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 Free Radicals 

What is a free radical

What is MDA

Free Radicals - where and how formed

Aging

Degenerative Diseases

Free Radical Test kit

Solutions to excessive free radicals

Antioxidant - Flax Hulls

Antioxidant - Fortified Flax Hulls (with broccoli sprouts)



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Strategic Health Marker

FREE RADICALS!



Degenerative Diseases caused by Free Radicals
  • Free radicals in the genesis of Alzheimer's disease
    J. S. Richardson - Department of Pharmacology, College of Medicine, University of Saskatchewan, Saskatoon, Canada.
    As part of an ongoing investigation of the role of oxygen free radicals in Alzheimer's disease (AD), the formation of peroxidation products, the activities of free radical defense enzymes, and the level of total iron were determined in autopsy brain tissue from donors with AD and from age-matched non-demented donors. Calcium uptake was also investigated in mitochondria harvested from fibroblasts grown in tissue culture from skin samples taken from brain donors. Compared to controls, homogenates of AD frontal cortex produced elevated levels of peroxidation products and this difference was amplified in a dose-dependent manner by iron (1 to 200 microM). Peroxidation produced by 200 microM iron was reduced dose dependently by the lazaroid U-74500A. The IC50 was 10 microM in AD cortex and 2.5 microM in controls. Superoxide dismutase (SOD), one of the free radical defensive enzymes, was reduced by 25 to 35% in AD frontal cortex, hippocampus and cerebellum. In other brain areas, SOD did not differ between AD and control. The activities of catalase and glutathione peroxidase were the same in AD and control samples. Endogenous iron levels were higher in AD frontal cortex (2.5 nmol/mg protein) than in controls (1.5 nmol/mg protein). Calcium uptake by AD fibroblast mitochondria is 50% lower than in controls under basal conditions. Following exposure to 200 microM iron, mitochondrial calcium uptake is increased by 58% in AD and by 38% in controls. Pretreatment with 200 microM U-74500A or 1 mM deferoxamine, prior to exposure to 200 microM iron, gave complete protection to control mitochondria but gave only partial protection to AD mitochondria. These studies indicate that in AD, both CNS and peripheral cells show increased sensitivity to oxygen free radicals. The source of this increased sensitivity has not yet been identified but could reflect either reduced free radical defenses or increased free radical formation or both. Work is underway using electron paramagnetic resonance spectrometry to determine in vivo, premortem free radical activity in AD patients.

  • Free radical oxidative damage and Alzheimer's disease
    EE Tuppo; LJ Forman
    There is increasing evidence that free radical-induced oxidative damage may play a role in the pathogenesis of Alzheimer's disease. Free radicals are reactive oxygen compounds that may attack and damage lipids, proteins, and DNA. The brain is especially sensitive to oxidative damage because of its high content of readily oxidized fatty acids, high use of oxygen, and low levels of antioxidants. Evidence for oxidative damage has been obtained from postmortem brain tissue as well as from living patients with Alzheimer's disease. Antioxidants such as vitamin E show promise that they may help in treating the disease.

  • Immaturity-dependent free radical activity in premature infants
    E Varsila, O Pitkanen, M Hallman and S Andersson - Children's Hospital, University of Helsinki, Finland.
    To examine the role of immaturity in the free radical-mediated rate of lipid peroxidation in premature infants, we studied 27 infants [gestational age, 27.1 (SD 2.4) wk; birth weight, 970 (SD 330) g]. Ethane and pentane were quantitated in expired air during the first 18 d of life. During the first 2 postnatal d ethane [24.1 (SEM 7.8) pmol x kg-1 x min-1] and pentane [24.2 (SEM 4.1) pmol x kg-1 x min-1] were stable but increased during d 5 to maxima of 79.1 (15.8) pmol x kg-1 x min-1 and 62.1 (8.1) pmol x kg-1 x min-1, respectively. Maximum ethane and pentane correlated with gestational age (r = -0.42, p = 0.03 and r = -0.52, p = 0.005, respectively) and birth weight (r = -0.38, p = 0.05 and r = -0.59, p = 0.001, respectively). Infants with high maximum expired ethane and pentane (exceeding 40 pmol x kg-1 x min-1) had higher odds of dying or having bronchopulmonary dysplasia than those with low ethane and pentane (odds ratio, 6.5; 95% confidence interval, 1.1 to 38.5; p < 0.05 for ethane and odds ratio, 5.6; 95% confidence interval, 1.1 to 29.3; p < 0.05 for pentane). We conclude that degree of prematurity is the single most important factor explaining free radical-mediated lipid peroxidation in premature infants. A therapeutic intervention to limit the effects of free radicals should be started during the 1st postnatal d in premature infants to be effective.

  • Prospects for the prevention of free radical disease, regarding cancer and cardiovascular disease
    K F Gey - Vitamin Unit, Institute of Biochemistry and Molecular Biology, University of Berne Berne, Switzerland
    (Abstract)
    Free radicals may be involved in the aetiology of cancer and cardiovascular diseases. In epidemiological studies poor plasma levels of all essential antioxidants are associated with increased relative risks; in particular, low levels of carotene and vitamin E with the risk of cancer and ischemic heart disease, respectively. The studies suggest that for optimal synergistic protection the plasma antioxidant levels should simultaneously exceed the threshold values of 28–30 µmol/l lipid-standardized vitamin E, 40–50 µmol/l vitamin C, 0.4–0.5 (µmol/l carotene and 2.2–2.8 µmol/l lipid-standardized vitamin A. However the preventive efficacy of an optional antioxidant status is still to be proven in randomized intervention trials. Although these antioxidant micronutrients may be the primary protective components of vegetable-rich ‘preventive’ diets, the potentials of other plant components await exploration, eg carotenoids other than ß-carotene, bioflavonoids and oxygen-sensitive B-vitamins.

