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

Download our android mobile app for more materials

ORDER NOW

COMPLETE MATERIAL  COST  N2,500 Or $10.  FRESH  PROJECT MATERIAL  COST 50,000 NAIRA FOR UNDERGRADUATE, OTHERS 100,000 -200,000 NAIRA.

Foreign Transaction For Dollars Payment :
Bank Name: GTBank
Branch Location: Enugu State,Nigeria.
Account Name: Chi E-Concept Int’l
 Account Number:  0117780667. 
Swift Code: GTBINGLA 
Dollar conversion rate for Naira is 175 per dollar. 

ATM CARD:  YOU CAN ALSO MAKE PAYMENT USING YOUR ATM CARD OR ONLINE TRANSFER. PLEASE CONTACT YOUR BANK SECURITY FOR GUIDE ON HOW TO TRANSFER MONEY TO OTHER BANKS USING YOUR ATM CARD. ATM CARD OR ONLINE BANK TRANSFER IS FASTER FOR QUICK DELIVERY TO YOUR EMAIL . OUR MARKETER WILL RESPOND TO YOU ANY TIME OF THE DAY. WE SUPPORT CBN CASHLESS SOCIETY. 

OR
PAY ONLINE USING YOUR ATM CARD. IT IS SECURED AND RELIABLE.

form>DELIVERY PERIOD FOR BANK PAYMENT IS  LESS THAN 24 HOURS

CALL OUR  CUSTOMERS CARE  OKEKE CHIDI C ON :  08074466939,08063386834.

AFTER PAYMENT SEND YOUR PAYMENT DETAILS TO

08074466939 or 08063386834, YOUR PROJECT TITLE  YOU WANT US TO SEND TO YOU, AMOUNT PAID, DEPOSITOR NAME, UR EMAIL ADDRESS,PAYMENT DATE. YOU WILL RECEIVE YOUR MATERIAL IN LESS THAN 2 HOURS ONCE WILL CONFIRM YOUR PAYMENT.

WE HAVE SECURITY IN OUR BUSINESS.   

MONEY BACK GUARANTEE

                                                   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;

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

MALARIA PARASITE AND ITS EFFECT TO HUMAN HEALTH (A CASE STUDY OF UNTH ENUGU)

complete material cost 5000 naira .  Order Now

ABSTRACTS

The detection of malaria parasite in the blood which was the major aim of this project was carried out and experimented data shows the existence of three species of the parasite in the human blood cell vis:

(a)     Plasmodium falciparium  (b) Plasmodium Malaria

(c ) Plasmodium Vivax. More over, the last remaining spp which is Plasmodium Ovale was not observed at all in the human blood cell.

Out of 150 specimens collected, 110 were found to be positive indicating that about 75% people in our country Nigeria were living under the shadow of this infectious disease.

Finally, in our finding. It was assumed that the group of people that are more subsetible to this malaria parasite were children under the age range of 1 to 10 and the pregnant women in the adult range. This finding was made after staining the thick and thin film using the different stains vis. Leishman, Giemsa, and field stains which enhances a clear observation of the morphological appearance of the organism under the microscopic view.

TABLE OF CONTENT

CHAPTER ONE

• INTRODUCTION

1.1    BACKGROUND INFORMATION

• STATEMENT OF PROBLEMS
• AIM AND OBJECTIVE OF THE STUDY
• HYPOTHESIS

CHAPTER TWO

• LITERATURE REVIEW

2.1    THE STAGES OF DIFFERENT SPECIES OF MALARIA PARASITE.

CHAPTER THREE

• MATERIALS AND METHOD

3.1    MATERIALS USED

• SAMPLE COLLECTION
• METHOD OF SAMPLE ANALYSIS
• PREPARATION OF BLOOD FILM
• PREPARATION OF BUTTER SOLUTION TO BE USED WITH GEMSA STAIN
• DIFFERENT BETWEEN THICLE AND THIN FILM

CHAPTER FOUR

• RESULTS AND DISCUSSION

4.1    TABULATION OF THE RESULT OBTAINED

• DISCUSSION

CHAPTER FIVE

• CONCLUSION
• REFERENCE

CHAPTER ONE

• INTRODUCTION

1.1   BACKGROUND INFORMATION

Malaria parasite is regarded as one of the most serous health problems facing almost the whole world today. It was noted that this parasitic disease is caused by species of protozoa called Plasmodium Spp. Within the compass of medical environment, malaria was known to be a parasitic disease that gets into human system through the pathogenic bite of an infected female anopheles mosquito. (Knudsen, 1992).

