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Molecular and Cellular Biochemistry

, Volume 368, Issue 1–2, pp 181–187 | Cite as

Vitamin E slows the progression of hypercholesterolemia-induced oxidative stress in heart, liver and kidney

  • Kailash PrasadEmail author
  • Erick D. McNair
  • A. Mabood Qureshi
  • Gudrun Casper-Bell
Article

Abstract

Vitamin E suppresses the hypercholesterolemia-induced oxidative stress in the heart. The objectives were to investigate if: (a) hypercholesterolemia-induced oxidative stress is similar in heart, liver, and kidney, and is dependent upon duration of hypercholesterolemia; and (b) vitamin E slows the progression of oxidative stress in these organs. The rabbits were assigned to 4 groups: I, regular diet (2 months); II, 0.25 % cholesterol diet (2 months); III, 0.25 % cholesterol diet (4 months); and IV, 0.25 % cholesterol diet (2 months) followed by 0.25 % cholesterol diet plus vitamin E (2 months). Blood samples were collected before and at the end of protocol for the measurement of total cholesterol (TC). Hearts, livers, and kidneys were removed at the end of the protocol under anesthesia for the measurement of oxidative parameters, malondialdehyde (MDA), and chemiluminescence (CL). The basal MDA levels in the heart, liver, and kidney of rabbits in Group I were similar, but increased to 14.65-, 3.18-, and 10.35-fold, respectively, with hypercholesterolemia. The increases in MDA levels were dependent upon the duration of hypercholesterolemia. Vitamin E did not alter the TC levels, but reduced the MDA levels in all organs. Hypercholesterolemia and vitamin E had variable effects on CL activity. In conclusion, (i) hypercholesterolemia induces oxidative stress in heart, liver, and kidney, the heart being the most and the liver the least susceptible to oxidative stress; (ii) oxidative stress is positively associated with duration of hypercholesterolemia; and (iii) vitamin E slows the progression of oxidative stress in these organs.

Keywords

Hypercholesterolemia Oxidative stress Heart Liver Kidney Vitamin E 

Notes

Acknowledgments

This study has been supported by a grant from the Heart and Stroke Foundation of Saskatchewan and College of medicine Research Fund of the University of Saskatchewan, Saskatoon, Canada. The technical assistance of Mrs. Barbara Raney is highly appreciated.

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Copyright information

© Springer Science+Business Media, LLC. 2012

Authors and Affiliations

  • Kailash Prasad
    • 1
    Email author
  • Erick D. McNair
    • 2
  • A. Mabood Qureshi
    • 3
  • Gudrun Casper-Bell
    • 4
  1. 1.Department of Physiology, College of medicineUniversity of SaskatchewanSaskatoonCanada
  2. 2.Department of SurgeryUniversity of Saskatchewan and Royal University HospitalSaskatoonCanada
  3. 3.Pathology and Laboratory MedicineUniversity of Saskatchewan and Royal University HospitalSaskatoonCanada
  4. 4.Department of MedicineUniversity of Saskatchewan and Royal University HospitalSaskatoonCanada

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