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252 ASHFAQ AHMAD et al.4. Ha H., Park J., Kim Y.S., Endou H.: YonseiMed. J. 45, 1049 (2004).5. Nakao A., Kaczorowski D.J., Sugimoto R.,Billiar T.R., McCurry K.R.: J. Clin. Biochem.Nutr. 42, 78 (2008).6. Nunomura A., Moreira P., Takeda A., SmithM., Perry G.: Curr. Med. Chem. 14, 2968(2007).7. Wei YH., Lu CY., Wei CY., Ma YS., Lee HC.:Chin. J. Physiol. 44, 1 (2001).8. Stipanuk M.H., Beck P.W.: Biochem. J. 206,267 (1982).9. Wang R.: FASEB J. 16, 1792 (2002).10. Yong Q.C., Pan T.-T., Hu L.-F., Bian J,-S.: J.Mol. Cell. Cardiol. 44, 701 (2008).11. Hosoki R., Matsuki N., Kimura H.: Biochem.Biophys. Res. Commun. 237, 527 (1997).12. Zanardo R.C.O., Brancaleone V., Distrutti E.,Fiorucci S., Cirino G., Wallace J.L.: FASEB J.20, 2118 (2006).13. Fiorucci S., Distrutti E., Cirino G., WallaceJ.L.: Gastroenterology 131, 259 (2006).14. Zhong G.Z., Chen F.R., Cheng Y.Q., Tang C.S.,Du J.B.: J. Hypertens. 21, 1879 (2003).15. Brunner F., Andrew P., Wˆlkart G., Zechner R.,Mayer B.: Circulation 104, 3097 (2001).16. Packer M., Bristow M.R., Cohn J.N., ColucciW.S., Fowler M.B., Gilbert E.M.: N. Engl. J.Med. 334, 1349 (1996).17. Ye S., Nosrati S., Campese V.M.:. J. Clin.Invest. 99, 540 (1997).18. Mazzali M., Hughes J., Kim Y.-G., J. JeffersonJ.A., Kang D.-H., Gordon K.L., Lan H.Y. et al.:Hypertension 38, 1101 (2001).19. Harisa G.E.I., Abo Salem O.M.., El-Sayed E.-S.M., Taha E.I., El-Halawany N.: Pak. J.Pharm. Sci. 4, 373 (2009).20. Whiteman M. Li L., Kostetski I., Chu S.H., SiauJ.L., Bhatia M.: Biochem. Biophys. Res.Commun. 343, 303 (2006).21. Ali M.Y., Ping C.Y., Mok Y.-Y.P., Ling L.,Whiteman M., Bhatia M., Moore P.K.: Br. J.Pharmacol. 149, 625 (2006).22. Hussain A.I., Anwar F., Hussain Sherazi ST.,Przybylski R.: Food Chem. 108, 986 (2008).23. Anwar F., Ali M., Hussain A.I., Shahid M.:Flavour Fragr. J. 24, 170 (2009).24. Hussain A.I., Anwar F., Chatha S.A.S., JabbarA., Mahboob S., Nigam P.S.: Braz. J.Microbiol. 41, 1070 (2010).25. Irvine J.C. Ritchie R.H., Favaloro J.L.,Andrews K.L., Widdop R.E., Kemp-HarperB.K.: Trends Pharmacol. Sci. 29, 601 (2008).26. Ferreira I.C.F.R., Baptista P., Vilas-Boas M.,Lillian Barros L.: Food Chem. 100, 1511(2007).27. Patel R.P., Levonen A.L., Crawford J.H.,Usmar D.V.M.: Cardiovasc. Res. 47, 474(2000).Received: 12. 12. 2013
Acta Poloniae Pharmaceutica ñ Drug Research, Vol. 72 No. 2 pp. 253ñ260, <strong>2015</strong> ISSN 0001-6837Polish Pharmaceutical SocietyCLINDAMYCIN: EFFECTS ON PLASMA LIPID PROFILEAND PEROXIDATION PARAMETERS IN RABBIT BLOOD PLASMAPRITESH DEVBHUTI 1 *, ACHINTYA SAHA 2 and CHANDANA SENGUPTA 31Division of Medicinal and Pharmaceutical Chemistry, Gupta College of Technological Sciences,Ashram More, G. T. Road, Asansol-713301, West Bengal, India2Department of Chemical Technology, University of Calcutta, Kolkata-700009, India3Division of Medicinal and Pharmaceutical Chemistry, Dept. of Pharmaceutical Technology,Jadavpur University, Kolkata-700032, IndiaAbstract: Alteration of plasma lipid profile and induction of lipid peroxidation may take place due to drugeffect, which may be correlated with adverse drug reactions and drug-induced toxicity. Considering this