De dood: een einde en een nieuw begin
Automatic self destruct
Voedselschaarste was in het verre verleden waarschijnlijk de reden dat de natuur bedacht heeft dat mensen nadat zij voor nageslacht gezorgd hadden beter dood konden gaan. Op deze manier had de volgende generatie ondanks een voedsel tekort een grotere kans om te overleven. Door onze huidige westerse cultuur van overvloed heeft deze vroegtijdige dood om voedsel te besparen zijn functie verloren. De moderne mens wil met de VUT, met de boot of camper de wereld rond en al helemaal niet dood.Andere oorzaken van veroudering
Naast deze "geprogrammeerde dood" is er nog een aantal andere oorzaken aan te wijzen die veroudering kunnen versnellen:- Schade door vrije radicalen, vooral in de mitochondria, de energie centrales van de cel.
- Een verminderde productie van de bio-energetische stof ATP. Hierdoor ontstaat een scala aan "ouderdomsklachten".
- Schade door een te hoog glucoseniveau in ons bloed waardoor de toxische stof AGES ontstaat.
Schade door vrije radicalen
Wat zijn vrije radicalen?
Bij de verbranding van vetzuren en glucose in de mitochondria, een soort energiecentrales binnen in onze cellen, komen veel afvalstoffen vrij. Dat zijn stoffen die tijdens het chemische proces een elektron (negatief geladen deeltje van een atoom) zijn kwijt geraakt of er een bij hebben gekregen. Dit zijn de vrije radicalen. Vrije radicalen, negatief of positief geladen, zijn bijzonder agressief. Ze willen graag een binding aan gaan met andere stoffen in de buurt om hun elektronen tekort (of overschot) te compenseren. Bijvoorbeeld met de wanden van je cellen of nog erger met je DNA materiaal. Zo ontstaat schade aan de celwanden of aan de informatie die in het DNA is opgeslagen. Het biochemische proces in onze cellen wordt vaak vergeleken met "fikkie stoken in een klerenkast" het is net zo gevaarlijk. Gelukkig blussen de anti-oxidanten en speciaal ontworpen enzymen de in de cel rondvliegende vonken.Vrije radicalen en veroudering
Wetenschappers zijn er van overtuigd dat de schade die wordt veroorzaakt door vrije radicalen een van de oorzaken is van veroudering. Bij de verbranding van glucose en vetzuren worden er in de mitochondria ongeveer 1000 miljoen vrije radicalen per cel per dag geproduceerd. Dit is een normaal gegeven want bij verbranding komen nu eenmaal schadelijke stoffen vrij. Maar dat is wel één van de reden waarom deze verbranding door middel van een membraan van de rest van de cel wordt afgescheiden.Ook in andere delen van het lichaam worden vrije radicalen geproduceerd. Bijvoorbeeld in vetweefsel. Ingewikkelde processen moeten deze vrije radicalen neutraliseren en de schade die reeds is ontstaan repareren. Vrije radicalen ontstaan in ons lichaam ook onder invloed van straling, (zon, röntgenfoto, bestraling bij kanker), maar ook door bestrijdingsmiddelen en kunstmest die we via voedsel binnen krijgen, sigaretten roken en door de nu alom aanwezige luchtverontreiniging.
Vooral de schade die ontstaat aan de mitochondria en de schade aan het DNA heeft grote gevolgen voor onze gezondheid en is direct van invloed op de snelheid van het verouderingsproces.
Referenties
- Melatonin reduces oxidant damage and promotes mitochondrial respiration: implications for aging
Melatonin has a number of properties as a consequence of which it could be beneficial to animals as they age. Of particular interest are its ubiquitous actions as a direct and indirect antioxidant and free radical scavenger. These findings, coupled with diminished melatonin production in advanced age, has prompted scientists to consider melatonin in the context of aging. As of this writing there is no definitive evidence to prove that melatonin alters the rate of aging, although data relating to melatonin deferring some age-related degenerative conditions is accumulating rapidly. - Melatonin as an antioxidant: biochemical mechanisms and pathophysiological implications in humans
This brief resume enumerates the multiple actions of melatonin as an antioxidant. Numerous in vitro and in vivo studies have documented the ability of both physiological and pharmacological concentrations to melatonin to protect against free radical destruction. Furthermore, clinical tests utilizing melatonin have proven highly successful; because of the positive outcomes of these studies, melatonin's use in disease states and processes where free radical damage is involved should be increased. - Role of oxidative stress in development of complications in diabetes
N epsilon-(carboxymethyl)lysine, N epsilon-(carboxymethyl)hydroxylysine, and the fluorescent cross-link pentosidine are formed by sequential glycation and oxidation reactions between reducing sugars and proteins. These compounds, termed glycoxidation products, accumulate in tissue collagen with age and at an accelerated rate in diabetes. - Will the 'good fairies' please prove to us that vitamin E lessens human degenerative disease?
