Influence of 12-week nicotine treatment and dietary copper on blood pressure and indices of the antioxidant system in male spontaneous hypertensive rats.
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 microgram Cu/g) for 14 d prior to nicotine treatment. SHR were inserted with tablets that released nicotine at a rate of 75 micrograms/h or placebo (control). Following tablet insertion, rats were fed a control diet (+Cu) (12.0 micrograms 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.
Bui
L M
LM
Department of Nutrition, University of California, Davis 95616-8669.
Keen
C L
CL
Dubick
M A
MA
D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D001794:Blood Pressure / Q000187:drug effects*; D001835:Body Weight / Q000187:drug effects; D003300:Copper / Q000172:deficiency / Q000494:pharmacology*; D004334:Drug Administration Schedule; D005979:Glutathione Peroxidase / Q000378:metabolism; D005980:Glutathione Reductase / Q000378:metabolism; D006973:Hypertension / Q000139:chemically induced / Q000201:enzymology / Q000378:metabolism; D008297:Male; D009538:Nicotine / Q000494:pharmacology*; D051381:Rats; D011918:Rats, Inbred SHR / Q000502:physiology*; D013482:Superoxide Dismutase / Q000378:metabolism; D014131:Trace Elements / Q000097:blood / Q000378:metabolism
D000975:Antioxidants; D014131:Trace Elements; D009538:Nicotine; D003300:Copper; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase