ABSTRACT
This work was done to ascertain the efficacy of the seed of Tetracarpidium conophorum on hydrogen peroxide induced oxidative stress in Wistar albino rats. Thirty five (35) male wistar albino rats weighing (120- 140g) were distributed into seven (7) groups of five rats each. Groups 2-6 were administered with hydrogen peroxide (1.0 ml/kg), while group 1 served as the normal control while group 2 serves as positive control Groups 3, 4, 5 and 6 were treated with vitamin C (100 mg/kg), 200, 400 and 800 mg/kg of the extract respectively for five days, Group 7 was administered 800 mg/kg b.w of the extract only. Blood was collected from the animals on the 7th day through occular puncture for assay of some biochemical parameters. The qualitative and quantitative analysis of the seed extract were determined using standard methods and showed that the extract contained terpenoids (4.36 ± 0.06 mg/g), Tannins (1.89 ± 0.11 mg/g), alkaloids (20.31 ± 0.30mg/g) and cardiac glycosides (12. 45 ± 0.08 mg/g), anthraquinones, saponins and steroids were not detected in the extract. Vitamins constituents of the extract were vitamin A (10.55 ± 2.67 mg/ 100g), vitamin C (13.09 ± 0.23 mg/ 100g) and vitamin E (5.77 ± 0.08 mg/ 100g). The mineral constituents indicated the presence of mg (133.59 ± 0.11 mg/ 100g), Ca (118.90 ± 0.01 mg/ 100g), Fe (3.67 ± 0.07 mg/ 100g), Zn (2.22 ± 0.01 mg/ 100g), Cu (1.54 ± 0.78 mg/ 100g). The acute toxicity test of the extract showed no toxicity up to 5000 mg/ kg b.w. Serum ALT activity significantly decreased (p< 0.05) in all the test groups compared to group 2. Serum AST and ALP activity decreased significantly (p< 0.05) in all the test groups except group 6 for ALP activity compared to the enzyme activities of normal and positive controls. A significant decrease (p< 0.05) was observed in the serum MDA concentration of rats in the test groups when compared to the group 2. A significant increase (p < 0.05) was observed in the serum GPx activity of groups 4, 6 and 7 compared to the GPx activity of group 2 rats. There was a significant increase (p < 0.05) in groups 4 and 7 compared to group 2. The serum cholesterol concentration showed a significant decrease (p < 0.05) in the test groups relative to those of the controls. There was a significant decrease (p < 0.05) in the serum LDL and TAGs of rats in the test groups when compared to the controls. The serum HDL of groups 5 and 7 increased significantly (p < 0.05) compared to the normal control and the positive control. The effect of the extract on lipid profile showed that it increased HDL at a concentration of 400mg/kg body. These antioxidant enzymes results support the claims made by several scientists that the plant could be used to scavenge free radicals in the system which often lead to the risk of various diseases.
1.1 Background of the study
CHAPTER ONE
INTRODUCTION
The use of various fruits, vegetables, nuts and various parts of plants in traditional medicine is as old as man (Evans, 2002). This lies outside the mainstream of orthodox or Western medicine, it has been estimated that two thirds of the world population (mainly in developing countries) rely on traditional medicine as their primary form of health care (Sumner, 2000). The use of traditional medicine cannot fade out in the treatment and management of diseases in the African continent and this could be attributed to the socio- cultural, socio-economic, lack of basic health care and qualified personnel (Elujoba et al.,
2005). Plants contain active components such as anthraquinones, flavonoids, glycosides, saponins, tannins, etc which posses medicinal properties that are harnessed for the treatment of different diseases (Chevalier, 2000). The active ingredients for a vast number of pharmaceutically derived medications contain the healing properties known as the active principles and are found to differ from plant to plant (Chevalier, 2000).Nuts vary considerably in their nutrient content and are sources of vitamins, antioxidants, proteins, essential amino acids, etc. (Fasuyi, 2006). They are included in meals mainly for their nutritional values. However, some are reserved for their medicinal values such as increase in brain health, decreased depression, increase in antioxidant levels; thus, helping to mop up free radicals which have been implicated in a number of diseases (Oladiyi et al., 2007).
