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

Research output: Contribution to journalArticle

8 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)67-78
Number of pages12
JournalBiological Trace Element Research
Volume46
Issue number1-2
DOIs
StatePublished - Oct 1994

Fingerprint

Blood pressure
Nicotine
Rats
Copper
Antioxidants
Blood Pressure
Nutrition
Liver
Diet
Therapeutics
Thiobarbituric Acid Reactive Substances
Plasmas
Hypertension
Thoracic Aorta
Tablets
Rat control
Ceruloplasmin
Trace Elements
Weighing
Selenium

Keywords

  • antioxidant enzymes
  • copper
  • drug-nutrient
  • hypertension
  • iron
  • manganese
  • nicotine
  • SHR
  • trace elements
  • zinc

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology
  • Biochemistry, Genetics and Molecular Biology(all)
  • Biochemistry, medical
  • Inorganic Chemistry
  • Clinical Biochemistry
  • Biochemistry

Cite this

Influence of 12-week nicotine treatment and dietary copper on blood pressure and indices of the antioxidant system in male spontaneous hypertensive rats. / Bui, Linh M.; Keen, Carl L; Dubick, Michael A.

In: Biological Trace Element Research, Vol. 46, No. 1-2, 10.1994, p. 67-78.

Research output: Contribution to journalArticle

@article{2089e2a56a934d4fa77baf241df5673c,
title = "Influence of 12-week nicotine treatment and dietary copper on blood pressure and indices of the antioxidant system in male spontaneous hypertensive rats",
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.",
keywords = "antioxidant enzymes, copper, drug-nutrient, hypertension, iron, manganese, nicotine, SHR, trace elements, zinc",
author = "Bui, {Linh M.} and Keen, {Carl L} and Dubick, {Michael A.}",
year = "1994",
month = "10",
doi = "10.1007/BF02790068",
language = "English (US)",
volume = "46",
pages = "67--78",
journal = "Biological Trace Element Research",
issn = "0163-4984",
publisher = "Humana Press",
number = "1-2",

}

TY - JOUR

T1 - Influence of 12-week nicotine treatment and dietary copper on blood pressure and indices of the antioxidant system in male spontaneous hypertensive rats

AU - Bui, Linh M.

AU - Keen, Carl L

AU - Dubick, Michael A.

PY - 1994/10

Y1 - 1994/10

N2 - 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.

AB - 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.

KW - antioxidant enzymes

KW - copper

KW - drug-nutrient

KW - hypertension

KW - iron

KW - manganese

KW - nicotine

KW - SHR

KW - trace elements

KW - zinc

UR - http://www.scopus.com/inward/record.url?scp=0028077052&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028077052&partnerID=8YFLogxK

U2 - 10.1007/BF02790068

DO - 10.1007/BF02790068

M3 - Article

C2 - 7888285

AN - SCOPUS:0028077052

VL - 46

SP - 67

EP - 78

JO - Biological Trace Element Research

JF - Biological Trace Element Research

SN - 0163-4984

IS - 1-2

ER -