OXIDATIVE STRESS LEVEL IN FEMALES WITH HEART DISEASES USING VITAMIN A, C AND E AS DETERMINANTS

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ABSTRACT

Heart disease is associated with elevated oxidative stress via increased generation of reactive oxygen species (ROS), and decline in antioxidant defences. Increased oxidative stress is thought to play a role in the development of cardiovascular diseases. The present study was carried out to see the levels of vitamin C, vitamin E and total antioxidant (AO) in hypertensive female patients with heart disease. Twenty-two patients (all women) with history of Hypertension from outpatient clinic unit of the State Central Hospital, Benin City, Edo State, Nigeria where studied. Eight control subjects (all women) with no history of hypertension and heart diseases were studied.

The raw group data of their age, weight, height, blood pressure and pulse rate of the subjects were obtained. They were selected on the basis of general physical examination Serum level of vitamin A, C and E were obtained using documented method. Serum levels of vitamin A,C, and E were 380.24±68.13 U/L and 135.69±21.32 U/L, 1.23±0.13 mg/dl and 1.20±0.09 mg/dl, 136.26±9.72 U/L and 185.41±1.84 U/L in experimental and control. Vitamin A shows significant increase with experimental when compared with control, but Vitamin C shows mild increase when experimental group was compared with control group, but did not attain significant at (p<0.05) and Vitamin E shows moderate significant decrease when experiment group compared with control group at (p<0.05). This study reveals a significant reduction in serum vitamin E level of hypertensive patients as compared to the controls with the mean vitamin C level showing no significant difference. In this research, the scientific data do not justify the use of antioxidant vitamin supplements for CVD risk reduction.

