HEPATOPROTECTIVE EFFECTS OF SENNA TORA LEAF EXTRACT ON CARBON TETRACHLORIDE INDUCED TOXICITY
Many of the developing countries including African countries like Nigeria practice traditional medicine as its main source of health care. This traditional medicine is normally gotten from plant origin [Rehan Ahmad et al, 2008, Stephen bent, 2008].Today nearly 88 percent of the global populations switch to plant derived medicines as their first line of defence for maintaining health and combating diseases [Kintzios et al,2006]. Presently there are about 60 types of medicinal plants that have been recognised in primary health care and are classified according to their pharmacological actions such as peptic ulcers, anti flatulence, laxative, antidiarrhoeal and anti hepatic [Viomolos et al,2003]. However in future the discovery of novel therapeutic agents will be only dependent on plant origin [Perumalsamy et al, 1999].
Senna tora is an example of traditional medicine with pharmacological actions as anticholesterolemic, antispasmodic, carninitative, emollients, ophthalmic and purgative [Polunin and Stainton,1984,Yeung,1985,Manandhar, 2002]. It can be cardiotonic, antiperiodic, anthelmintic and expectorant and can also be used in treating cough,leprosy ,ringworm ,colic,flatulence, constipation and other disorders[Natureserve,2007]. Senna tora formally regarded as cassia tora is capable of suppressing the production of prostaglandins and other inflammatory agonists such as cytokines, histamine, kinin and free radical.manila,1998 buttressed his observations confirming its use in the treatment of constipation, edema and liver protection in Korea.
Liver, the largest internal organ of the human body performs more than five hundred functions, all of which are very vital to life. The liver can regenerate or grow back cells that have been destroyed by short term injury or disease, but if the liver is damaged repeatedly over a long period of time, it may undergo irreversible changes which permanently interferes with its function.
Carbon tetrachloride is a toxic substance that interrupts the liver and its functions. This is to say that it damages the liver when ingested.CCL4 is stable in the presence of air and light, it is also inflammable. Despite its toxic effect on the liver, it is useful as grain fumigant ,pesticide etc. Equilibrium of the body fluids and secretions are altered as a result of carbon tetrachloride. For instance lipid metabolism, cholesterol metabolism and biotransformation functions of the liver are terminated or altered in the presence of CCL4.Thus carbon tetrachloride is lethal. The liver produces some enzyme such as aspartate amino transaminases, alkaline phosphatase, lactate dehydrogenase,gamma glutamyl transferase etc which catalyses the biochemical activities of the body, and on the attack of CCL4 to the liver ,these enzymes will not be produced.
Free radicals are highly reactive compounds with uneven number of electrons in their outermost orbit. This can react with cellular compounds like unsaturated fatty acids and can generate new free radicals which result in irreversible biochemical injury like membrane damage, apotosis and cell necrosis. Antioxidants scavenge free radicals and stop the subsequent reactions hence protecting the macromolecules and cellular environment from toxicity and degeneration [Hong B.O. Shao et al, 2008].The oxygen consumption inherent in cell growth leads to the generation of series of reactive oxygen species [ROS].The ROS are molecules such as superoxide anion radicals and hydroxyl radicals[OH]. ROS may be very damaging attacking the lipids of cell membrane and DNA mutation which may further propagate the propagation of many diseases[Valontao et al 2002,Gulcin et al 2003]. Reactive oxygen species are continuously produced during normal Physiological events and are removed by antioxidants defence mechanism [Buyukokuroglu et al,2001]. Many results have shown that some of the cassia species have acquired antimicrobial substances and antioxidant activities.
1.1 AIMS OF THE RESEARCH
The aim of this research is to find out hepatoprotective effects of senna tora leaf extract on carbon tetrachloride induced toxicity.
Anders, M. W, and Jakobson, J. (1985). Biotran S Formation of Halogenated Solvents – Second J. Work Environ Health, 11(Sup PL I):23-32.
Armstrong, R. N. (1993). Glutathione S – Transferees; Structure and Mechanism of an Archetypical Detoxification Enzyme. Advanced Enzymolgy, 69:144. Available Online at http//www.biotrius /lLab/cancer/html.
Bagnasco, F. M., Shrines, B. and Muslim, A. M. (2001). Carbon Tetrachloride Poisoning: Adiographic Findings. NY State J. Med, 78:646-647.
Betteridge, D. J. (2000). What is Oxidative Stress Metabolism, 49:3-8.
Burk R. F, Patel, K. and Iane, J.M. (1984). Reduced Glutathione Protection Against Carbon Tetrachloride Induced Hepatic Miciosomal Lipid Peroxidation and Covalent Binding in the Rat. J. Clin Invest, 74:1996 – 2001.
Buttler, J. C. (1961). Liver in Toxication. J. Pharmacol Exp The. 143: 311-319.
Crawford, M. C. (2003). Current Diagnosis and Treatment on Cardiology. 2nd Edition. New York: Lang Medical Books/McGraw-Hill Medical Publishing Division pp 1529.
sKndo, A (1992). The Discovery and Development of HMG CoA Reductase Inhibiters. http://en.wikipedia. Org/wiki/statin.
Gamble, J. S (1972). A Manual of Indian Timbers, Bishen Singh mahandra pal Singh.
Ganett, R. R and Grishman, C. M (1999). Cholesterol: Garrett and Grishman Biochemistry, 2nd Edition. Thomson Books Coole, USA. Pp.03 – 350.
Halliwell, B., Muicia, M.A., Chirico, S and Aruome, O. I (1995). Free Radicals and Antioxidants in Food and Invivo: What they do and how they work Crit Rev Food Sci. Nutri., 35:7 – 20.
