RESEARCH on Neurodegeneration: Antioxidant Therapeutic Potential

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RESEARCH ON NEURODEGENERATION: ANTIOXIDANT THERAPEUTIC POTENTIAL AT PUBMED
Oxid Med Cell Longevity Epub 2013 Jul 28.
SOD1 and DJ-1 Converge at Nrf2 Pathway: A Clue for Antioxidant Therapeutic Potential in Neurodegeneration.
Abstract: Neurodegenerative diseases share diverse pathological features and among these oxidative stress (OS) plays a leading role. Impaired activity and reduced expression of antioxidant proteins have been reported as common events in several aging-associated disorders. In this review paper, we first provide an overview of the involvement of reactive oxygen species- (ROS-) induced oxidative damage in Parkinson’s disease (PD) and amyotrophic lateral sclerosis (ALS). Subsequently, we focus on DJ-1 and SOD1 proteins, which are involved in PD and ALS and also exert a prominent role in the interaction between redox homeostasis and neurodegeneration. Interestingly, recent studies demonstrated that DJ-1 and SOD1 are both tightly connected with Nrf2 protein, a transcriptional factor and master regulator of the expression of many antioxidant/detoxification genes. Nrf2 is emerging as a key neuroprotective protein in neurodegenerative diseases, since it helps neuronal cells to cope with toxic insults and OS. We herein summarize the recent literature providing a detailed picture of the promising therapeutic efficacy of Nrf2 natural and synthetic inducers as disease-modifying molecules for the treatment of neurodegenerative diseases. http://www.ncbi.nlm.nih.gov/pubmed/23983902
NRF2 PATHWAY PIC

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http://www.ncbi.nlm.nih.gov/pubmed/16413416
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RESEARCH on Hemochromatosis & Oxidative Stress

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RESEARCH ON HEMOCHROMATOSIS and OXIDATIVE STRESS AT PUBMED

Elevated hepatic iron activates NF-E2-related factor 2-regulated pathway in a dietary iron overload mouse model.
Source: Dept of Microbiology and Immunology, Milton S Hershey Medical Center, The Penn State College of Medicine,
Hershey, Pennsylvania 17033, USA.
Abstract: Hepatic iron overload has been associated classically with the genetic disorder hereditary hemochromatosis. More recently, it has become apparent that mild-to-moderate degrees of elevated hepatic iron stores observed in other liver diseases also have clinical relevance. The goal was to use a mouse model of dietary hepatic iron overload and isobaric tag for relative and absolute quantitation proteomics to identify, at a global level, differentially expressed proteins in livers from mice fed a control or 3,5,5-trimethyl-hexanoyl-ferrocene (TMHF) supplemented diet for 4 weeks. The expression of 74 proteins was altered by ≥ ±1.5-fold, showing that the effects of iron on the liver proteome were extensive. The top canonical pathway altered by TMHF treatment was the NF-E2-related factor 2 (NRF2-)-mediated oxidative stress response. Because of the longstanding association of elevated hepatic iron with oxidative stress, the remainder of the study was focused on NRF2. TMHF treatment upregulated 25 phase I/II and antioxidant proteins previously categorized as NRF2 target gene products.  Immunoblot analyses showed that TMHF treatment increased the levels of glutathione S-transferase (GST) M1, GSTM4, glutamate-cysteine ligase (GCL) catalytic subunit, GCL modifier subunit, glutathione synthetase, glutathione reductase, heme oxygenase 1, epoxide hydrolase 1, and NAD(P)H dehydrogenase quinone 1. Immunofluorescence, carried out to determine the cellular localization of NRF2, showed that NRF2 was detected in the nucleus of hepatocytes from TMHF-treated mice and not from control mice. We conclude that elevated hepatic iron in a mouse model activates NRF2, a key regulator of the cellular response to oxidative stress. http://www.ncbi.nlm.nih.gov/pubmed/22649188

2005 Study Results: Protandim, the NRF2 Activator, Reducing Oxidative Stress

2005_study_results

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http://www.ncbi.nlm.nih.gov/pubmed/16413416
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Disclaimer: PROTANDIM DOES NOT CLAIM TO TREAT, MITIGATE, DIAGNOSE, CURE, OR PREVENT ANY DISEASE.

RESEARCH on Parkinson’s & Oxidative Stress

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RESEARCH ON PARKINSON’S and OXIDATIVE STRESS AT PUBMED

Gene. 2013 Aug 15. pii: S0378-1119(13)00993-1. doi: 10.1016/j.gene.2013.07.085. [Epub ahead of print]

The novel role of mitochondrial induced oxidative stress and genetic mutations in Parkinson’s disease.

