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Adaramoye OA, Azeez AF, Ola-Davies OE. Ameliorative Effects of Chloroform Fraction of Cocos nucifera L. Husk Fiber Against Cisplatin-induced Toxicity in Rats. Pharmacognosy Res. 2016;8(2):89-96doi: 10.4103/0974-8490.172658.
Adaramoye, O. A., Azeez, A. F., & Ola-Davies, O. E. (2016). Ameliorative Effects of Chloroform Fraction of Cocos nucifera L. Husk Fiber Against Cisplatin-induced Toxicity in Rats. Pharmacognosy research, 8(2), 89-96. https://doi.org/10.4103/0974-8490.172658
Adaramoye, Oluwatosin Adekunle, et al. "Ameliorative Effects of Chloroform Fraction of Cocos nucifera L. Husk Fiber Against Cisplatin-induced Toxicity in Rats." Pharmacognosy research vol. 8,2 (2016): 89-96. doi: https://doi.org/10.4103/0974-8490.172658
Adaramoye OA, Azeez AF, Ola-Davies OE. Ameliorative Effects of Chloroform Fraction of Cocos nucifera L. Husk Fiber Against Cisplatin-induced Toxicity in Rats. Pharmacognosy Res. 2016 Apr-Jun;8(2):89-96. doi: 10.4103/0974-8490.172658. PMID: 27034598; PMCID: PMC4780144.
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Pharmacognosy Res. 2016 Apr-Jun;8(2):89-96. doi: 10.4103/0974-8490.172658.

Ameliorative Effects of Chloroform Fraction of Cocos nucifera L. Husk Fiber Against Cisplatin-induced Toxicity in Rats.

Pharmacognosy research

Oluwatosin Adekunle Adaramoye, Adesola Fausat Azeez, Olufunke Elizabeth Ola-Davies

Affiliations

  1. Department of Biochemistry, Faculty of Basic Medical Sciences, University of Ibadan, Ibadan, Nigeria.
  2. Department of Veterinary Physiology, Biochemistry and Pharmacology, Faculty of Veterinary Medicine, University of Ibadan, Ibadan, Nigeria.

PMID: 27034598 PMCID: PMC4780144 DOI: 10.4103/0974-8490.172658

Abstract

BACKGROUND: Cisplatin (Cis) is used in the treatment of solid tumors and is known to elicit serious side effects.

OBJECTIVE: The present study investigated the protective effects of chloroform fraction of Cocos nucifera husk fiber (CFCN) against Cis-induced organs' damage and chromosomal defect in rats. Quercetin (QUE), standard antioxidant, served as positive control.

MATERIALS AND METHODS: Thirty male Wistar rats were assigned into six groups and treated with corn oil (control), Cis alone, Cis + CFCN, CFCN alone, Cis + QUE, and QUE alone. QUE and CFCN were given at 50 and 200 mg/kg/day, respectively, by oral gavage for 7 days before the rats were exposed to a single dose of Cis (10 mg/kg, intraperitoneal) at the last 36 h of study.

RESULTS: Administration of Cis alone caused a significant (P < 0.05) increase in the levels of serum creatinine and urea by 72% and 70%, respectively, when compared with the control. The activity of serum aspartate aminotransferase was significantly (P < 0.05) increased while alanine aminotransferase and alkaline phosphatase were insignificantly (P > 0.05) affected in Cis-treated rats. Furthermore, the activities of hepatic and renal catalase, superoxide dismutase, glutathione S-transferase, glutathione peroxidase, and levels of reduced glutathione were significantly (P < 0.05) decreased in Cis-treated rats with concomitant elevation of malondialdehyde. Cis exposure increased the frequency of micro nucleated polychromatic erythrocytes (mPCE) by 92%. Pretreatment with CFCN inhibited lipid peroxidation, enhanced the activities of some antioxidative enzymes and reduced the frequency of mPCE.

CONCLUSIONS: Chloroform fraction of CFCN may protect against organs damage by Cis. Further studies are required to determine the component of the plant responsible for this activity.

SUMMARY: Cisplatin (Cis) is used in the treatment of solid tumors and is known to elicit serious side effects. This study investigated the protective effects of chloroform fraction of Cocos nucifera husk fiber (CFCN) against Cis-induced organs' damage while quercetin (QUE) served as standard antioxidant.Thirty male Wistar rats were assigned into six groups and treated with corn oil (Control), Cis alone, Cis + CFCN, CFCN alone, Cis + QUE and QUE alone.QUE and CFCN were given at 50 and 200 mg/kg/day respectively by oral gavage for seven days before the rats were exposed to a single dose of Cis (10mg/kg, i.p.) at the last 36 h of study. Results indicate that administration of Cis caused a significant (P<0.05) increase in the levels of serum creatinine and urea by 72% and 70% respectively.The activity of serum aspartate aminotransferase was significantly (P <0.05) increased while alanine aminotransferase and alkaline phosphatase were insignificantly (P>0.05) affected in Cis-treated rats.The activities of hepatic and renal catalase, superoxide dismutase, glutathione-s-transferase, glutathione peroxidase and levels of reduced glutathione were significantly (P<0.05) decreased in Cis-treated rats with concomitant elevation of malondialdehyde.Cis exposure increased the frequency of micronucleated polychromatic erythrocytes (mPCE) by 92%.Pretreatment with CFCN inhibited lipid peroxidation, enhanced the activities of some antioxidative enzymes and reduced the frequency of mPCE. The findings suggest that CFCN may protect against organs damage by cisplatin.Further studies are required to determine the component of the plant responsible for this activity.

