I radicali liberi sono molecole non equilibrate, centrate su ossigeno o azoto e per bilanciare se stesse, asportano elettroni da altre molecole, provocando uno squilibrio e, di conseguenza, provocando danni al corpo umano.
La mancanza di anti-ossidante cellulare di difesa provoca un accumulo di radicali liberi, che quindi danneggia le membrane, le proteine e tutto il resto fino ai mitocondri cellulari. È interessante notare che allo stesso modo che l’infiammazione è ritenuta presenti e/o causa di malattie che vanno dall’artrite all’Alzheimer, la mancanza di anti-ossidanti di difesa (squilibrio Redox) sta seguendo la stessa via. (1)
Arthritis and Rheumatism, rivista mensile ufficiale della American College of Rheumatology, che ha effettuato una grande analisi delle proteine nei pazienti con artrite reumatoide, anche recentemente ha pubblicato uno studio che coinvolge un meccanismo cellulare per la progressione dell’artrite reumatoide. Questo meccanismo è il percorsi di ossidazione / riduzione cellulare (Redox). La sua deregolazione si ritiene causa dell’avanzamento dell’artrite reumatoide mentre la sua regolazione è in fase di studio per lo sviluppo di farmaci anti-cancro (2, 3). Questi studi recenti stanno prendendo di mira o coinvolgendo lo squilibrio Redox nelle malattie che vanno dall’artrite reumatoide all’Alzheimer, nello stesso modo in cui sono iniziati gli studi sul ruolo dell’infiammazione e, successivamente, sono diventati il centro dell’attenzione.
Secondo lo studio pubblicaot su Antioxidant and Redox Signaling Journal, l’ossidazione delle proteine da parte dei radicali liberi può presentare un significato fisiologico e patologico e, inoltre, la modifica delle proteine attraverso i radicali liberi sarebbe in correlazione con malattie come l’Alzheimer. È interessante notare che anche lo studio in Journal of Arthritis and Rheumatism, ha riferito che dallo screening differenziale di 100 proteine, è risultato essere un fattore predominante la deregolazione delle proteine da riduzione dell’ossidazione nei sinoviociti di tipo fibroblasto (FLS), che può contribuire alla sviluppo e nella progressione dell’artrite reumatoide. (2)
Inoltre, secondo il Dipartimento di Medicina Interna dell’Università di Miami, il Redox cellulare è regolato da tre sistemi che contrastano i radicali liberi. Due dei sistemi di cui sopra sono regolati da glutatione. Troppi radicali liberi provocano l’ossidazione del glutatione. (3)
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1. Can J Physiol Pharmacol. 1987 Sep;65(9):1805-15.
2. Arthritis Rheum. 2011 Oct 17
3. Drugs. 2011 Jul 30;71(11):1385-96
[…]
Studies Are Pointing to Oxidative Damage As a Significant Risk Factor in The Development And Progression of Diseases, Ranging From Arthritis to Alzheimer
A newly published study, which entailed 10 years of research, is shedding a more deserving light to another important health risk factor: lack of antioxidant defense, which has been implicated in many diseases, ranging from Arthritis to Alzheimer. Going back to 1987, when the first study suggested a common factor (inflammation) in diseases ranging from Arthritis to Alzheimer, at least, 1459 other studies have followed, only investigating the role and association of inflammation in the development and progression of Alzheimer. Nutri-Med Logic Corp states that the lack of anti-oxidant defense in the development and progression of diseases is as important as the role of inflammation, if not more.
Miami, Florida (PRWEB) January 15, 2012
Nutri-Med Logic Corp: A newly published study, in Antioxidant and Redox Signaling Journal, implicates the imbalance between the anti-oxidant defense and free radicals as contributing factor in improper protein formation and would correlate with neurodegenerative diseases such as Alzheimer.
Free radicals are molecules that are not balanced and could be either oxygen or nitrogen centered and in order to balance themselves, they takeaway electrons from other molecules, causing an imbalance and, consequently, exerting damage to the human body.
Lack of cellular anti-oxidant defense causes an accumulation of the free radicals, thus, damaging cellular membranes, proteins and all the way up to the mitochondria.
Interestingly, in the same manner that inflammation was first suggested to be present and/or cause diseases ranging from Arthritis to Alzheimer, lack of anti-oxidant defense (redox imbalance) is following the same pathway. (1)
Arthritis and Rheumatism, an official monthly journal of the American College of Rheumatology, which involved a large-scale protein analysis in Rheumatoid Arthritis patients, also recently published a study implicating a cellular mechanism for the progression of Rheumatoid Arthritis. This mechanism is the cellular oxidation/reduction (Redox) pathways. Its dysregulation is proposed to advance Rheumatoid Arthritis and its regulation is being studied for the development of anti-cancer drugs. (2, 3)
These recent studies are targeting or implicating the Redox imbalance in diseases ranging from Rheumatoid Arthritis to Alzheimer, in the same manner that studies in the role of inflammation began and, later, became the focus of attention.
