Influence of 12-week nicotine treatment and dietary copper on blood pressure and indices of the antioxidant system in male spontaneous hypertensive rats

  • Linh M. Bui
  • Carl L. Keen
  • Michael A. Dubick
Article
Received:
Accepted:

Abstract

Nicotine treatment and copper (Cu) deficiency have been associated with an increased production of reactive oxygen species that may contribute to the development and/or progression of cardiovascular diseases (CVD). The present study investigated the influence of dietary Cu intake on the response to chronic nicotine treatment in spontaneous hypertensive rats (SHR) with respect to tissue trace mineral levels, several components of the oxidant defense system, and lipid peroxidation rates. SHR weighing 100–110 g were fed a Cu deficient diet (−Cu) (0.5 μg Cu/g) for 14 d prior to nicotine treatment. SHR were inserted with tablets that released nicotine at a rate of 75 μg/h or placebo (control). Following tablet insertion, rats were fed a control diet (+Cu) (12.0 μg Cu/g) or the −Cu diet. Nicotine treatment lasted for 12 wk. Blood pressure (BP) was higher in nicotine-treated SHR than in control SHR at wk 3; BP was unaffected by diet. BP was higher in +Cu nicotine-treated SHR at wk 6 compared to −Cu nicotine and control rats. BP was not affected by nicotine or diet at wk 2. Liver, heart, and brain Cu levels and liver, heart, and red cell CuZn superoxide dismutase and plasma ceruloplasmin oxidase activities were lower in the −Cu SHR than in the +Cu SHR. Liver Fe levels were higher and plasma Fe levels were lower in the −Cu rats than in the +Cu rats. Liver selenium-dependent-glutathione peroxidase (Se-GSH-Px) activity was lower in the −Cu rats than in the +Cu rats; heart and thoracic aorta Se-GSH-Px activity was unaffected by −Cu diet. Thoracic aorta, liver, and heart GSH-reductase activities were unaffected by treatments. Plasma thiobarbituric acid reactive substances (TBARS) were higher in the −Cu than in the +Cu SHR. Liver and heart TBARS production was similar among the groups. These data show that nicotine can exacerbate the development of high BP in susceptible individuals; Cu deficiency did not exacerbate the effects of nicotine.

Index Entries

SHR trace elements antioxidant enzymes nicotine hypertension drug-nutrient zinc copper iron manganese 
This is a preview of subscription content, log in to check access.