Source: Molecular Physiology and Biophysics Laboratory, Department of Biological Sciences, Oakland University, Rochester, MI 48309

Abstract: Parkinson’s disease (PD) is recognized as one of the most advanced neurodegenerative diseases that produces pathogenic effects on an individual’s substantia nigra, a site of neurotransmitter dopamine. Memory and cognitive function are hindered by this disorder. It is understood that PD is age-related; as age increases, the chance of onset responds accordingly. Although genetic heritability influences the disease, the definite cause is unknown. A current hypothesis associates mitochondrial dysfunction, specifically reactive oxygen species (ROS), and oxidative stress (OS) as the fundamental agents of deterioration. Certain genetic mutations can also contribute to the mitochondrial misbalance producing OS. OS refers to the disequilibrium of free radicals and antioxidants saturated with ROS. Minor amounts of ROS are essential for normal physiological functions, playing a critical role in many biological processes. However, vast quantities of ROS production cause intracellular deregulation leading to continuous damage to critical cellular components such as membrane lipids, proteins, and DNA. This review expands on the specific impact of mitochondrial production of free radicals and its correlation to the neurodegeneration in Parkinson’s disease. http://www.ncbi.nlm.nih.gov/pubmed/23954870

OXIDATIVE_STRESS_PIC

Figure 10

Mitochondrial dysfunction is associated with neurodegeneration through many mechanisms. It can directly trigger cell death pathways that culminate in neuronal apoptosis or necrosis, disrupt calcium homestasis, and cause UPS dysfunction and oxidative stress. Dissecting the role of mitochondrial dysfunction in neurodegeneration is complicated by the fact that many of these downstream effects can themselves contribute to mitochondrial defects.

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Protandim is the ONLY product that has been scientifically proven to reduce oxidative stress by 40% in 30 days. http://www.ncbi.nlm.nih.gov/pubmed/16413416
Watch ABC Primetime Investigative Report on Protandim www.ABCreport.net

Disclaimer: PROTANDIM DOES NOT CLAIM TO TREAT, MITIGATE, DIAGNOSE, CURE, OR PREVENT ANY DISEASE.

RESEARCH on Atherosclerotic Disease & Oxidative Stress

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RESEARCH ON ATHEROSCLEROTIC DISEASE & OXIDATIVE STRESS AT PUBMED

Targeting Cellular Antioxidant Enzymes for Treating Atherosclerotic Vascular Disease. 2013 Mar;21(2):89-96.
Abstract: Atherosclerotic vascular dysfunction is a chronic inflammatory process that spreads from the fatty streak and foam cells through lesion progression. Therefore, its early diagnosis and prevention is unfeasible. Reactive oxygen species (ROS) play important roles in the pathogenesis of atherosclerotic vascular disease. Intracellular redox status is tightly regulated by oxidant and antioxidant systems. Imbalance in these systems causes oxidative or reductive stress which triggers cellular damage or aberrant signaling, and leads to dysregulation. Paradoxically, large clinical trials have shown that non-specific ROS scavenging by antioxidant vitamins is ineffective or sometimes harmful. ROS production can be locally regulated by cellular antioxidant enzymes, such as superoxide dismutases, catalase, glutathione peroxidases and peroxiredoxins. Therapeutic approach targeting these antioxidant enzymes might prove beneficial for prevention of ROS-related atherosclerotic vascular disease. Conversely, the development of specific antioxidant enzyme-mimetics could contribute to the clinical effectiveness.

http://www.ncbi.nlm.nih.gov/pubmed/24009865

HEART VALVES
Consider PROTANDIM®, The Nrf2 Activator “Game Changer”!

A fundamental synergistic new approach to antioxidant therapy!
Clinical studies of Protandim® resulted in:
30% Increase in SOD Production
54% Increase in Catalase Production
300% Increase in Glutathione Peroxidase Production

PROTANDIM 40 IN 30 DAYSProtandim® is the ONLY product that has been scientifically proven to reduce oxidative stress by 40% in 30 days.
http://www.ncbi.nlm.nih.gov/pubmed/16413416
Watch ABC Primetime Investigative Report on Protandim www.ABCreport.net
Disclaimer: PROTANDIM DOES NOT CLAIM TO TREAT, MITIGATE, DIAGNOSE, CURE, OR PREVENT ANY DISEASE.

RESEARCH on Aging, Longevity & Oxidative Stress

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RESEARCH ON AGING, LONGEVITY and OXIDATIVE STRESS AT PUBMED

Exploring the Role of Genetic Variability and Lifestyle in Oxidative Stress Response for Healthy Aging and Longevity Abstract: Oxidative stress is both the cause and consequence of impaired functional homeostasis characterizing human aging. The worsening efficiency of stress response with age represents a health risk and leads to the onset and accrual of major age-related diseases. In contrast, centenarians seem to have evolved conservative stress response mechanisms, probably derived from a combination of a diet rich in natural antioxidants, an active lifestyle and a favorable genetic background, particularly rich in genetic variants able to counteract the stress overload at the level of both nuclear and mitochondrial DNA. The integration of these factors could allow centenarians to maintain moderate levels of free radicals that exert beneficial signaling and modulator effects on cellular metabolism. Considering the hot debate on the efficacy of antioxidant supplementation in promoting healthy aging, in this review we gathered the existing information regarding genetic variability and lifestyle factors which potentially modulate the stress response at old age. Evidence reported here suggests that the integration of lifestyle factors (moderate physical activity and healthy nutrition) and genetic background could shift the balance in favor of the antioxidant cellular machinery by activating appropriate defense mechanisms in response to exceeding external and internal stress levels, and thus possibly achieving the prospect of living a longer life. http://www.mdpi.com/1422-0067/14/8/16443

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Protandim is the ONLY product that has been scientifically proven to reduce oxidative stress by 40% in 30 days. http://www.ncbi.nlm.nih.gov/pubmed/16413416
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Watch ABC Primetime Investigative Report on Protandim www.ABCreport.net
Disclaimer: PROTANDIM DOES NOT CLAIM TO TREAT, MITIGATE, DIAGNOSE, CURE, OR PREVENT ANY DISEASE.