Holly. S. (1996). Lipid Peroxidation Occur via Metabolic Intermediates. Marnett L. J. Mutation Research 1997 Man 8; 424:83 – 95.
Jones P; Katonek 5, Laurora I. Hunning Shake D. (1998). Comparative Dose Efficiency Study of Atorvastation.
Kenaga B. (1995). Tissue Levels of Carbon Tetrachloride After Gastric Infusions. Proc Nati. Acad. Sci. USA. 98 – 83.
Ken, B. (2004). Reversing Liver Damage: 515. John Wiley and Sons, New York. Available Online at http//www.pubmodcentral.Nih/gov/articte–renderartid.
Khurana, V., Bejjanki. H.R., Caldito. G., Owens. M.W. (2007). Stations Reduce the Risk of Lung Cancer in Humans a Large Case Control Study of us Verterans. http://en. Wikipedia. Org/wiki/stin.
Klein, Barbara E.K., Ronald M.D., Kristine G., Losa M. (2006). Statin Use and Incident Nuclear Cataract. http:en. Wikipedia. Org/wiki/ statin.
Kim, H. J. Odendhal, S. & Bruckner, J. V (1995). Effect of Dosing Vehicles on the Acute Hepatoxicity of Carbon Tetrachloride in Rats. Toxicol. Allp. Pharmacol; 102, 34 – 49.
Manaudhau, N. P. (2002). Plants and People of Nkpal, Timber Press Oregon ISBN 0 – 85 192 – 527 – 6.
Manila, (1998). Medical Plants in the Republic of Korea. World Health Organization ISBN 92 – 9061 – 120 -0.
Marchard, C., McLean, S. and plea G.L. (1990). The Effect of SKF. 525A on the Distribution 259: 2135 – 2143. Available on Link at http://www.inchem. Org/documents ehk/ehc/ek 28. html.
MC Gregor, D. and Lang M. (1996). Carbon Tetrachloride; Genetic Effects and other Modes of Action. Mutate Res, 366: 181 – 195.
Muphy, S. D., and Malley, S. (1969). Effects of Carbon Tetrachloride on Induction of Liver Enzymes by Acute Stress of Corticosterones Toxtcol, Appl Pharmacol, 15: 117 – 130.
Moss, D.W.; Henderson, A.R. and Kachmar, J.R. (1986). Enzymes. In N. W. Tietz(ed); Textbook of Clinical Chemistry (Philade/Phin: W.B. Saunders), Pp. 619 – 663.
Munoz Torres, E., Paz Bouza, J. I, A bad Hernandez. M. M, Alonso Martin, M.J. and Lopez Brano A. (1988). Experimental Carbon Tetrachloride Induced Cirrhosis of the Liver. Int J. Tissue React, X: 245 – 251.
Murray, R.K., Granner, D.K., Mayeis, P.A. and Rod Owel. V.W. (2003). Harper’s Biochemistry 26th ed. McGraw Publisher, New York.
Nakata, R. Tsukamoto I., Miyoshi, M. and Kojo S. (1985). Liver Regeneration After Carbon Tetrachloride Intoxication in the Rat, Biochem Pharmacol, 34: 586-588. Available online at http://www.inchem/org/documents/ehc/ehc/ehc 208. html.
National Library of Medicine (1997). Hazardous Substances Data Bank – Bethseda, Maryland National Library of Medicine National Toxicology Information Programme. Available Online at http://www.inchem.org/document ehc/ehc/ehc 208. htm.
Packer, J.E., Slater, T.F. and Wilson, R.L., (1978). Reactions of the Carbon Tetrachloride Related Peroxy Free Radical (CCL3O20) with Amino Acids: Pulse Radiolysis Evidence Life Sci,. 23: 2617 – 2620. Available online at http://www.inchem.org/documents/ehc/ehc/ehc. 208 html.
Paul, B. B, and Rublistein, D. (1993). Metabolism of Carbon Tetrachloride and Chloroform by the Rat. J. Pharmacol E x Ther, 141: 141 – 148.
Rej, R., and Horder, M. (1983). Aspartate Aminotransferase. In Methods of Enzymatic Analysis. Bergmeyer H. U., Bergmeyer J. Grasse M. Eds Wein. Hein, verlag chemic 3:416- 433.
Sies, H. (1997). Oxidative Stress; Oxidants and Antioxidants. Exp Physiol 82: 291 – 295. Available Online at http:/www.pdf Health.com /drug info./nm drug profiles/nuts up drugs/glu 0126. shtml.
Song, Z Joshi – Barve, S., and McClain, C. J. (2004). A Drances in Alcoholic Liver Disease. Curr Gastroenterol Rep, 6:21 – 76.
Withey, J.R., Collins, B.T., and Collins, P.G. (1983). Effects of Vehicle on PharmaCokinetics and Uptake of Four Halogenated Hydrocarbons from the Gastrointestinal Tract of the Rat. J. APPL Toxicol, 3:249 – 253. Retrieved July 1 2010 from http:/www.inchem.org/documents/ehc/ehc/ehc 208. html.
Wolozin B, Wang S.W., Li N.C., Lec. H., Tee. T.A., Kazis L.E. (2007). Sima Stain is Associated. With a Reduced Incidence of Dementia and Parkinson’s Diseases. http://en wikipedia. Org/Wiki/ statin.
Versus S. Moastatin, Pravastatin, Lovastatin and Fluvastatin in Patients with Hypercholesterolemia. Http://en.wiki Redia. Org/Wiki/Statin.