Malaria parasite was also found to be mostly infective to the children under 5-6years and pregnant women, this is because this group of people usually build antibodies which do not prevent the endemic disease of the parasite, but tolerate the victim to a point where it is not consistently lethal (WHO 1986). In the year 1880

Alphonsus lavaran first observed this parasite at it merizoit stage and was published in the B “Bullentine de Aeademic de medicine pariss”. Futher findings on this malaria parasite was carried on by Italian doctors. Which includes Golgi manson, Baslianelli etc. This people observed the mechanism of spreading and the life cycle of the parasite. It was also estimated that 270 million new malaria infection occur worldwide along with 110million cases of illness and 2million deaths, where 25% of childrens death in Africa aere attributed to malaria parasite (WHO 1986).

Malaria parasite being a parasite which falls into protozoa called sporozoa. It means that they are spore formers, their life cycle involves and alternation of generation, one which is sexual and the other asexual method of reproduction. The sexual and asexual generation in this parasite take place in two different hosts. In a complex life cycle like this where the parasite has two host, the definite and the intermidiate host. In the definite host, the parasite carries out the sexual part of the reproduction of which female anopheles mosquito is the host which the asexual part will be carried on in the intermediate host which is in the human blood system (Franklin and wehrle 1948).

According to cheesBrough (1987) this plasmodium Spp which is the causative agent of this malaria parasite are of four varieties species that attacks man. They are (a) Plasmodium Viax which cause tartian malaria, or vivax malaria (b) Plasmodium Malaria, the cause of quatain malaria also called malaria malariae ( c) Plasmodium Oval that causes oval malaria and finally (d) Plasmodium Falciparum which is the agent of malignant tartian malaria. With skill and experience these organs and the differet disease they cause can be possibly differetiate from each other.

LIFE CYCLE.

Among all the mosquitoes that suck blood, it is the female species that has the quality capable of sucking blood, the male mosquitoes are vegetarians which means plant feeders, they feed on the plant juice which they suck. It is the female mosquito in the genus anopheles that bites man to suck blood, and in the process inject the malaria parasite in the body system.

Infecteous mosquito contain in their salivary gland plasmodia which occur in spindle – shaped form known as sporaozonite. Once a mosquito that is parasitise by this organism feeds on the host liver (intermediate host), it inject the sporozoites, these migrate to the host liver where in the parenchymal cells they multiplies asexually. This pact of cycle is known as exo-erythrocytic schizogony, exo-erythrocytic indicates that it take place outside the red cell, “schizogony” literally meaning splitting generation. This Malaria Parasite leaves the liver cells, enter red blood cells, and begin the erythrocytic schizogony phase.

While para-erythrocytic cycle continue in the parenchymal cell of the liver. The exception being plasmodium falagraum which do not undergo paraerythrocytic schizogony cycle in the red cell the malaria parasite grows in size making use of globin in haemoglobin as its source of protein as amino acid, the residual product collects as a pigment.

Then division of the protozoan nucleus occur. At this point, the multinucleated organism inside a red cell is called schizont or segmneter. And a separate nucleus which is surrounded by its own cytoplasm is called a merozorite. The number of the nuclear division and hence the number of merozoite formed varies from species to species and this factor is very useful for the identification of the type of species involved. The red cell containing mature merozorite disintergrate, and merozorites thus released invade new red blood cells, becoming trophozorites and the cycle continues.

Because of the significant exception of the Placsmodium Falciparum of not undergoing para –erythrocytic cycle, different drugs and other control measure are used against this paganism in erythrocytic and para-erythrocytic cycle, Plasmodium Falciparum being relatively easier to control than other species. Mostly often but not all parasitised red blood cells give raise to merozoites. Some plasmodia in red cells ultimately and differently develops either into two sexual forms viz: the macro gametocyte (Female) or microgamatocyte (male) or as the asexual form which continues the cycle in the human system.

The gametocytes develop no further in man and will survive only when the are ingested by female anopheles mosquito. Parenthentically, all the four species of malaria parasite mentioned above can be transmitted from one intermediate host to another by either transfusion of blood or congenitally the gametocytes ingested by a mosquito undergo further development, from each microgamatocyte, about a dozen or so mobile, flagella like microgametes are formed. Then in the stomach of mosquito there occurs a union of the micro-gametesand macro – gametes resulting in the formation of zygote, which proceeds to develop into an ookinete.