fact,the present in vivo study was carried out to evaluate the effect of clindamycin on plasma lipid profile and peroxidationparameters alone and in combination with ascorbic acid, a promising antioxidant. After administeringdrug and antioxidant alone and in combination in rabbit, it was found that clindamycin had mild lipid peroxidationinduction and profile alteration capacity, which can be arrested on co-administration of ascorbic acid.Keywords: clindamycin, adverse drug reactions, lipid peroxidation, lipid profile, ascorbic acidDuring the passage of transport, drug has tocross many barriers, most of which are lipoidal innature. Interaction of drug with membrane lipidsmay lead to alteration in lipid pattern and composition,as well as lipid peroxidation, which is a measureof the membrane damage. Lipid peroxidation isthe oxidative deterioration of polyunsaturated lipids(1). It is a highly destructive process that induces awide variety of alterations in the structure and functionof cellular membranes (2), and an importantcause of certain diseases or disorders, like diabetesmellitus, gastric ulcer, neurodegenerative diseases(3), atherosclerosis (4), aging (5) etc. Indomethacininducedgastric mucosal damage (6) and doxorubicin-inducedcardiomyopathy (7) are the consequencesof drug-induced lipid peroxidation andreactive oxygen species (ROS) formation.A drug may also induce changes in plasmalipid profile (8-11). A lipid profile is a measure ofthree components: cholesterol (Ch), triglycerides(Tg), and lipoproteins (LP) (high and low density).Total cholesterol (TCh) comprises all the cholesterolfound in various lipoproteins, such as high densityLP (HDL), low density LP (LDL) and very low densityLP (VLDL). High density lipoprotein cholesterol(HDL-Ch) is believed to play a key role in theprocess of reverse cholesterol transport that promotesthe efflux of excess cholesterol from vesselwall to the liver for excretion (12, 13). On the contrary,low density lipoprotein cholesterol (LDL-Ch)contains the high percentage of cholesterol, and isresponsible for cholesterol deposit on the arterialwall, resulting in coronary symptom like atherosclerosis.Very low density lipoprotein cholesterol(VLDL-Ch) is a large group of macromolecules synthesizedand secreted mainly by liver and intestinalmucosal cells, and contains large quantities of Tg(14). Tg is the neutral fat metabolite found in the tissueand blood and may contribute to the disordersrelated to coronary heart disease (CHD) (15).Phospholipid (PL) is one of the major componentsof total lipid (TL) present in the biological membrane.Evidence suggests that oxidized PL (a majorlipid of LDL-Ch) is formed in atherogenesis andplays an important role in the oxidative modificationduring LDL-Ch oxidation (16). Elevated lipid profileis associated with many diseases. Diabeticpatients have increased level of TCh, Tg, LDL-Ch,VLDL-Ch and decreased level of HDL-Ch (17).CHD is also associated with elevated level of bloodTCh, Tg, LDL-Ch and decreased HDL-Ch (18).Blood TCh, HDL-Ch and LDL-Ch are found to be* Corresponding author: e-mail: priteshdevbhuti@yahoo.co.in253
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