Vitamin E prevents oxidative modification of brain and lymphocyte band 3 proteins during aging.

Poulin, Jeff E.; Cover, Cathleen; Gustafson, Monica; Kay, Marguerite M. B.

doi:10.1073/pnas.93.11.5600

Cited by 21 publications

(12 citation statements)

References 17 publications

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“…To achieve this, different antioxidants were proposed. It was shown that vitamin E is able to prevent lipofuscin accumulation in mouse brain cells (36), lipid oxidation in aged at kidneys (84), and protein oxidation in brain cells and lymphocytes (82). Vitamin E appears to stabilize various homeostatic functions in elderly individuals (74).…”

Section: Preventionmentioning

confidence: 99%

Proteasomal Defense of Oxidative Protein Modifications

Poppek

Grune

2006

Antioxidants & Redox Signaling

111

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The proteasome has an important role in the degradation of normal, damaged, mutant, or misfolded proteins. This includes the degradation of normal and regulatory proteins in the cellular metabolism and additionally the removal of damaged proteins as a stress response. The two well-described proteasome regulators, the 11S and the 19S regulators, forming together with the 20S 'core' proteasome various forms of the proteasome, including the ATP-stimulated 26S proteasome. As a result of aerobic metabolism, reactive oxygen species (ROS) are constantly generated during the lifetime of biological organisms. Consequently a permanent generation of oxidative damage takes place. This includes the formation of oxidatively modified proteins. These oxidized protein derivatives tend to aggregate, and accumulation of these aggregates may lead to cell death. To prevent this, such oxidatively modified proteins are selectively recognized and either repaired or degraded by the proteasome. The current knowledge of the repair systems and the degradation mechanism is reviewed here. The possible interactions between the ubiquitin-proteasome-system, the chaperone system, the protein repair mechanisms, and other antioxidative defense strategies are highlighted.

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Section: Preventionmentioning

confidence: 99%

Proteasomal Defense of Oxidative Protein Modifications

Poppek

Grune

2006

Antioxidants & Redox Signaling

111

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“…Abnormalities in each of these processes occur in AD and can be linked to neuronal death and brain dysfunction. Some of these pathological changes are also related to aging and are additionally altered in AD by common or divergent mechanisms (Quadri et al, 1996;Poulin et al, 1996;Eckert et al, 1997a;Eckert et al, 1997b;Schindowski et al, 2000). Cell culture experiments also suggest that defects in the cellular calcium stores, ability to handle oxidative stress, and to respond to metabolic impairment, link the FADcausing PS1 mutations to the disease process (Mattson et al, 2001).…”

Section: Neuromolecular Medicinementioning

confidence: 99%

Impact of Aging: Sporadic, and Genetic Risk Factors on Vulnerability to Apoptosis in Alzheimer's Disease

Schindowski

Kratzsch

Peters

et al. 2003

NMM

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The identification of specific genetic and amyloid precursor protein [APP] mutations) and environmental factors responsible for Alzheimer's disease (AD) has revealed evidence for a shared pathway of neuronal death. Moreover, AD-specific cell defects may be observed in many other nonneuronal cells (e.g., lymphocytes). Thus, lymphocytes may serve as a cellular system in which to study risk factors of sporadic, as well as genetic AD in vivo. The aim of our present study was to clarify whether lymphocytes bearing genetic or sporadic risk factors of AD share an increased susceptibility to cell death. Additionally we examined whether a cell typespecific vulnerability pattern was present and how normal aging, the main risk factor of sporadic AD, contributes to changes in susceptibility to cell death. Here, we report that lymphocytes affected by sporadic or genetic APP and PS1 AD risk factors share an increased vulnerability to cell death and exhibit a similar cell type-specific pattern, given that enhanced vulnerability was most strongly developed in the CD4 + T-cell subtype. In this paradigm, sporadic risk factors revealed the highest impact on cell type-specific sensitivity of CD4 + T cells to apoptosis. In contrast, normal aging results in an increased susceptibility to apoptosis of both, CD4 + and CD8 + T cells.

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“…4 Our recent studies show that supplementation with ascorbic acid improves neutrophil phagocytic function, humoral immunity, and antioxidants in aging humans. 5,6 Compounds able to restore reduced glutathione are of therapeutic interest to ensure the antioxidative function of glutathione within the cell.…”

Section: Introductionmentioning

confidence: 99%

α-Lipoic Acid Enhances Reduced Glutathione, Ascorbic Acid, and α-Tocopherol in Aged Rats

Arivazhagan¹,

Samuel²,

Elango³

et al. 2002

Journal of Anti-Aging Medicine

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It is hypothesized that a reduction in the level of antioxidants with age leads to an impairment in the quenching of free radicals, which in turn increases the risk of succumbing to ageassociated disorders. Male albino rats of Wistar strain (both young and aged rats) were treated with lipoic acid for 7 and 14 days. Analyses were carried out in blood, liver, kidney, and brain for lipid peroxidation, reduced glutathione, ascorbic acid, and a-tocopherol. The levels of reduced glutathione, and vitamins C and E were found to be lowered in aged rats, whereas the level of lipid peroxidation was found to be high. After intraperitoneal administration of lipoate (a thiol antioxidant) to the aged rats, a time-dependent reduction in the level of lipid peroxidation and elevation in the levels of reduced glutathione, and vitamins C and E were observed. From our observations, we conclude that lipoic acid, a dithiol, normalizes lipid peroxidation and prevents the oxidation of reduced glutathione, possibly through recycling mechanisms, thereby maintaining normal metabolic function. Thus, lipoic acid supplementation could be beneficial in minimizing age-associated disorders where free radicals are the major cause. 265

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Vitamin E prevents oxidative modification of brain and lymphocyte band 3 proteins during aging.

Cited by 21 publications

References 17 publications

Proteasomal Defense of Oxidative Protein Modifications

Proteasomal Defense of Oxidative Protein Modifications

Impact of Aging: Sporadic, and Genetic Risk Factors on Vulnerability to Apoptosis in Alzheimer's Disease

α-Lipoic Acid Enhances Reduced Glutathione, Ascorbic Acid, and α-Tocopherol in Aged Rats

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