Recent research about the role of free radical derivatives of oxygen and nitrogen in biological systems has highlighted the possibility that antioxidants, such as vitamin E, that prevent these processes in vitro may be capable of carrying out a similar function in living organisms in vivo. There is increasing evidence that free radical reactions are involved in the early stages, or sometimes later on, in the development of human diseases, and it is therefore of particular interest to inquire whether vitamin E and other antioxidants, which are found in the human diets, may be capable of lowering the incidence of these diseases. - Antioxidants and immune response in aged persons: overview of present evidence
The oxidant-antioxidant balance is an important determinant of immune cell function, including maintaining the integrity and functionality of membrane lipids, cellular proteins, and nucleic acids and controlling signal transduction and gene expression in immune cells. Optimal amounts of antioxidants are needed for maintenance of the immune response across all age groups. This need might be more critical, however, in aged persons. Age-associated dysregulation of immune response, particularly of T cell-mediated function, is well documented. The well-known age-related increase in free radical formation and lipid peroxidation contributes, at least in part, to this phenomenon. We summarize animal and human studies undertaken by ourselves as well as other investigators on the effects of antioxidants, vitamin E, beta-carotene, and glutathione on the immune response of aged persons. The underlying mechanisms for the antioxidant nutrients' effects as well as their health implications for aged persons are discussed. - Oxidative damage and mitochondrial decay in aging
We argue for the critical role of oxidative damage in causing the mitochondrial dysfunction of aging. Oxidants generated by mitochondria appear to be the major source of the oxidative lesions that accumulate with age. Several mitochondrial functions decline with age. The contributing factors include the intrinsic rate of proton leakage across the inner mitochondrial membrane (a correlate of oxidant formation), decreased membrane fluidity, and decreased levels and function of cardiolipin, which supports the function of many of the proteins of the inner mitochondrial membrane. Acetyl-L-carnitine, a high-energy mitochondrial substrate, appears to reverse many age-associated deficits in cellular function, in part by increasing cellular ATP production. Such evidence supports the suggestion that age-associated accumulation of mitochondrial deficits due to oxidative damage is likely to be a major contributor to cellular, tissue, and organismal aging. - Mitochondrial decay in aging
Several mitochondrial functions decline with age. The contributing factors include, the intrinsic rate of proton leakage across the inner mitochondrial membrane (a correlate of oxidant formation), decreased membrane fluidity, and decreased levels and function of cardiolipin, which supports the function of many of the proteins of the inner mitochondrial membrane. Oxidants generated by mitochondria appear to be the major source of the oxidative lesions that accumulate with age. Evidence supports the suggestion that age-associated accumulation of mitochondrial deficits due to oxidative damage is likely to be a major contributor to cellular, tissue, and organismal aging. - Mutation and oxidative damage of mitochondrial DNA and defective turnover of mitochondria in human aging
Accumulation of somatic mutations in the mitochondrial DNA (mtDNA) is a major contributor to human aging and degenerative diseases. Rapid progress has been made in unraveling the molecular changes associated with aging. MtDNA mutations are likely early molecular events associated with human aging that may be responsible for the age-dependent decline in mitochondrial respiratory functions. - Oxidative stress, mitochondrial DNA mutation, and impairment of antioxidant enzymes in aging
Mitochondria do not only produce less ATP, but they also increase the production of reactive oxygen species (ROS) as by-products of aerobic metabolism in the aging tissues of the human and animals. It is now generally accepted that aging-associated respiratory function decline can result in enhanced production of ROS in mitochondria. Moreover, the activities of free radical-scavenging enzymes are altered in the aging process. - Mitochondrial theory of aging matures--roles of mtDNA mutation and oxidative stress in human aging
Mitochondrial theory of aging, a variant of free radical theory of aging, proposes that accumulation of damage to mitochondria and mitochondrial DNA (mtDNA) leads to aging of humans and animals. It has been supported by the observation that mitochondrial function declines and mtDNA mutation increases in tissue cells in an age-dependent manner. Age-related impairment in the respiratory enzymes not only decreases ATP synthesis but also enhances production of reactive oxygen species (ROS) through increased electron leakage in the respiratory chain. - An Integrated View of Oxidative Stress in Aging: Basic Mechanisms, Functional Effects and Pathological Considerations
Aging is an inherently complex process that is manifested within an organism at genetic, molecular, cellular, organ and system levels. Although the fundamental mechanisms are still poorly understood, a growing body of evidence points towards reactive oxygen species (ROS) as one of the primary determinants of aging. The "oxidative stress theory" holds that a progressive and irreversible accumulation of oxidative damage caused by ROS impacts on critical aspects of the aging process and contributes to impaired physiological function, increased incidence of disease, and a reduction in lifespan. - Oxidative stress and protein aggregation during biological aging