LIST OF TABLES

Table 4.1: shows the effect of hypertension

on the blood pressure, enzyme and non

enzyme antioxidants in hypertensive

female patients – – – – – – 62

TABLE OF CONTENTS

PAGE

Cover page – – – – – — – – -i

Title page – – – – – – – – – – -ii

Certification – – – – – – – – -iii

Dedication – – – – – – – – – -iv

Acknowledgements – – – – – – – – -v

Abstract – – – – – – – – – – -vi

List of tables and figure – – – – – – – -vii

Table of content – – – – – – – – -vii

CHAPTER ONE

1.1 INTRODUCTION – – – – – – – – –1

1.2 Aims and Objectives – – – – – – -5

1.3 Scope of study – – – – – – – – -6

1.4 Significance of study: – – – – – – -6

CHAPTER TWO

2.0 LITERATURE REVIEW – – – – – – – 7

2.1 HEART DISEASE – – – — – – 7

2.2 TYPES OF HEART DISEASE — – – – – – 8

2.2.2 Hypertensive heart disease — – – – – -8

2.2.3 Heart failure – – – – – – – – -8

2.2.4 Cor pulmonale or pulmonary heart disease — -9

2.2.5 Valvular heart disease – – – — — 9

2.2.6 Cerebrovascular disease – – – – – — -9

2.2.7 Congenital heart disease – – – — -10

2.3 Epidemiology of Cardiovascular Disease – – – -10

2.4 Risk factors – – – – – – — — -11

2.5 OXIDATIVE STRESS – – – – – — -13

2.6 Physiological Sources of Reactive Oxidant

Species in Cells – – – – – —- 13

2.6.1 Mitochondrial respiration as a source

of reactive oxidant species in cells – – – – -14

2.6.2 NADH/NADPH oxidase system as a source of

reactive oxidant species in the cell – – – – -17

2.6.3 Xanthine oxido-reductase system as a source of

reactive oxidant species in the cell – – – – – -20

2.6.4 NOS uncoupling as a source of reactive

oxidant species in the cell. Uncoupled NO – — 21

2.7 Reactive Oxidant Species Formation and

Cardiovascular Disease – – – – – — 21

2.7.1 Oxidative stress and endothelial

Dysfunction in aterosclerosis – – – - – – -24

2.7.2 Oxidative stress and hypertension – — – — 31

2.7.3 Oxidative stress and cardiovascular ischemia – — -33

2.7.4 Oxidative stress and heart failure – – – – -35

2.7.5 Oxidative stress and postoperative arrhythmias – – -39

2.8 Antioxidants and Cardiovascular Disease – -39

2.8.1 Antioxidants – – – – – — — -40

2.8.2 The Use of Antioxidants – – – – – — -42

2.8.3 Dietary Intervention and Risk of

Cardiovascular Disease – – – – – – – -42

2.8.4 Antioxidants and Cardiovascular Risk — – — -45

2.8.5 Vitamin C and Cardiovascular Disease — – — -48

2.8.6 Vitamin E and Cardiovascular Disease – — -51

CHAPTER THREE

3.0 MATERIALS AND METHOD – – – — -56

3.1 MATERIALS – – – – – – — — -56

3.1.1 Instruments – – – – – – – — -56

3.1.2 Apparatus and glass wares – – – – — -56

3.1.3 Reagents – – — – – – – — — -57

3.1.4 Specimen – – – – – – — -57

3.1.5 Blood Serum – – – — – – — — -57

3.2 METHODS – – – – – – — -57

3.2.1 Study group – – – – – — — -57

3.2.2 Clinical assessment – – – — — -58

3.2.3 Sample collection and preservation – – – – —58

3.3 SAMPLE ANALYSIS – – – – – — — -58

3.3.1 Serum vitamin E estimation – – – – — -58

3.3.2 Serum Vitamin A estimation – – – – — -60

3.3.3 Serum Vitamin C estimation – – – – — -60

3.4 STATISTICAL ANALYSIS – – – – — — -61

CHAPTER FOUR

4.0 RESULTS — – – – – – – -62

CHAPTER FIVE

5.0 DISCUSSION – – – – – – – – — 64

5.1 Conclusion – – – – – – – – – 67

References

CHAPTER ONE

1.1 INTRODUCTION

Heart disease(cardiovascular disease), defined as coronary artery disease, hypertensive heart disease, congestive heart failure, peripheral vascular disease, and atherosclerosis including cerebral artery disease and strokes, is the leading cause of death in the United States and disability in the world today, (Thom, 1989).

In the United States, the heart disease death toll is nearly one million each year, and in 2002 the estimated cost of heart disease treatment was $326.6 billion, (Shekelle et al., 2003). To provide early prognosis and better therapies for preventing and curing these diseases, an understanding of the basic pathophysiologic mechanisms of heart disease is essential. Growing evidence indicates that oxdant stress production of reactive oxygen species (ROS) and other free radicals under pathophysiologic conditions is integral in the development of cardiovascular diseases (CVD).

Free radicals are molecules containing one or more unpaired electrons in atomic or molecular orbital, (Gutteridge et al., 2000). Reactive free radicals play a crucial part in different physiological processes ranging from cell signaling, inflammation and the immune defense, (Elahi et al., 2006).

There is increasing evidence that abnormal production of free radicals lead to increased stress on cellular structures and causes changes in molecular pathways that underpins the pathogenesis of several important human diseases, including heart disease, neurological disease and cancer and in the process of physiological ageing, (Pacher 2008; Vassalle et al., 2008). One of the major contributors of oxidative stress is the reactive oxygen species (ROS) family of molecules. These include free radicals such as superoxide anion (O₂-), hydroxyl radical (HO-), lipid radicals (ROO-) and nitric oxide (NO). Other reactive oxygen species, hydrogen peroxide (H₂O₂), peroxynitrite (ONOO-) and hypochlorous acid (HOCl), although are not free radicals but they have oxidizing effects that contribute to oxidative stress. ROS has been implicated in cell damage; necrosis and cell apoptosis due to its direct oxidizing effects on macromolecules such as lipids, proteins and DNA, (Izakovic et al., 2006). Production of one free radical can lead to further formation of radicals via sequential chain reactions, (Cronin et al., 2005).

Understanding the contribution of free radical stress in the pathogenesis of disease will allow us to study the development of oxidative stress; a condition that occurs due to an imbalance between cellular production of oxidant molecules and the availability of appropriate antioxidants species that defend against them. In physiological conditions, cells would increase activities of antioxidant enzymes and other antioxidant defenses to counteract occurrence of oxidative stress, (Brunzini et al., 2004). These include radical scavengers such as vitamin E, A, beta carotene and vitamin C, Manganese dependent superoxide dismutase such as manganese superoxide dismutase (Mn-SOD), Copper/Zinc superoxide dismutase (Cu/Zn SOD), glutathione peroxidase, glutathione reductae and catalase (CAT).

Decreased risk of cardiovascular death has been associated with higher blood levels of vitamin C and E. In addition, vitamin C, vitamin E, and A have demonstrated antioxidant effects, including beneficial effects on oxidation of low-density lipoprotein. There is evidence that these vitamins affect other risk factors for CVD such as hypertension. Vitamin E may also reduce coronary artery blockage by decreasing blood platelet aggregation. Thus, it was reasonable to expect that supplementation with these antioxidants would decrease the risk of developing CVD.

Large numbers of people are taking antioxidants with the expectation that they will prevent disease. As part of a natural defense system, antioxidants can mitigate the activity of free radicals and other oxidative species that have been implicated in the development of heart disease, (Krzanowski, 1991; Duthie et al., 1999). The epidemiologic and observational literature has suggested a beneficial effect of antioxidant-rich foods, as well as specific antioxidants, on the risk of CVD and stroke, (Asplund, 2002; Tribble, 1999). Because oxidative functions also contribute positively to the health of the cell by their participation in energy metabolism, biosynthesis, detoxification, and cellular signaling, a balance is clearly required between the pro-oxidants and the antioxidant defense system to maintain health, (German et al., 2001).

1.2 Aims and Objectives

The aim of this study is to determine the efficacy of three antioxidants, vitamin E, vitamin C, and A, for the prevention and treatment of cardiovascular disease (CVD) or modification of known risk factors for heart diseases in hypertensive female patients

Specifically, the objective of this study is to determine;

The vitamin A level in hypertensive patient with heart disease.
The vitamin C level in hypertensive patient with heart disease.

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