References

  1. 1.
    O. Auerbach, E. C. Hammond, and L. Garfinkel,New Engl. J. Med. 273, 775–779 (1965).PubMedGoogle Scholar
  2. 2.
    G. C. Hunter, M. A. Dubick, C. L. Keen, and C. D. Eskelson,Proc. Soc. Exp. Biol. Med. 196, 273–279 (1991).PubMedGoogle Scholar
  3. 3.
    A. Kershbaum, S. Bellet, E. R. Dickstein, and L. J. Feinberg,Circ. Res. 9, 631–638 (1961).PubMedGoogle Scholar
  4. 4.
    W. P. Castelli,Am. J. Med. 76, 4–12 (1984).PubMedCrossRefGoogle Scholar
  5. 5.
    R. C. Sharma, D. W. Crawford, D. M. Kramsch, A. Sevanian, and Q. Jiao,Arterioscler. Thromb. 12, 403–415 (1992).PubMedGoogle Scholar
  6. 6.
    M. S. Latha, P. L. Vijayammal, and P. A. Kurup,Indian J. Med. Res. 98, 44–49 (1993).PubMedGoogle Scholar
  7. 7.
    M. A. Dubick and C. L. Keen,Biol. Trace Elem. Res. 31, 97–109 (1991).PubMedGoogle Scholar
  8. 8.
    C. T. Dollery,Am. J. Med. 82, 2–8 (1987).PubMedCrossRefGoogle Scholar
  9. 9.
    P. S. Prabha, U. N. Das, R. Koratkar, P. Sagar, and G. Ramesh,Prostaglandins Leukot. Essent. Fatty Acids 41, 27–33 (1990).PubMedCrossRefGoogle Scholar
  10. 10.
    C. L. Keen, M. S. Clegg, F. Ferrell, G. C. Hunter, and M. A. Dubick, inBiology of Copper Complexes, J. R. J. Sorenson, ed., Humana, Totowa, NJ, pp. 141–153 (1987).Google Scholar
  11. 11.
    M. Uysal, H. Bulur, D. Sener, and H. Oz,Int. J. Clin. Pharmacol. Ther. Toxicol. 24, 474–476 (1986).PubMedGoogle Scholar
  12. 12.
    G. M. Rubanyl,Free Rad. Biol. Med. 4, 107–120 (1988).CrossRefGoogle Scholar
  13. 13.
    D. M. Medeiros, D. Bagby, G. Ovecka, and R. McCormick,J. Nutr. 121, 815–824 (1991).PubMedGoogle Scholar
  14. 14.
    J. Davidson, D. M. Medeiros, and R. L. Hamlin,J. Nutr. 122, 1566–1575 (1992).PubMedGoogle Scholar
  15. 15.
    S. Reiser, A. Powell, C. Y. Yang, J. J. Canary,Nutr. Rep. Int. 36, 641–649 (1987).Google Scholar
  16. 16.
    K. G. Allen and L. M. Klevay,Atherosclerosis 29, 81–93 (1978).PubMedCrossRefGoogle Scholar
  17. 17.
    L. M. Klevay,Nutr. Rep. Int. 35, 999–1005 (1987).Google Scholar
  18. 18.
    D. M. Medeiros,Nutr. Res. 7, 231–235 (1987).CrossRefGoogle Scholar
  19. 19.
    B. N. Wu, D. M. Medeiros, and K. N. Lin, and B. M. Thorne,Nutr. Res. 4, 305–314 (1984).CrossRefGoogle Scholar
  20. 20.
    M. Fields, R. J. Ferretti, J. C. Smith Jr., and S. Reiser,Life Sci. 34, 763–769 (1984).PubMedCrossRefGoogle Scholar
  21. 21.
    C. Frieden,Clin. Physiol. Biochem. 4, 11–19 (1986).PubMedGoogle Scholar
  22. 22.
    J. R. Prohaska,J. Nutr. 121, 355–363 (1991).PubMedGoogle Scholar
  23. 23.
    P. Lowney, M. E. Gershwin, L. S. Hurley, J. S. Stern, and C. L. Keen,Biol. Trace Elem. Res. 16, 1–18 (1987).CrossRefGoogle Scholar
  24. 24.
    P. P. Lau, M. A. Dubick, G. S. M. Yu, P. R. Morrill, and M. C. Geokas,Toxicol. Appl. Pharmacol. 104, 457–465 (1990).PubMedCrossRefGoogle Scholar
  25. 25.
    L. P. Schacter, B. C. Delvillano, E. M. Gordon, and B. L. Klein,Am. J. Hematol. 19, 137–144 (1985).PubMedCrossRefGoogle Scholar
  26. 26.
    M. S. Clegg, C. L. Keen, B. Lonnerdal, and L. S. Hurley,Biol. Trace Elem. Res. 3, 107–115 (1981).CrossRefGoogle Scholar
  27. 27.
    S. Marklund and G. Marklund,Eur. J. Biochem. 47, 469–479 (1974).PubMedCrossRefGoogle Scholar
  28. 28.
    R. A. Lawrence and R. F. Burk,Biochem. Biophys. Res. Commun. 71, 952–958 (1976).PubMedCrossRefGoogle Scholar
  29. 29.
    K. M. Rogers and R. C. Augusteyn,Exp. Eye Res. 27, 719–721 (1978).PubMedCrossRefGoogle Scholar
  30. 30.
    M. M. Bradford,Anal. Biochem. 72, 248–254 (1976).PubMedCrossRefGoogle Scholar
  31. 31.
    K. H. Schosinsky, H. P. Lehmann, and M. F. Beeler,Clin. Chem. 20, 1556–1563 (1974).PubMedGoogle Scholar
  32. 32.
    C. G. Fraga, B. E. Leibovitz, and A. L. Tappel,Free Radic. Biol. Med. 4, 155–161 (1988).PubMedCrossRefGoogle Scholar
  33. 33.
    K. Yagi,Meth. Enzymol. 105, 328–336 (1984).PubMedCrossRefGoogle Scholar
  34. 34.
    N. L. Benowitz,Annu. Rev. Med. 37, 21–32 (1986).PubMedCrossRefGoogle Scholar
  35. 35.
    J. M. C. Gutteridge,Ann. Clin. Biochem. 15, 293–448 (1979).Google Scholar
  36. 36.
    I. R. Garret and M. W. Whitehouse, inCopper in Animals and Man, vol 2, J. M. Howell, J. M. Gawthom, eds., CRC Press, Boca Raton, FL, pp. 107–122 (1987).Google Scholar
  37. 37.
    I. M. Goldstein, H. B. Kaplan, H. S. Edelson, and G. Weissman,J. Biol. Chem. 254, 4040–4045 (1979).PubMedGoogle Scholar
  38. 38.
    S. K. Jain and D. M. Williams,Am. J. Clin. Nutr. 48, 637–640 (1988).PubMedGoogle Scholar
  39. 39.
    J. S. Rosenbaum, S. Zidenberg-Cherr, and C. L. Keen,Alcohol 8, 473–479 (1991).PubMedCrossRefGoogle Scholar

Copyright information

© Humana Press Inc. 1994

Authors and Affiliations

  • Linh M. Bui
    • 1
  • Carl L. Keen
    • 1
    • 2
  • Michael A. Dubick
    • 1
    • 3
    • 4
  1. 1.Department of NutritionUniversity of California, DavisDavis
  2. 2.Department of Internal MedicineUniversity of California, DavisDavis
  3. 3.Division of Military Trauma ResearchLetterman Army Institute of ResearchPresidio of San Francisco
  4. 4.US Army Institute of Surgical ResearchFt. Sam Houston

Personalised recommendations