Advances in age pigment research

Porta, Eduardo A.

doi:10.1016/0167-4943(91)90036-p

Cited by 77 publications

(34 citation statements)

References 72 publications

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“…Severe oxidized and cross-linked proteins have reached the third stage of oxidative modification and are not longer accessible for proteolytic degradation. Such proteins tend to build hydrophobic and insoluble aggregates and are preliminary stages of the socalled lipofuscin (35)(36)(37), an indegradable and nonexocytosable material; in the literature sometimes also referred to as ''age pigment'' (38) or ''ceroid'' (39). If the proteolytic systems of the cell (40)(41)(42) fail to degrade oxidized proteins in time, the likelihood of cross-linking events increases and lipofuscin is formed.…”

Section: Protein Oxidation In Mammalian Cellsmentioning

confidence: 99%

The proteasome and its role in the degradation of oxidized proteins

2008

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SummaryThe generation of free radicals and the resulting oxidative modification of cell structures are omnipresent in mammalian cells. This includes the permanent oxidation of proteins leading to the disruption of the protein structure and an impaired functionality. In consequence, these oxidized proteins have to be removed in order to prevent serious metabolic disturbances. The most important cellular proteolytic system responsible for the removal of oxidized proteins is the proteasomal system. For normal functioning, the proteasomal system needs the coordinated interaction of numerous components. This review describes the fundamental functions of the 20S ''core'' proteasome, its regulators, and the roles of the proteasomal system beyond the removal of oxidized proteins in mammalian cells. IUBMBIUBMB Life, 60(11): 743-752, 2008

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Section: Protein Oxidation In Mammalian Cellsmentioning

confidence: 99%

The proteasome and its role in the degradation of oxidized proteins

2008

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“…The basic formation mechanisms of both lipofuscin and ceroid are believed to be the same. The difference is that ceroid forms rapidly during any period in the life of any tissue, whereas lipofuscin accumulates only slowly within postmitotic cells and is more resistant to digestion (Porta, 1991). Although the mechanisms by which such pigments are formed are unknown at present, they are mostly believed to be a consequence of carbonyl/amine reactions (Chio and Tappel, 1969;Desay and Tappel, 1963;Hidalgo and Zamora, 1993a;Yin et al 1995;Yin, 1996), among which oxidized lipid/protein reactions play a significant role.…”

Section: The Role Of Lipids In Nonenzymatic Browningmentioning

confidence: 99%

The role of lipids in nonenzymatic browning

Hidalgo¹,

Zamora²

2000

Grasas y Aceites

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RESUMEN El papel de los lípidos en el pardeamiento no enzimáticoEn este trabajo se hace una revisión del papel de los lípidos en el pardeamiento no enzimático de alimentos mediante el estudio de las reacciones proteína/lípido oxidado en comparación con otras reacciones donde ocurre también este oscurecimiento: la reacción de Maillard, el pardeamiento producido por el ácido ascórbico, y las reacciones de las quinonas con los grupos amino. Los mecanismos propuestos para estas reacciones de producción de color y fluorescencia, así como la formación de melanoidinas, lipofuscinas y productos coloreados de bajo peso molecular son discutidos de forma comparada, concluyendo que el papel de los lípidos en estas reacciones no parece ser muy diferente del papel de los carbohidratos en el Maillard o de los fenoles en el pardeamiento enzimático. Estas reacciones carbonil-amino parecen ser un grupo de reacciones secundarias que ocurren de forma gradual, son parcialmente reversibles, son universales e inevitables y ocurren en alimentos y en sistemas biológicos. Sin embargo, la mayoría de estos resultados han sido obtenidos en sistemas modelo y estudios adicionales deberían ser abordados en sistemas más cercanos a los alimentos y a lo seres vivos, lo que debería repercutir en un mejor entendimiento del pardeamiento no enzimático y, en definitiva, nos daría una visión más completa de la bioquímica de los alimentos y de los seres vivos. PALABRAS-CLAVE: Interacciones proteína-lípido oxidado Pardeamiento no enzimático Reacción de MaillardReacciones amino-carbonilo. SUMMARY The role of lipids in nonenzymatic browningThe role of lipids in nonenzymatic browning is studied by reviewing oxidized lipid/protein reactions in comparison with other reactions where the production of browning is known: the Maillard reaction, the ascorbic acid browning, and the quinone/amine reactions. The mechanisms proposed in these reactions for production of color and fluorescence, as well as the formation of melanoidins, lipofuscins, and low molecular weight colored products are discussed comparatively, concluding that the role of lipids in these reactions does not seem to be very different to the role of carbohydrates in the Maillard reaction or the phenols in the enzymatic browning. These carbonyl-amine reactions seem to be a group of gradual, partially reversible, universal, and inevitable side reactions in both food and biological systems. However, most of these results were obtained in model systems and additional studies should be carried out in systems closer to real foods or living beings, which should provide a more complete understanding of nonenzymatic browning, and, therefore, to afford a much more comprehensive knowledge of food and human biochemistry. KEY-WORDS: Amino-carbonyl reactions Maillard reactionNonenzymatic browning Oxidized lipid-protein interactions.

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“…For example, the yeast Saccharomyces cerevisiae accumulates extrachromosomal ribosomal DNA circles (ECR) and depolarized mitochondria with age (Sinclair and Guarente 1997;Hughes and Gottschling 2012), while old Caenorhabditis elegans nematodes accumulate lipofuscin (Klass 1977), an insoluble aggregate of oxidized proteins and lipids (Toth 1968;Porta 1991), in their intestinal cells. In higher eukaryotes, damaged organelles and proteins accumulate in long-lived postmitotic tissues, such as skeletal muscles, heart, liver, and brain (Schmucker 2005;Chaudhary et al 2011;Szweda et al 2003).…”

mentioning

confidence: 99%

p62/SQSTM1 at the interface of aging, autophagy, and disease

Bitto

Lerner

Nacarelli

et al. 2014

AGE

124

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Advanced age is characterized by increased incidence of many chronic, noninfectious diseases that impair the quality of living of the elderly and pose a major burden on the healthcare systems of developed countries. These diseases are characterized by impaired or altered function at the tissue and cellular level, which is a hallmark of the aging process. Age-related impairments are likely due to loss of homeostasis at the cellular level, which leads to the accumulation of dysfunctional organelles and damaged macromolecules, such as proteins, lipids, and nucleic acids. Intriguingly, aging and age-related diseases can be delayed by modulating nutrient signaling pathways converging on the target of rapamycin (TOR) kinase, either by genetic or dietary intervention. TOR signaling influences aging through several potential mechanisms, such as autophagy, a degradation pathway that clears the dysfunctional organelles and damaged macromolecules that accumulate with aging. Autophagy substrates are targeted for degradation by associating with p62/SQSTM1, a multidomain protein that interacts with the autophagy machinery. p62/SQSTM1 is involved in several cellular processes, and its loss has been linked to accelerated aging and to age-related pathologies. In this review, we describe p62/SQSTM1, its role in autophagy and in signaling pathways, and its emerging role in aging and age-associated pathologies. Finally, we propose p62/ SQSTM1 as a novel target for aging studies and ageextending interventions.

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Advances in age pigment research

Cited by 77 publications

References 72 publications

The proteasome and its role in the degradation of oxidized proteins

The proteasome and its role in the degradation of oxidized proteins

The role of lipids in nonenzymatic browning

p62/SQSTM1 at the interface of aging, autophagy, and disease

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