liver disease. Gut, 47 (5), 710-716. http://dx.doi.org/10.1136/gut.47.5.710.
Ljubuncic P & Bomzon A (2006), Liver disease, oxidative stress and ursodeoxycholic acid," in Liver Diseases: Biochemical Mechanisms and New Therapeutic Insights, S. Ali, S. L. Friedman, and D. A. Mann, Eds., Science, New Hampshire, NH, USA.
Majno G & Joris I (2004), Cells, Tissues, and Disease, Princi-pals of General Pathology, 2nd Edi. Oxford University Press, New York and Oxford.
Nebbia C (2001), Biotransformation enzymes as determinants of xenobiotic toxicity in domestic animals.Vet J., 161(3): 238-52. http://dx.doi.org/10.1053/tvjl.2000.0561.
Parke DV and Piotrowski J (1996), Glutathione: Its role in detoxification of reactive oxygen species and environmental chemicals. Acta Pol. Toxicol, 4(1).
Purucker E, Wernze H & Krandik G (1995), Glutathione in plasma, liver and kidney in the development of CCl4-induced cirrhosis of the rat. Res Exp Med. 195, 193-200. http://dx.doi.org/10.1007/BF02576788.
Recknagel RO, Glende EA, Dolack JA, Walter RL (1992), Mechanism of carbon tetrachloride toxicity. Pharmacol ther, 43, 139-154. http://dx.doi.org/10.1016/0163-7258 (89)90050-8.
Sharma S (1977) Rasa Ratna Samuchhaya, Published by Motilal Banrasidas, New Delhi, 72-108.
Teli P, Jadhav J & Kanase A (2014), Comparison of abhrak bhasma and silicon dioxide efficacy against single dose of carbon tetrachloride induced hepatotoxicity in rat by evaluation of lipid peroxidation. International journal of pharmaceutical science and research, 2 (7): 186-196.