According to the study, in Antioxidant and Redox Signaling Journal, protein oxidation by free radicals may present physiological and pathological significance and, further, the modification of proteins through free radicals would correlate with diseases such as Alzheimer.
Interestingly, the study in Journal of Arthritis and Rheumatism, also reported that from screening 100 differential proteins, down-regulation of oxidation reduction-related proteins in Fibroblast-like synoviocytes (FLS) was found to be a predominant factor, which may contribute to the development and progression Rheumatoid Arthritis. (2)
Additionally, according to The Department of Internal Medicine of University of Miami, the cellular redox is regulated by three systems that counteract with free radicals . Two of the above systems are regulated by glutathione. Too much of free radicals causes oxidation of glutathione. (3)
in 1996, an anti-oxidant researcher at University of Berkeley, California, Dr. Packer, a professor of molecular and cell biology discovered that R-Alpha Lipoic Acid, a nutrient, increased the production of Glutathione.
R-Alpha Lipoic Acid (also known as R-Lipoic Acid) is a biologically significant (active) compound produced by human body and found in many foods. R-Alpha Lipoic Acid, not only increases the internal anti-oxidant “glutathione”, but also amongst its many other vital properties inactivates free radicals. (4)
In animal studies, R-Alpha Lipoic Acid has easily crossed the blood-brain barrier and reached peak levels in the cerebral cortex, spinal cord and peripheral nerves within 30 minutes of administration. (5)
R-Lipoic Acid is hydrophilic (liquid soluble) and lipophilic (fat soluble) and easily penetrates cell membranes and reaches high intracellular concentrations within 30 seconds of its administration. (6)
In conclusion agrees with these recent studies relating to redox imbalance and the development and progression of diseases such as Arthritis and Alzheimer but adds that an anti-oxidant of choice should be an anti-oxidant capable of reaching the entire body.
Nutri-Med Logic Corp. is a producer of dietary supplements, including a Pharmaceutical Grade R-Alpha Lipoic Acid, the dietary supplement of choice for the Diabetics, in Germany for more than 40 years.
Nutri-Med Logic Corp is also producer of a Natural, Balanced, Deodorized and Concentrated Omega-3, which is also a Pharmaceutical Grade Omega-3;
Producer of PolyEnylPhosphatidylCholine (PPC 425mg), an extract of soy and the recommended dietarty supplement for those with Fatty Liver and Alcoholic Liver Disease, in Europe for about 50 years.
Nutri-Med Logic’s products are Formulated Based on Nutritional Logic, made from the highest quality raw materials that are manufactured in pharmaceutical facilities, encapsulated in pharmaceutical facilities and packaged in pharmaceutical facilities.
It must be noted that the studies, sources or statements above and/or below have not been evaluated by The FDA and, thus, one should not relate the cause of any diseases, stated herein, to lack of the dietary supplements, stated herein, nor equate their supplementation to prevention, treatment or cure.
1. Can J Physiol Pharmacol. 1987 Sep;65(9):1805-15.
2. Arthritis Rheum. 2011 Oct 17
3. Drugs. 2011 Jul 30;71(11):1385-96
4. Toxicology and Applied Pharmacology, Vol. 182, Issue 1, 1 July 2002, PPs 84-90.
5. Neurotoxicology 2001;22:577-592.
6. Archives of Biochemistry and Biophysics 1989;273:389-395.
Fonte del seguente articolo PubMed
Redox Proteomics in Selected Neurodegenerative Disorders: From Its Infancy to Future Applications.
Source
1 Department of Chemistry, Center of Membrane Sciences, Sanders-Brown Center on Aging, University of Kentucky , Lexington, Kentucky.
Abstract
Abstract Several studies demonstrated that oxidative damage is a characteristic feature of many neurodegenerative diseases. The accumulation of oxidatively modified proteins may disrupt cellular functions by affecting protein expression, protein turnover, cell signaling, and induction of apoptosis and necrosis, suggesting that protein oxidation could have both physiological and pathological significance. For nearly two decades, our laboratory focused particular attention on studying oxidative damage of proteins and how their chemical modifications induced by reactive oxygen species/reactive nitrogen species correlate with pathology, biochemical alterations, and clinical presentations of Alzheimer’s disease. This comprehensive article outlines basic knowledge of oxidative modification of proteins and lipids, followed by the principles of redox proteomics analysis, which also involve recent advances of mass spectrometry technology, and its application to selected age-related neurodegenerative diseases. Redox proteomics results obtained in different diseases and animal models thereof may provide new insights into the main mechanisms involved in the pathogenesis and progression of oxidative-stress-related neurodegenerative disorders. Redox proteomics can be considered a multifaceted approach that has the potential to provide insights into the molecular mechanisms of a disease, to find disease markers, as well as to identify potential targets for drug therapy. Considering the importance of a better understanding of the cause/effect of protein dysfunction in the pathogenesis and progression of neurodegenerative disorders, this article provides an overview of the intrinsic power of the redox proteomics approach together with the most significant results obtained by our laboratory and others during almost 10 years of research on neurodegenerative disorders since we initiated the field of redox proteomics. Antioxid. Redox Signal. 00, 000-000.