In a normal cell, there is an appropriate pro-oxidant/antioxidant balance. However this balance can be shifted towards the prooxidant following the ingestion of certain chemicals or drugs when the levels of antioxidants are low; this gives rise to oxidative stress and results in cell damage if prolonged or massive (Murray et al., 2009). Thus oxidative stress is a metabolic perturbation of homeostasis. On the other hand, antioxidants are a complex and diverse group of molecules that protect key biological sites from oxidative damage (Murray et al., 2009).Lipid peroxidation is a degenerative process involving peroxidative decomposition of unsaturated fatty acids mediated by free radical or reactive oxygen species (Gutteridge and Halliwell, 1995).
Recently oxidative stress has been linked to many age associated diseases including heart diseases, cancer, atherosclerosis as well as brain disorders (Singh et al., 1995). It can also lead to inhibition of some metabolic enzymes (Devasagayam et al., 2004).
Fortunately, aerobic organism have evolved very effective defense system against oxidative assault, this is due to the consistency of both hydrophilic (GSH, Vit C) and lipophilic (Vit E,
Carotenoid pigment) antioxidant compounds or scavengers and specific antioxidant enzymes including superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase. Epidemiological studies have shown strong correlation between plasma antioxidant vitamin levels and mortality rates from heart disease (Schafer and Buettner, 2001).
Hence, oxidative stress is one of the common causes of health disorders posing a great threat to global health care. Medicinal plants are currently being used in various parts of the world especially in the civilized world in the treatment of several diseases such as artherosclerosis, heart disease, brain disorder etc (Ajaiyeoba and Fadare, 2006).
Most nuts contain antioxidant enzymes as well as antioxidant vitamins (A, C, E). Tetracarpidium conophorum nuts used as snack in various countries of the world have been shown to have positive effects on oxidative stress (Oke, 1995).Due to their ability to increase poly unsaturated fatty acids, good cholesterol (HDL) antioxidant vitamins in several parts of the world.Hence there is need to investigate the effect of chloroform-methanol extract of T. conophorum nuts on hydrogen peroxide induced oxidative stress markers and possibly advocate their inclusion in food preparations for everyone and especially for the elderly and this has necessitated this research.
1.2 Tetracarpidium conophorum
Tetracarpidium conophorum (Walnut) consists of families of Juglandaceae (English Walnut), Euphorbiaceae (African Walnut) and Olacaceae (African Walnut (Dalziel) 1937). Each family has its own peculiar characteristics but they have some things in common such as the nuts. Juglandaceae, is mostly found in Southeast Europe to Japan and more widely in the New world. Tetracarpidium conophorum (family Euphorbiaceae) is found in Nigeria and Cameroun while coula edulis (family Olacaceae) which is also referred to as African Walnut is found in Congo, Gabon and Liberia (Wikipedia, 2008).
Tetracarpidium conophorum is a climbing shrub 10-20 feet long, it is known in the Southern Nigeria as Ukpa (Igbo), Western Nigeria as awusa or asala (Yoruba). It is known in the littoral and the Western Cameroun as Kaso or ngak (Dalziel, 1937). It is found in Uyo, Akamkpa, Akpabuyo, Lagos, Kogi, Ogbomoso and Ibadan. The plant is cultivated principally for the nuts which are cooked and consumed as snacks (Oke, 1995).
The plant is glabrous with deciduous male flowers leaving the females at the base of the raceme (Petrova, 1980).
A bitter taste is usually observed upon drinking water immediately after eating the nuts. This could be attributed to the presence of chemical substances such as alkaloid (Ayodele, 2003). The seeds contain ascorbic acid and heavy metals, amino acids and fatty acids (Oyenuga, 1997) reported on the amino acid and fatty acid compositions of the nuts and on the use of its leaf juice have been used for the treatment of prolonged and constant hiccups.