Biological aging is a fundamental process that represents the major risk factor with respect to the development of cancer, neurodegenerative, and cardiovascular diseases in vertebrates. It is, therefore, evident that the molecular mechanisms of aging are fundamental to understand many disease processes. In this regard, the oxidation and nitration of intracellular proteins and the formation of protein aggregates have been suggested to underlie the loss of cellular function and the reduced ability of senescent animals to withstand physiological stresses. - Free radical theory of aging: an update: increasing the functional life span
Aging is the progressive accumulation of diverse, deleterious changes with time that increase the chance of disease and death. The basic chemical process underlying aging was first advanced by the free radical theory of aging (FRTA) in 1954: the reaction of active free radicals, normally produced in the organisms, with cellular constituents initiates the changes associated with aging. The involvement of free radicals in aging is related to their key role in the origin and evolution of life. Aging changes are commonly attributed to development, genetic defects, the environment, disease, and an inborn aging process (IAP). The latter produces aging changes at an exponentially increasing rate with age, becoming the major risk factor for disease and death for humans after the age of 28 years in the developed countries. In them the IAP limits human average life expectancy at birth (ALE-B)--a rough measure of the healthy life span--to about 85 years; few reach 100 years and only one is known to have lived to 122 years. In these countries, improvements in living conditions (ILC) have gradually raised ALE-Bs to 76-79 years, 6-9 years less than the limit imposed by aging, with no change in the maximum life span (MLS). The extensive studies based on the FRTA hold promise that ALE-B and the MLS can be extended, the ALE-B possibly by a few years, and the MLS somewhat less. - The free radical theory of aging
Aging is the accumulation of changes that increase the risk of death. Aging changes can be attributed to development, genetic defects, the environment, disease, and an inborn process: the aging process. The latter is the major risk factor for disease and death after age 28 in the developed countries. In these countries, average life expectancies at birth (ALE-B) now range from 76 to 79 years, 6-9 years less than the limit of approximately 85 years imposed by aging. Aging changes may be caused by free radical reactions. The extensive studies based on this possibility hold promise that the ALE-B can be extended to >85 years and the maximum life span increased. - The role of AGEs in aging: causation or correlation
Over a dozen advanced glycation end-products (AGEs) have been identified in tissue proteins by chemical or immunological methods. Of these, about half are known to accumulate with age in collagen at a rate that correlates with the half-life of the collagen. Although AGEs in proteins are probably correlative, rather than causative, with respect to aging, they accumulate to high levels in tissues in age-related chronic diseases, such as atherosclerosis, diabetes, arthritis and neurodegenerative disease. Inhibition of AGE formation in these diseases may limit oxidative and inflammatory damage in tissues, retarding the progression of pathophysiology and improve the quality of life during aging. - Involvement of advanced glycation end-products (AGEs) in Alzheimer's disease
The advanced stage of the glycation process (one of the post-translational modifications of proteins) leads to the formation of advanced glycation end-products (AGEs) and plays an important role in the pathogenesis of angiopathy in diabetic patients. It has recently become clear that AGEs also influence physiological aging and neurodegenerative diseases such as Alzheimer's disease (AD) and amyotrophic lateral sclerosis (ALS).
SITE MAP
Maagdarmstoornissen: Candida infectie - Prikkelbaredarmsyndroom - Crohn - Colitus Ulcerosa - CVS/ME: Chronische vermoeidheid Syndroom - Diabetische complicaties: Bloeduiker stabilisatie - Neuropathie - Retinopathie - Nefropathie - Hart- en vaatziekten: Cardiomyopathie en Hartfalen - Hoge bloeddruk - Cholesterol verlaging - Aderverkalking (atherosclerose) - Spataderen - Levensverlenging: 100 jaren jong - DHEA - Melatonine - 65+ - Kanker: - Ondersteuningstherapie bij kanker - Bot en gewrichtsaandoeningen: - Artrose - Artritis - Osteoporose - Fibromyalgie: - Fibromyalgie - Urinewegaandoeningen: - Prostaatklachten - Blaasontsteking - Vrouwenklachten: Menopauze - Premenstrueelsyndroom - Overgewicht: - Overgewicht - SLIM - Oogaandoeningen: Staar - Slecht zien Andere artikelen: - HPU - Astma - Multiple Sclerose - Psoriasis - Depressie
Maagdarmstoornissen: Candida infectie - Prikkelbaredarmsyndroom - Crohn - Colitus Ulcerosa - CVS/ME: Chronische vermoeidheid Syndroom - Diabetische complicaties: Bloeduiker stabilisatie - Neuropathie - Retinopathie - Nefropathie - Hart- en vaatziekten: Cardiomyopathie en Hartfalen - Hoge bloeddruk - Cholesterol verlaging - Aderverkalking (atherosclerose) - Spataderen - Levensverlenging: 100 jaren jong - DHEA - Melatonine - 65+ - Kanker: - Ondersteuningstherapie bij kanker - Bot en gewrichtsaandoeningen: - Artrose - Artritis - Osteoporose - Fibromyalgie: - Fibromyalgie - Urinewegaandoeningen: - Prostaatklachten - Blaasontsteking - Vrouwenklachten: Menopauze - Premenstrueelsyndroom - Overgewicht: - Overgewicht - SLIM - Oogaandoeningen: Staar - Slecht zien Andere artikelen: - HPU - Astma - Multiple Sclerose - Psoriasis - Depressie