Keywords: Antioxidant; Cisplatin; Clastogenicity; Cocos nucifera; Lipid peroxidation

References

  1. Asian Pac J Cancer Prev. 2015;16(3):991-6 - PubMed
  2. Tumour Biol. 2014 Jul;35(7):6445-54 - PubMed
  3. J Lab Clin Med. 1963 May;61:882-8 - PubMed
  4. Cancer. 2014 Sep 1;120(17):2684-93 - PubMed
  5. Toxicol In Vitro. 2006 Mar;20(2):187-210 - PubMed
  6. Life Sci. 1996;59(22):1881-90 - PubMed
  7. Lab Anim Res. 2014 Dec;30(4):174-80 - PubMed
  8. Anticancer Res. 1992 May-Jun;12(3):885-98 - PubMed
  9. Int J Biol Sci. 2009 Jun 28;5(5):466-73 - PubMed
  10. Nat Rev Drug Discov. 2005 Apr;4(4):307-20 - PubMed
  11. Science. 1973 Feb 9;179(4073):588-90 - PubMed
  12. Saudi J Biol Sci. 2015 Mar;22(2):227-31 - PubMed
  13. Oxid Med Cell Longev. 2014;2014:476430 - PubMed
  14. Food Chem Toxicol. 2014 Dec;74:98-106 - PubMed
  15. J Pharmacol Sci. 2015 Jan;127(1):117-26 - PubMed
  16. Environ Toxicol. 2016 Jul;31(7):855-65 - PubMed
  17. Asian Pac J Cancer Prev. 2015;16(3):1117-22 - PubMed
  18. J Biol Chem. 1974 Nov 25;249(22):7130-9 - PubMed
  19. Planta Med. 2015 Mar;81(4):286-91 - PubMed
  20. J Med Food. 2015 Jul;18(7):802-9 - PubMed
  21. J Clin Pathol. 1957 Nov;10(4):394-9 - PubMed
  22. Environ Toxicol. 2016 May;31(5):624-36 - PubMed
  23. Biomed Res Int. 2015;2015:167235 - PubMed
  24. Klin Wochenschr. 1965 Feb 1;43:174-5 - PubMed
  25. J Dairy Sci. 1970 Feb;53(2):227-32 - PubMed
  26. BMC Complement Altern Med. 2013 May 16;13:107 - PubMed
  27. Pharmacogn Rev. 2010 Jul;4(8):118-26 - PubMed
  28. J Reprod Fertil. 1964 Oct;8:149-55 - PubMed
  29. J Ethnopharmacol. 2007 Sep 5;113(2):248-51 - PubMed
  30. Toxicol Mech Methods. 2015;25(5):347-54 - PubMed
  31. Methods Enzymol. 1978;52:302-10 - PubMed
  32. J Biol Chem. 1969 Nov 25;244(22):6049-55 - PubMed
  33. J Pept Sci. 2014 Dec;20(12):909-15 - PubMed
  34. Environ Toxicol Pharmacol. 2015 Jan;39(1):392-404 - PubMed
  35. Mutat Res Genet Toxicol Environ Mutagen. 2015 Jan 1;777:7-16 - PubMed
  36. Liver Transpl. 2005 Sep;11(9):1031-47 - PubMed
  37. Fundam Appl Toxicol. 1988 Aug;11(2):343-58 - PubMed
  38. J Biol Chem. 1951 Nov;193(1):265-75 - PubMed
  39. Lancet. 1994 Sep 10;344(8924):721-4 - PubMed
  40. Equine Vet J. 2012 Mar;44(2):214-20 - PubMed
  41. Prog Mol Biol Transl Sci. 2015;131:471-508 - PubMed
  42. Am J Clin Pathol. 1957 Jul;28(1):56-63 - PubMed
  43. Gastroenterology. 1965 Sep;49(3):256-61 - PubMed
  44. Free Radic Biol Med. 1998 Jul 15;25(2):196-200 - PubMed
  45. Gynecol Obstet Invest. 2015;79(2):119-25 - PubMed
  46. J Inflamm (Lond). 2015 Feb 08;12:10 - PubMed
  47. Shanghai Kou Qiang Yi Xue. 2014 Apr;23(2):219-23 - PubMed

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