Toxicological implications of Margaritaria discoidea aqueous seed extract on Na+, K+-ATPase specific activity, glucose and serum electrolytes level in wistar rats

 
 
 
  • Abstract
  • Keywords
  • References
  • PDF
  • Abstract


    The effect of aqueous seed extract of Margaritaria discoidea on Na+ K+ ATPase activity and toxicity studies of its seed extract were investigated in albino rats. The study involved oral administration of different doses of the aqueous extract to groups of male albino rats at 25, 50,100, and 200mg/kg body weight resulted in significant (p<0.05) decrease in sodium, potassium and glucose levels while chloride and calcium ions showed a significant (p<0.05) increase relative to control. The seed extract also showed significant (p<0.05) decrease in Na+ K+ ATPase specific activity in a dose dependent manner relative to control. The median lethal dose (LD50) of this extract in mice was established at 316.2mg/kg body weight using probit of mortality. The results showed that the acute toxicity potency of the aqueous extract of the seeds was practically non-toxic. The study showed that seeds of Margaritaria discoidea could be toxic if not consumed in moderate quantities.


  • Keywords


    ATPase activity; Probit; Lethal Dose (LD50); Margaritaria discoidea.

  • References


      [1] Amusan OOG, Nonhlanhia AS, Priscilla SD, Fortunate GS. 2007. Some Swazi phytomedicines and their constituents. Afri. J. of Biotechno. Bioline International 6(3): 267-271.

      [2] Amusan OOG, Sukati NA, Shongwe MS. 2005b.Some phytomedicines from Shiselweni region of Swaziland.S .Nat. Rem. 5: 19-25.

      [3] Badole B, Gupta KC, Sastry MS. 2006.Anti-hyperglyceamic activity of Fagonia mollisus in diabetic rats. Nat. II. Pharmacognoscy, 34; 681-691.

      [4] Burkill HM, 1994. The useful plants of West Tropical Africa (2nd ed) 167-168.

      [5] Davidson BA. 1989. Principles and practice of medicine. Churchill Livingstone (6thed) 23-62.

      [6] Davidson BA. 2005. Principles and practice of medicine. Churchill Livingstone (10thed) 46-58.

      [7] Devlin TM.2006. Textbook on Biochemistry with Clinical Correlation. McGraw Hill Company. 234-276.

      [8] Farnsworth NR. 1990. Bioactive compound from plants in: Chardwick D.J, March J. (edns). Ciba Foundation symposium, 154, Wiley, Chichester, 42-57.

      [9] Gill SA. 1992. Chemical constituents of indigenous plants of Swaziland. UNISWA .I. Agnc. Sci. Tech. 4: 30-35.

      [10] Guyton CA, Hall JE. 1996. Textbook of medical physiology (9thedn). Philadelphia, PAW.B. Saunders Company. 50-72.

      [11] Harold V. 1988.Practical Clinical Biochemistry. ELBS books. (4thedn). 485-516.

      [12] Javorková V, Pechánová O, Andriantsitohaina R, Vrbjar N.2004. Effect of polyphenolic compounds on the renal Na+, K+-ATPase during development and persistence of hypertension in rats. Exp Physiol. 89(1):73-81. http://dx.doi.org/10.1113/expphysiol.2003.002613.

      [13] Jorgensen PL, Pedersen, PA. 2001. Structure-function relationships of Na+, K+, ATP, or Mg2+ binding and energy transduction in Na+ K+-ATPase. Biochem. Biophys. Acta.1505: 57-74. http://dx.doi.org/10.1016/S0005-2728(00)00277-2.

      [14] Krediyyeh SI, Usta J. 2008.Diurectic effect and mechanism of action of Parley.Pubmed.1-5.

      [15] Lambert JDH, Ryden PA and Esikuri EE. 2005. Capitalizing on the Bio-Economic value of multi-purpose plant for rehabilitation of dry land in Sub-saharan Africa World Bank, Washington D.C, USA. 11-14.

      [16] Lavorkoraet V, Pechanova O, Andraintsitohiana R, Vrbjar N. 2003. Effect of polyphenolic compounds on the renal Na+, K+-ATPase during the restoration of normal tension after experimentally induced hypertension in rats. Exp. Physiol. 88:475-482. http://dx.doi.org/10.1113/eph8802553.