  • The role of free radicals in muscular dystrophy
    James G. Tidball1* and Michelle Wehling-Henricks2 - 1 Department of Physiological Science, University of California - Los Angeles, Los Angeles, California, United States 2 Department of Physiological Science, University of California - Los Angeles, 90095, California, United States
    Null mutation of members of the dystrophin protein complex can cause progressive, and possibly fatal, muscle wasting. Although these muscular dystrophies arise from mutation of a single gene that is expressed primarily in muscle, the resulting pathology is complex and multi-systemic. Prior to the identification of the deficient proteins that underlie muscular dystrophies such as Duchenne muscular dystrophy (DMD), oxidative stress was proposed as a major cause of the disease. Now, current knowledge indicates that interactions between the primary genetic defect and disruptions in the production of free radicals contribute these diseases. In this review, we focus on the pathophysiology of dystrophin-deficiency in humans with DMD and the mdx mouse model of DMD. Current evidence indicates three routes through which free radical production can be disrupted in dystrophin-deficiency and promote pathology. First, constitutive differences in free radical production can disrupt signaling in muscle and other tissues and exacerbate pathology. Second, tissue responses to the pathology can shift free radical production to promote cellular injury and dysfunction. Finally, behavioral differences in the affected individual can cause changes in the production free radicals and contribute to disease. Unfortunately, the complexity of the free radical mediated processes that are perturbed in muscular dystrophy makes it difficult to develop therapies founded on systemic administration of anti-oxidants. More mechanistic knowledge of the specific disruptions of free radicals that underlie major features of muscular dystrophy is needed to develop more targeted therapeutic approaches.

  • Iron, Free Radicals and Oxidative Injury
    Joe M McCord, University of Colorado Health Sciences Center, Denver, Colorado
    The ability of transition metal ions to undergo facile 1-electron oxidation or reduction makes them obvious potential chemical partners for reactions involving biological free radicals. It is not coincidental that superoxide dismutases, the enzyme that catalytically destroy, the superoxide radical (O2) by alternately oxidising and reducing it, have been found containing 3 transition metals (Cu, Mn or Fe) at their active sites. Iron is by far the most abundant transition metal in the human body because of its roles in oxygen binding and transport and electron transport. It provides opportunites for the cause of diseases related to iron absorption, transport and metabolism as well as for the excerbation of mechanisms of disease involving free radical injury

  • Oxygen-derived free radicals and postischemic myocardial dysfunction ("stunned myocardium")
    R. Bolli, Department of Medicine, Baylor College of Medicine, Houston, Texas
    Experimental studies have demonstrated that myocardium reperfused after reversible ischemia exhibits prolonged depression of contractile function ("stunning"), which is associated with various ultrastructural, biochemical, vascular and other functional abnormalities. Clinical observations suggest that stunning occurs in many situations (for example, rest and exercise-induced angina, myocardial infarction with early reperfusion, open heart surgery, transplantation) and thus may contribute significantly to morbidity among patients with coronary artery disease. In recent years an increasing number of studies have provided indirect evidence that postischemic myocardial dysfunction may be mediated in part by the generation of reactive oxygen species, such as superoxide radical (.O2), hydrogen peroxide (H2O2) and hydroxyl radical (.OH). Thus, it has been shown that the recovery of the stunned myocardium is enhanced by agents that either scavenge oxygen metabolites, such as superoxide dismutase and catalase, N-2-mercaptopropionylglycine and dimethylthiourea, or prevent their generation, such as allopurinol, oxypurinol and desferrioxamine. More recent experiments utilizing electron paramagnetic resonance spectroscopy have directly demonstrated that reperfusion after a reversible ischemic episode is associated with a burst of free r adical production. At present, the evidence supporting the free radical hypothesis is suggestive but not conclusive. Definitive demonstration of the role of oxy-radicals will require careful studies measuring the production of these species in conscious animal models of postischemic dysfunction. If confirmed, the free radical hypothesis will provide not only new important insights into the pathophysiology of ischemic injury, but also a rationale for developing clinically applicable interventions.


    Looking for an effective antioxidant to control excessive free radicals?
    Consider Osumex Flax Hulls which has a high ORAC value of 19,600 and a powerful antioxidant. It is also a most nutritious fibre!


    **ORAC (Oxygen Radical Absorbance Capacity) is a method of measuring antioxidant capacities of different foods


    Osumex Free Radical Test kit - see sample kit below



    Malondialdehyde (MDA) is a by-product of free radical activity and this is what the test kit measures.

    It is recommended that you test at least once a week, if excessive free radical activity is found, until it is brought under control, or once a month or at least once every few months to make sure free radicals in the body are not running rampant!





    "The natural way to better health"



    The above information is provided for general educational purposes only. It is not intended to replace competent health care advice received from a knowledgeable healthcare professional. You are urged to seek healthcare advice for the treatment of any illness or disease.
    The Food Standards Agency (UK) has not evaluated these statements. This product is not intended to diagnose, treat, cure, or prevent any disease.



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