This Ookinete is a worm like. It migrates to the stomach wall of the mosquito where it transforms to another form known as oasyst. Then within the oosyst repeated nuclear division occur. The mature Coyest breaks with the release of thousands of sporozoites into the content of the osqito. Sporozoites now migrate to the salivary gland of the mosquito where they are ready again to be injected into the intermediate host (man) for another cycle. The cycle in the mosquito take 1 to 3 weeks. In mana the time from mosquito bite to first Symtoms and hus the time for the pre-erythrocytic and

The typical incubation periods in vagary, ovale malaria, and falciparum malaria are on the order of 14 – 17 , 10 – 14, 28, 8 – 10 days respectively this period occasionally may be much longer in vivase 16-12 mouths and malaria (years) disease condition.

1.2    STATEMENT OF PROBLEMS

A repeatedly report about malaria parasite infection has arise several years long ayo and presently, causing reguar fever, continuous chill, vomiting, headache, shortage of blood and other relative sickness which forms to symptom of the infection.

The estimate of the incident of this parasite according to WHO (1986) shows that about 270 miollion new malaria infection occure worldwide with the occompaniment of 110 and 2 million case of illness and death respectively. Where 25% or childrens death in Africa are altributed to malaria (W H O 1986)

1.3 AIM AND OBJECTIVE OF THE STUDY

AIM:  To determine malaria parasite in the blid all and it’s effect to the human health

THE SPECIFIC OBJECTIVE ARE:

• To identify varieties of Plasmodium Spp. And the different stages of the parasite in the blood sample
• To identify the effects of the parasite in the blood cell ogan infected person
• To proffer preventive measures to reduce the incidence of this infection and it’s mortality rate amony children in the area where there is large infection of malaria parasite.

1.4    HYPOTHESIS

Hi:     Malaria parasite is high among children under 5-6 years and pregnant women.

H0:   Malaria parasite is not high among children and pregnant women.

INTRAOCULAR PRESSURE MARKERS IN MALARIAL INFECTED MICE RECEIVING PHYLLANTHUS  AMARUS  TREATMENT

Download our android mobile app for more materials

ORDER NOW

COMPLETE MATERIAL  COST  N2,500 Or $10.  FRESH  PROJECT MATERIAL  COST 50,000 NAIRA FOR UNDERGRADUATE, OTHERS 100,000 -200,000 NAIRA.

Foreign Transaction For Dollars Payment :
Bank Name: GTBank
Branch Location: Enugu State,Nigeria.
Account Name: Chi E-Concept Int’l
 Account Number:  0117780667. 
Swift Code: GTBINGLA 
Dollar conversion rate for Naira is 175 per dollar. 

ATM CARD:  YOU CAN ALSO MAKE PAYMENT USING YOUR ATM CARD OR ONLINE TRANSFER. PLEASE CONTACT YOUR BANK SECURITY FOR GUIDE ON HOW TO TRANSFER MONEY TO OTHER BANKS USING YOUR ATM CARD. ATM CARD OR ONLINE BANK TRANSFER IS FASTER FOR QUICK DELIVERY TO YOUR EMAIL . OUR MARKETER WILL RESPOND TO YOU ANY TIME OF THE DAY. WE SUPPORT CBN CASHLESS SOCIETY. 

OR
PAY ONLINE USING YOUR ATM CARD. IT IS SECURED AND RELIABLE.

form>DELIVERY PERIOD FOR BANK PAYMENT IS  LESS THAN 24 HOURS

CALL OUR  CUSTOMERS CARE  OKEKE CHIDI C ON :  08074466939,08063386834.

AFTER PAYMENT SEND YOUR PAYMENT DETAILS TO

08074466939 or 08063386834, YOUR PROJECT TITLE  YOU WANT US TO SEND TO YOU, AMOUNT PAID, DEPOSITOR NAME, UR EMAIL ADDRESS,PAYMENT DATE. YOU WILL RECEIVE YOUR MATERIAL IN LESS THAN 2 HOURS ONCE WILL CONFIRM YOUR PAYMENT.

WE HAVE SECURITY IN OUR BUSINESS.   

MONEY BACK GUARANTEE

ABSTRACT

Phyllanthus amarus has been consistently reported as a rich herb having medicinal value and ethnomedical importance. It has been used to eliminate gallstone, malaria and some other aliments, but the effect of its use on changes in ocular glucose, proteins and lipids — analytes that influence intraocular pressure, has not been fully documented. So, in this study, the effect of ethanolic leaf extract of Phyllanthus amarus on the levels of ocular glucose, proteins and lipids was investigated using homogenized ocular tissue of experimental mice. Forty five (45) adult mice weighing between 22-27g were randomly divided into 9 groups  and used for the study. Group 1: normal control (uninfected and untreated mice) Group 2: malaria control (mice infected with plasmodium berghei and untreated) Group 3: parasitized (infected with P. Berghei treated with 100mg/kg P. amarus) Group 4: parasitized (infected with P. Berghei treated with 200mg/kg P. amarus) Group 5: parasitized (infected with P. Berghei treated with 300mg/kg P. amarus)

Group 6: parasitized (infected with P. Berghei treated with 5mg/kg chloroquine)

Group 7: uninfected but treated with 100mg/kg P .amarus Group 8: uninfected but treated with 200mg/kg P. amarus Group 9: uninfected but treated with 300mg/kg P. amarus .Each group was treated for

7days and on the 8th day the animals were scarificed under chloroform anaesthesia after an overnight fast. The mice eyes were carefully excised, rinsed in cold normal saline and prepared for the biochemical analysis of glucose, proteins and lipids using standard methods. Results show that Phyllanthus amarus administration (irrespective of dose) did not significantly (p>0.05) alter ocular glucose and protein levels, but increased (p<0.05) lipids (cholesterol and triglycerides) concentrations when compared with control values. The altered ocular lipid homeostasis may have some biochemical implications and clinical significance. This should be validated in further studies.

LIST OF TABLES

Table 1: glucose in the serum of p. berghei infected and uninfected mice treated with phyllanthus amarus leaf extract.    ———————————————————        25

Table 2: changes in blood cholesterol and triglyceride induced by plasmodium berghei infected mice    ——————————————————————————–       26

Table 3:  changes in blood albumin and total protein induced by p. berghei infected mice    —————————————————————————————————        27

Cover         ——————————————————————–      i

Title            ——————————————————————–    ii

Certification   —————————————————————-     iii

Dedication      ————————————————————–       iv

Acknowledgement   ——————————————————         v

Abstract         —————————————————————       vi

List of Tables   ————————————————————-     vii

Table of contents   ——————————————————-       viii

CHAPTER ONE

• INTRODUCTION ———————————————————————–      1

1.1.1 BACKGROUND OF STUDY    ——————————————————-      1

1.2 STATEMENT OF PROBLEM    ——————————————————-        3

1.3 OBJECTIVE OF STUDY    ————————————————————-        4

1.4 SIGNIFICANCE OF STUDY    ——————————————————–        4

1.5 HYPOTHESIS    ————————————————————————–     5

1.6 BRIEF REVIEW OF RELEVANT LITERATURE    ———————————     5

1.7 BIOMAKERS   —————————————————————————-    5

1.8 RETINOPATHY    ————————————————————————   6

1.9 MUSCULAR ODEMA   —————————————————————–    6

1.10 WHAT IS MALARIA?    ———————————————————    7

1.11 CAUSES OF MALARIA       ———————————————————–     8

1.12 EPIDEMIOLOGY OF MALARIA         ———————————————-     8

1.13 GLOBAL AND GEOGRAPHICAL DISTRIBUTION OF MALARIA..   ——        9

1.14TRANSMISSION AND LIFE CYCLE OF PLASMODIUM PARASITE   —–      11

1.15 LIFE CIRCLE OF PLASMODIUM PARASITE   ———————————–    12

CHAPTER TWO   ——————————————————————————    14

2. 0MATERIALS AND METHOD ——————————————————– 14

2.1 MATERIALS    —————————————————————————–    14

2.2 METHODS    ——————————————————————————–   14

2.2.1 ANIMALS CARE AND HANDLING    ———————————————    14

2.2.2 ANIMAL GROUPING AND INOCULATION WITH PLASMODIUM BERGHEI    —————————————————————————————————–     15

2.2.3 ANIMAL SACRIFICE AND COLLECTION OF SPECIMEN    —————-     16

2.2.4 ANALYSIS OF SPECIMEN   ———————————————————-   16

2.3 GLUCOSE ESTIMATION    ———————————————————–    16

2.3.1 REACTION PRINCIPLE    ———————————————————-     16

2.3.2 PROCEDURE    ———————————————————————–     17

2.4 TOTAL CHOLESTEROL ESTIMATION    ——————————————   17

2.4.1 PRINCIPLE    ————————————————————————–     17

2.4.2 EQUATION    ————————————————————————–    17

2.4.3 PROCEDURE    ————————————————————————    18

2.4.4 CALCULATION    ———————————————————————   19

2.5. TRIGLYCERIDE ESTIMATION    —————————————————    19

2.5.1 PRINCIPLE    ————————————————————————–     19

2.5.2 EQUATION    —————————————————————————   20

2.5.3 PROCEDURE    ———————————————————————–     20

2.5.4 CALCULATION    ——————————————————————–    21

2.6 TOTAL PROTEIN ———————————————————————-     21

2.6.1 PRINCIPLE    ————————————————————————–     21

2.6.2 PROCEDURE    ———————————————————————–     21

2.6.3 CALCULATION    ——————————————————————–     22

2.7 ALBUMIN ———————————————————————————–22

2.7.1 PRINCIPLE    ————————————————————————–      22

2.7.2 PROCEDURE    ———————————————————————–      23

2.7.3 CALCULATION    ——————————————————————–     23

2.7.4 STATISTICAL ANALYSIS ————————————————————– 24

CHAPTER THREE    —————————————————————————   25

3.0 RESULTS    ———————————————————————————-   25

CHAPTER FOUR    —————————————————————————–   28

4.0 DICUSSION    ——————————————————————————    28

4.1 CONCLUSION    —————————————————————————– 29

REFERENCES   —————————————————————————30

CHAPTER ONE

1.1     INTRODUCTION

1.1.1. BACKGROUND OF STUDY

Nature can be considered as the ultimate chemist, about 80% of the world inhabitants still depend on natural products that have inspired chemists and physicians for years because of their rich structural diversity and complexity considerable advances have been obtained for the understanding of natural product biosynthesis in the recent decades.

Malaria, a mosquito borne infectious disease is endemic in the tropical and sub tropical regions of the world (Ahimanah et al., 2000). It is a deadly disease which lowers life expectancy and a major cause of infant mortality in highly endemic areas (WHO, 2011).

Malaria infection in humans and animals is caused by the Plasmodium. Several species of Plasmodium have the ability to cause malaria in animals, including rodents (mice). These parasites are not direct practical concern to man or his domestic animals. The interest of these parasites is that they are practical model organism in the laboratory for the experimental study of human malaria.

Plasmodium berghei is considered a comparable genetic model to human There is a high degree of genetic conservation this up to 99% (pennachio, 2003) and it is well established that mice also exhibit natural differences in susceptibility to malaria infection (Greenberg et al., 1954). P. berghei is transmitted by Anopheles mosquito and it infects the liver after being injected into the blood stream by the bite of the infected female mosquito. After a few days of development and multiplication, these parasites leave the liver and invade erythrocyte (red blood cells). The multiplication causes Anemia and damage essential organs in the body. P. berghei infection also affects the brain and can cause cerebral complications in laboratory mice.

The plant, phyllanthus schumach (Euphorbiaceac) is commonly known as bhuirali Usually occurs in Asain, Maharashitra, Burma, Nicobar, Islands malesia and America. Phyllanthus amarus schumach is a native to Americans (van Holthoon, 1999). Phyllanthus amarus is small, erect, annual herb that grows 30-40cm in height which is indigenous to the rain forests of the Amazon and other tropical areas throughout the world including America, India and Nigeria. The Spanish name of the plant, chanca piedra, means stone breaker, wind breaker, gulf leaf flower or gala of wind (Celia, A.  et al., 2006).

Phyllanthus amarus is an Ayurvedic system of medicine which is used in the problems of stomach, genitourinary system, liver, kidney, and spleen, it plays an important role in Ayurvedia, an Indian system of medicine and it is used to treat jaundice, gastropathy, diarrhea, dysentery, fevers, scabies, gential, infections, ulcers, and wounds (Patel et al., 2011).

The different plant parts are ethnobotanically used in various diseases and disorders. For example, the leaves are used as expectorant and diaphoretic and the fruits as carminative, laxative, astringent. Diuretic and tonic to the liver. The juice or extract of its thinner roots and young leaves are taken internally to stimulate the kidney. Heyne recorded its uses in the Dutch  Indies (Indonesia) for stomach, aches, gonorrhoea and children cough (Karuna,  et al., 2009).

Research have shown that the plant has demonstrated anti-viral property against hepatitis B virus (Boeira  et al., 2 011), hepatoprotective (Amin,  et al., 2013), anticarcinogenic (Rajeshkumar,  et al., 2002), antimutagenics, anti-nociceptive and anti-inflammatory (Obidike,  et al., 2010), anti-diabetics (Okoli, et al., 2011) and antilipidermic (Khanna,  et al.,  2002) activities.

1.2 STATEMENT OF PROBLEM

Since malaria has been speculated to alter biochemical functions of organs of the body such as brain, liver, heart, and spleen, this research is designed to know if such biochemical alternations also include changes in the intraocular pressure markers in experimental mice. Phyllanthus amarus is a medicinal herb used for the treatment of several diseases including malarial infection. In southern Nigeria the utilization of Phyllanthus amarus is popular but whether it improves or disturbs