1.2.1 Scientific classification of Tetracarpidium conophorum
Kingdom: Plantae Division: Magnoliophyta Class: Magnoliopsida Order: Malpighiales Family: Janiroidea Genus: Tetracarpidium Species: conophorum
Govarts (2003)
1.2.2 Medicinal, Nutritional and Industrial importance of Tetracarpidium conophorum
1.2.2.1 Medicinal uses of Tetracarpidum conophorum (Walnuts)
Tetracarpidium conophorum is a medicinal plant widely cultivated for the production of its seeds. The seed have been implicated in Southern Nigeria ethno medicine as a male fertility agent (Ajaiyeoba and Fadare, 2006). The seed is used in the treatment of indigestion, constipation and diarrhea (Wolters, 2009). The seed is a good source of vitamins. Alkaloids are the most efficient plant substances used therapeutically. Pure isolated alkaloids and the synthetic derivatives are used as the basic medicinal agent because of their analgesic, antispadomic and bacterial properties. This is why the seed is believed to stop asthma and is prescribed to be taken between bouts of asthma, but not for acute asthma. It is used for the elderly as a constipation cure (Wikipedia, 2009). The presence of tannins in the seed of Tetracarpidium conophorum can support its strong use for healing of haemorrhoids, frost bite and varicose ulcers in herbal medicine (Igboko, 1983, Maduiyi, 1983).
Walnuts have been reported as having Chelating ability which in turn could account for its high antioxidant activity which have been compared to the use of dimercapto- succinic acid (DMSA). 2, 3- dimercapto -1- propanesulfonic acid (DMPS) and alpha lipoic acid (ALA) (Muanya, 2012).
Walnuts are a good source of protein, vitamin C, folic acid and vitamin E, they also have an extremely high level of polyunsaturated fat and are a good source of omega 3- fatty acids (Cortes et al., 2006) such as linoleic acid, alpha-linolenic acid (ALA) and arachidonic acids. Regular intake of Walnuts in the diet helps to lower, total as well as LDL or ‘bad cholesterol’ and increases HDL or “good cholesterol” levels in the blood. Walnuts are a rich source of many phytochemical substances that may contribute to their overall anti- oxidant activity, including melatonin, ellagic acid, Vitamin E, Carotenoid and poly phenolic compounds. These Compounds have potential health effects against Cancer, aging, inflammation and neurological diseases (Reiter et al., 2005).Walnuts Oil has flavourful nutty aroma and excellent astringent properties, applied locally, it helps to keep the skin well protected from dryness. It has also been used in cooking and as ‘carrier or base oil’ in traditional medicines in massage therapy, aromatherapy in pharmaceutical and cosmetic industry (Fortin, 1996).
1.2.2.2 Nutritional uses of Tetracarpidium conophorum (Walnuts)
Walnuts are excellent sources of vitamin E, not in the alpha tocopherol but in the gamma-tocopherol, particularly in studies of cardio vascular health of men, this gamma-
tocopherol form has been found to provide significant protection from heart problems and maintaining the integrity of cell membranes of mucous membranes and skin by protecting it from harmful oxygen radicals. (Blomhoff et al., 2006).
Some phytonutrients found in walnut for example, the quinine juglone are found in virtually no other commonly eaten food. Others’ such as the tannin-tellimagrandin or the flavonol morin are also rare and valuable as antioxidants and anti inflammatory nutrients. These anti- inflammatory and anti- oxidant phytonutrients also help explain the decreased risk of certain cancers- including prostate cancer and breast cancer (Fukuda et al., 2003). Walnut are packed with many important B- Complex groups of vitamins such as riboflavin, niacin, thiamine, pantothenic acid, Vitamin B6, and Folates.
They are also a rich source of mineral salts such as mangenese, copper, potassium,
calcium, iron, magnesium, zinc and selenium. Copper is a cofactor for many vital enzymes, including cytochrome c- oxidase and superoxide dismutase. Zinc is a co- factor in many enzymes that regulate growth and development, sperm generation, digestion and nucleic acid synthesis. Selenium is an important micro nutrient which functions as a co-factor for anti- oxidant enzymes such as glutathione peroxidases. (Esminger et al., 1983). Walnuts oil has flavourful nutty aroma used in salad dressings and also used as an edible oil in cooking.
1.2.2.3 Industrial uses of Tetracarpiduim conophorum (Walnuts)
Locally, the oil has been used as a moisturizer to keep the skin well protected from dryness. The bark is used as dye in clothing and textile industry because it contains a juice that will readily stain anything it comes into contact with. Walnut hulls contain phenolic compounds (ferulic acid, vanillic acid, coumaric acid, syringic acid, myricetrin juglone (Cosmulesc et al., 2010) and regiolone (Liu et al., 2007). Black Walnut heartwood is heavy, hard strong and durable with a chocolate brown colour. Walnut shells are used as thickener in paint and plastic industry, a filler in explosives and for cleaning and polishing, used as abrasive element in home soap making (Liu et al., 2007).The floor of the Globe Theatre in Elizabethan London was made of Walnut shells and compacted down to a very hard and polishable surface.
1.3 Oxidative Stress
Oxidative stress is an imbalance between the systemic manifestation of reactive oxygen species and a biological system’s inability to readily detoxify the reactive intermediates or to repair the resulting damage (Murray et al.,2009). Disturbances in the
normal redox state of cells can cause toxic effects through the production of peroxides and free radicals that damage all components of the cell including proteins, lipids and DNA.
In humans and animals, oxidative stress is thought to be involved in the development of many diseases or may exacerbate their symptoms (Proctor et al., 1984, Proctor, 1989) These include cancer, (Halliwell, 2001), Parkinson’s disease, Alzeihmer’s disease, atherosclerosis, heart failure, myocardial infarction, schizophrenia, Bipolar disorder, fragile X syndrome, sickle cell disease, autism and chronic fatigue syndrome (Gwen et al.,2005).
Oxidative stress is a term used to refer to the shift towards the pro-oxidants in the pro- oxidative/ antioxidants balance that can occur as a result of an increase in oxidative metabolism (Manda et al., 2009). ROS reactions with biomolecules such as lipid, protein and DNA, produce different types of secondary radicals like lipids radicals, non-sugar and base derived radicals, amino acid radicals depending upon the nature of the ROS (Niki et al.,
2005). These radicals in the presence of oxygen are converted to peroxyl radicals. Peroxyl radicals are critical in biosystems, these reactions exert oxidative stress on the cells, tissues and organs of the body. The biological implications of such reactions depends on several factors like site of generation, nature of the substrate, activation of repair mechanisms, redox status among many others (Koppeno, 1993; Goldstein et al., 1993).
1.3.1 Chemical and biological effects of oxidative stress.
Chemically, oxidative stress is associated with increased production of oxidizing species or a significant decrease in the effectiveness of antioxidant defenses, such as glutathione (Schafer and Buettner, 2001). The effects of oxidative stress depend upon the size of these changes, with a cell being able to overcome small perturbations and regain its original state. However, more severe oxidative stress can cause cell death and even moderate oxidation can trigger apoptosis, while more intense stresses may cause necrosis (Lennon et al., 1991).
Production of reactive oxygen species is a particularly destructive aspect of oxidative stress. Such species include free radicals and peroxides. Some of the less reactive of these species (such as superoxide) can be converted by oxidoreduction reactions with transition metals or other redox cycling compounds (including quinines) into more aggressive radicals that can cause extensive cellular damage (Valko et al., 2005). The major portion of long term effects is inflicted by damage on DNA (Evans and Cooke, 2004). Most of these oxygen – derived species are produced at a low level by normal aerobic metabolism. Normal cellular defense mechanisms destroy most of these. Likewise, any damage to cells is constantly
repaired. However, under the severe levels of oxidative stress that cause necrosis, the damage causes ATP depletion, preventing controlled apoptotic death and causing the cell to simply fall apart (Lelli et al., 1998, Lee and Shacter, 1999).
1.3.2 Oxidative stress and diseases
Oxidative stress is suspected to be implicated in neurodegenerative diseases including Lou Gehrig’s disease, Parkinson’s disease, Alzheimer’s disease, and Huntington’s disease (Patel and Chu 2011). Indirect evidence via monitoring biomarkers such as reactive oxygen species, and reactive nitrogen species production, antioxidant defense mechanism indicates that oxidative damage may be involved in the pathogenesis of these diseases (Nunomura et al., 2005), while cumulative oxidative stress with disrupted mitochondrial respiration and mitochondrial damage are related with Alzheimer’s disease, Parkinson’s disease, and other neurodegenerative diseases (Ramalingam and Kim, 2012).
Oxidative stress is thought to be linked to certain cardiovascular disease, since oxidation of LDL in the vascular endothelium is a precursor to plaque formation. Oxidative stress also plays a role in the ischemic cascade due to oxygen reperfusion injury following hypoxia. This cascade includes both strokes and heart attacks. Oxidative stress has also been implicated in chronic fatigue syndrome (Nijs et al., 2006). Oxidative stress also contributes to tissue injury following irradiation and hyperoxia as well as in diabetes.
1.3.3 Free Radical generations / Reactive oxygen species.
Free radicals can be defined as those atoms or molecules containing one or more unpaired electrons in their outer most shell and mostly is very reactive due to the presence of these unpaired electron(s) (Knight, 1998), Reactive oxygen species (ROS) is a collective name given to both oxygen free radicals and non oxygen free radicals (Mittler, 2002). Reactive oxygen species can also be used to refer to a group of oxidants.
1.3.3.1 Sources of Free radicals
1. Electron Transport Chain
Production of superoxide and hydrogen peroxide usually takes place in the mitochondria of a cell (Valko et al., 2004; Nelson et al., 2006). The mitochondria electron transport chain is the main source of ATP in the mammalian cell; hence, it is essential for life. During energy transduction, a small number of electrons “leak” to oxygen prematurely,
forming the oxygen free radical superoxide, which has been implicated in the pathophysiology of a variety of diseases (Valko et al., 2007).
2. Stress responses and defence pathways. (Phagocytosis)
Reactive oxygen species are nature’s response to external and internal stimuli. This is done in most cases to defend the body against foreign pathogenic and or parasitic invasion for instance; the killing of parasites during disease and infection states has been hypothesized. The hydroxyl radical, OH, is the neutral form of the hydroxide ion. The hydroxyl radical has a high reactivity, making it a very dangerous radical with a very short in vivo half- life of
approximately 10-9 s (Pastor et al., 2000). Thus, when produced in vivo, OH reacts close to
its site of formation. Cellular productions of these ROS are enhanced during stress and can posed threat to cells, but it is also thought that ROS act as signals for the activation of stress- response and defence pathways (Mittler, 2002). Thus, ROS can be viewed as cellular indicators of stress and as secondary messengers involved in the stress- response signal transduction pathway (Valko et al., 2005). Over- accumulation of ROS can result in cell death (Toykuni, 1999). ROS-induced cell death can result from oxidative processes such as membrane lipid peroxidation, protein oxidation, enzyme inhibition and DNA and RNA damage (Etsuo et al., 1991).