      [17] Leong PKK, Manahan DT. 2006. Measurement of Na+,K+-ATPase activity, total enzyme activity in tissue homogenate. J. of Medic. and Biomedic. Research, 281(28): 2882 -2883.

      [18] Lochhead HB, Purcell MK. 1951. Some recent changes in blood gas methods applied to the Van Slyke volumetric apparatus. Amer. J. Clin. Path.21: 877.

      [19] Lowry OH, Rosenbrough NJ, Farr A. Randall RJ. 1951 Protein measurement with the Folin phenol reagent. J Biol Chem; 193:265-275.

      [20] Magyar CE, Wang J, Azuna KK, McDonough AA. 1995. Reciprocal regulation of cardiac NA+, K+-ATPase and Na/Ca exchanger. Hypertension, thyroid hormone development. Am. J. Physiol, 269: 675-682.

      [21] Manasi D., Jayanta KP, Prasanna, PP. 2008. Phytochemical and anti- microbial screening of extracts of Aquilariaagal locha Roxb. Afri. J. of Biotechnology. 7(20): 3531-3534.

      [22] McCance, RA, Shipp HL.1931.The micro-determination of sodium in biological materials Biochem. J., 25(5): 1845–1848. http://dx.doi.org/10.1042/bj0251845.

      [23] McDonald, CE. Chen, LL. 1965. Lowry modification of the Folin reagent for determination of proteinase activity. Anal. Biochem, 10: 175-186. http://dx.doi.org/10.1016/0003-2697(65)90255-1.

      [24] Miller LC, Tainter MC. (1944). Estimation of LD50 and its error by means of logarithmic–probit graph paper. Proc.Soc.Exp. Biol. Med. 57:21-24.

      [25] NIH publication Guide for the care and use of laboratory animals. 2011. (8thEdn) Committee for the Update of the Guide for the Care. National Academies Press Washington DC.

      [26] Schorderet M. (1992).Pharmacologie des concepts fondamentanxaux applications thérapeutiques. Editions slatkine Geneve. Edition frison- Roche Paries.33-34.

      [27] Sweadner KJ, Herrars VL, Amato S, Moellmahn A, Gibbons DK, Repke KR. 1994.Immunologic identification of Na+, K+-ATPase isoform in myocardium. Isoform change in deoxycorticosterone acetate-salt hypertension. Cirs. Res. 74:669-678. http://dx.doi.org/10.1161/01.RES.74.4.669.

      [28] Tietz NW.1976. Fundamentals of Clinical Chemistry, 2nd ed.) , W.B. Saunders Co., Philadelphia, pp. 243.

      [29] Trouve P, Carra F, Belikova I, Leclercq C, Dakkli F, Sonfir L, Coquard I, Ramirez–Gill Charlemagner .D. 2000. Na+, K+-ATPase µ2 – isoform expression in guinea pig hearts during transition from compasation to decompasation. Am.J. Physiol Heart Circ. Physiol, 279: 1972-1981.

      [30] Veronika J, Olga P, Ramaroson A, Norbert V. 2004. Effect of polyphenolic compounds on the renal Na+ ,K+-ATPase during development and persistence of hypertension in rats. Experimental physiology. Physiological Society. 89 (1): 71-81.

      [31] Vrbjar N, Bernatova 1, Pechanova, O. 1999a. Functional alterations of Cardiac Na+,K+-ATPase in L-Name induced hypertension. Gen. Physiol Biophys 18(suppl. 1), 10-12.

      [32] Vrbjar N, Bernatova 1, Pechanova O. 1999b. Changes of sodium and ATP affinities of the renal Na+, K+-ATPase during and after nitric oxide deficient hypertension. Mol. Cel.Biochem., 202: 141-147. http://dx.doi.org/10.1023/A:1007097617502.

      [33] Vrbjar N, Javorka V, Pechanova O. 2002.Changes of sodium and ATP affinities of the renal Na+ , K+-ATPase during and after nitric oxide deficient hypertension. Physiol. Res. 51: 475-482.


 

View

Download

Article ID: 6660
 
DOI: 10.14419/ijpt.v4i2.6660




Copyright © 2012-2015 Science Publishing Corporation Inc. All rights reserved.