3. Metal catalysts
Metals such as iron, copper, chromium, vanadium and cobalt are capable of redox cycling in which a single electron may be accepted or donated by the metal. This action catalyzes reactions that produce reactive radicals and can produce reactive oxygen species (Pratviel, 2012). The most important reactions are probably Fenton’s reaction and the Haber- Weiss reaction, in which hydroxyl radical is produced from reduced iron and hydrogen peroxide. The hydroxyl radical then can lead to modifications of amino acids (e.g. meta- tyrosine and ortho-tyrosine formation from phenylalanine), carbohydrates, initiate lipid peroxidation, and oxidized nucleobases. Most enzymes that produce reactive oxygen species contain one of these metals. The presence of such metals in biological systems in an uncomplexed form (not in a protein or other protective metal complex) can significantly increase the level of oxidative stress. In humans, hemochromatosis is associated with increased tissue iron levels, Wilson’s disease with increased tissue levels of copper and chronic manganism with exposure to manganese ores. The reaction of transition metals with proteins oxidated by reactive oxygen species or reactive nitrogen species can yield reactive
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products that accumulate over time and contribute to aging and disease. For example, in Alzheimer’s patients, peroxidized lipids and proteins accumulate in lysosomes of the patient’s brain cells (Devasagayam et al., 2004)
4. Non- metal catalysts
Certain organic compounds in addition to metal redox catalysts can also produce reactive oxygen species. One of the most important classes of these are the quinines. Quinines can redox cycle with their conjugate semiquinones and hydroquinones, in some cases catalyzing the production of superoxide from dioxygen or hydrogen peroxide from superoxide. Oxidative stress generated by the reducing agent uric acid may be involved in the Lesch- Nyhan syndrome, stroke, and metabolic syndrome. Likewise, production of reactive oxygen species in the presence of homocysteine may figure in homocystinuria, as well as atherosclerosis, stroke, and Alzheimers.
1.4 Hydrogen Peroxide (H2O2)
Hydrogen peroxide is a lipid soluble radical or oxidant formed by dismutation by the enzyme SOD in the inactivation of destructive superoxide ions by converting them to hydrogen peroxide which is in turn transformed into water and oxygen by the enzyme catalase. Peroxisomes are known to produce H2O2, but not O2, under physiologic conditions (Valko et al., 2004). Peroxisomes are major sites of oxygen consumption in the cell and participate in several metabolic functions that use oxygen. Oxygen consumption in the peroxisome leads to H2O2 production, which is then used to oxidize a variety of molecules (Forman et al., 2010). This organelle also contains catalase, which decomposes hydrogen peroxide and presumably prevents accumulation of this toxic compound. Thus, the peroxisome maintains a delicate balance with respect to the relative concentrations or activities of these enzymes to ensure no net production of ROS (Juranek and Bezek, 2005). When peroxisomes are damaged and their H2O2 consuming enzymes down regulated, H2O2 releases into the cytosol which is significantly contributing to oxidative stress (Juranek and Bezek, 2005). Proteins can undergo direct and indirect damage following interaction with ROS resulting into peroxidation, changes in their tertiary structure, proteolytic degradation, protein- protein cross linkages and fragmentation (Yu, 1994). Although, DNA is a stable, well- protected molecule, ROS can interact with it and cause several types of damage such as modification of DNA bases, single and double strand DNA breaks, loss of purines (apurinic
sites), damage to the deoxyribose sugar, DNA- protein cross linkage and damage to the DNA
repair system (Droge, 2002).
1.5 Lipid Peroxidation
Lipid peroxidation is a well-established mechanism of cellular injury in both plants and animals, and is used as an indicator of oxidative stress in cells and tissues. It is the process in which free radicals “steal” electrons from the lipids in cell membranes, resulting in cell damage. This process proceeds by a free radical chain reaction mechanism (Marnett,
1999). Lipid peroxidation is an autocatalytic free radical- medicated destructive process whereby poly-unsaturated fatty acids in cell membranes undergo degradation to form lipid hydroperoxides (Moore and Robert, 1998). Lipid peroxidation of cellular structures, a consequence of increased oxygen free radicals, is thought to play an important role in atherosclerosis and micro vascular complications of diabetes mellitus which is consequent from oxidative stress (Soliman, 2008).Lipid peroxidation triggers the loss of membrane integrity, causing increased cell permeability, enzyme inactivation, structural damage to DNA and cell death (Halliwell, 1992). Initiation is the step in which a fatty acid radical is produced. The most notable initiators in living cells are reactive oxygen species (ROS), such as OH and HO, which combines with a hydrogen atom to make water and a fatty acid radical. The fatty acid radical is not a very stable molecule, so it reacts readily with molecular oxygen, thereby creating a peroxyl- fatty acid radical. This too is an unstable specie that reacts with another free fatty acid, producing a different fatty acid radical and lipid peroxide, or cyclic peroxide if it had reacted with itself (Koppeno, 1993; Goldstein et al., 1993). This cycle continues, as the new fatty acid radical reacts in the same way. Lipid peroxides are unstable and decompose to form a complex series of compounds including reactive carbonyl compounds.
When a radical reacts with a non- radical, it always produces another radical, which is why the process is called a “chain reaction mechanism”. The radical reaction stops when two radicals react and produce a non- radical specie (Juranek and Bezek, 2005). This happens only when the concentration of radical species is high enough for there to be a high probability of collision of two radicals. Hence, the generation of free radicals lead to lipid peroxidation and formation of severe damage in tissues (Soliman, 2008). Cellular membranes are vulnerable to the oxidation by ROS due to the presence of high concentration of unsaturated fatty acids in their lipid components. ROS reactions with membrane lipids cause lipid peroxidation, resulting in formation of lipid hydroperoxide (LOOH) which can further decompose to an aldehyde such as malondialdehyde, 4- hydroy nonenal (4-HNE) or form cyclic endoperoxide, and hydrocarbons (Trangvarasittichai et al., 2009).
Living organisms have evolved different molecules that speed up termination by catching free radicals and, therefore, protecting the cell membrane. One important such antioxidant is vitamin E. Other anti- oxidants made within the body include the enzymes superoxide dismutase, catalase and perioxidase. If not terminated fast enough, there will be damage to the cell membrane, which consists mainly of lipids (Seiler et al., 2008).
1.5.1 Malondialdehyde
By-products of lipid peroxidation such as conjugated dienes and malondialdehyde (MDA). MDA is generated as a relatively stable end product from the oxidative degradation of poly- unsaturated fatty acids (PUFA). This free radical- driven lipid peroxidation has been causatively implicated in the aging process, atherosclerosis, Alzheimer’s disease and cancer (Niki et al., 2005). Serum MDA has been used as a biomarker of lipid peroxidation and has served as an indicator of free radical damage (Tangvarasittichai et al., 2009). Malondialedehyde is a highly reactive three carbon dialdehyde that occurs naturally and exits primarily in an enol form. It is a toxic compound that reacts with DNA to form covalently- bonded adducts with deoxyadenosine and deoxyguanosine, an event that can cause a mutagenic transformation within DNA (Nordberg and Amer, 2001). Additionally, Malondialedehyde can interact with several functional groups on proteins and lipoproteins, altering their chemical behaviour and possibly contributing to carcinogenesis and mutagenesis (Ogugua and Ikejiaku, 2005). Due to its highly reactive nature, Malondialedehyde also functions as an electrophile that can cause toxic stress within the cell and is, therefore, a potent marker for measuring the overall level of oxidative stress within an organism (Conn, 1995; Del- Rio et al., 2005; Soliman, 2008; Tangvarasittichai et al., 2009).
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EFFECT OF CHLOROFORM- METHANOL EXTRACT OF TETRACARPIDIUM CONOPHORUM NUTS (WALNUTS) ON OXIDATIVE STRESS MARKERS IN HYDROGEN PEROXIDE INDUCED WISTAR ALBINO RATS>
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