Acceleration of Tissue Aging in Chickens Caused by Oxidative Stress Using Allopurinol and Detected by Cellular Humoral Chemiluminescence

Vascular calcification is a ubiquitous pathology of aging. Oxidative stress, persistent DNA damage, and senescence are major pathways driving both cellular and tissue aging, and emerging evidence suggests that these pathways are activated, and even accelerated, in patients with vascular calcification. The DNA damage response—a complex signaling platform that maintains genomic integrity—is induced by oxidative stress and is intimately involved in regulating cell death and osteogenic differentiation in both bone and the vasculature. Unexpectedly, a posttranslational modification, PAR (poly[ADP-ribose]), which is a byproduct of the DNA damage response, initiates biomineralization by acting to concentrate calcium into spheroidal structures that can nucleate apatitic mineral on the ECM (extracellular matrix). As we start to dissect the molecular mechanisms driving aging-associated vascular calcification, novel treatment strategies to promote healthy aging and delay pathological change are being unmasked. Drugs targeting the DNA damage response and senolytics may provide new avenues to tackle this detrimental and intractable pathology.

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The Roles of mitochondrial dysfunction and Reactive Oxygen Species in Aging and Senescence

Current Molecular Medicine ◽

10.2174/1566524021666210218112616 ◽

2021 ◽

Vol 21 ◽

Cited By ~ 1

Author(s):

Aliabbas Zia ◽

Tahereh Farkhondeh ◽

Ali Mohammad Pourbagher-Shahri ◽

Saeed Samarghandian

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Mitochondrial Dna ◽

Aging Process ◽

Replicative Senescence ◽

Reactive Oxygen ◽

Antioxidant Defenses ◽

Oxygen Species ◽

Mitochondrial Dna Mutation ◽

Tissue Aging

: The aging process deteriorates organs' function at different levels, causing its progressive decline to resist stress, damage, and disease. In addition to alterations in metabolic control and gene expression, the rate of aging has been connected with the generation of high amounts of Reactive Oxygen Species (ROS). The essential perspective in free radical biology is that reactive oxygen species (ROS) and free radicals are toxic, mostly cause direct biological damage to targets, and are thus a major cause of oxidative stress. Different enzymatic and non-enzymatic compounds in the cells have roles in neutralizing this toxicity. Oxidative damage in aging is mostly high in particular molecular targets, such as mitochondrial DNA and aconitase, and oxidative stress in mitochondria can cause tissue aging across intrinsic apoptosis. Mitochondria's function and morphology are impaired through aging, following a decrease in the membrane potential by an increase in peroxide generation and size of the organelles. Telomeres may be the significant trigger of replicative senescence. Oxidative stress accelerates telomere loss, whereas antioxidants slow it down. Oxidative stress is a crucial modulator of telomere shortening, and that telomere-driven replicative senescence is mainly a stress response. The age-linked mitochondrial DNA mutation and protein dysfunction aggregate in some organs like the brain and skeletal muscle, thus contributing considerably to these post-mitotic tissues' aging. The aging process is mostly due to accumulated damage done by harmful species in some macromolecules such proteins, DNA, and lipids. The degradation of non-functional, oxidized proteins is a crucial part of the antioxidant defenses of cells, in which the clearance of these proteins occurs through autophagy in the cells, which is known as mitophagy for mitochondria.

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Aging is associated with hypoxia and oxidative stress in adipose tissue: implications for adipose function

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.00059.2011 ◽

2011 ◽

Vol 301 (4) ◽

pp. E599-E607 ◽

Cited By ~ 42

Author(s):

Le Zhang ◽

Philip J. Ebenezer ◽

Kalavathi Dasuri ◽

Sun Ok Fernandez-Kim ◽

Joseph Francis ◽

...

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Adipose Tissue ◽

Visceral Fat ◽

Subcutaneous Fat ◽

Reactive Oxygen ◽

The Body ◽

Oxygen Species ◽

Fat Depots ◽

Tissue Aging

As a part of aging there are known to be numerous alterations which occur in multiple tissues of the body, and the focus of this study was to determine the extent to which oxidative stress and hypoxia occur during adipose tissue aging. In our studies we demonstrate for the first time that aging is associated with both hypoxia (38% reduction in oxygen levels, Po2 21.7 mmHg) and increases reactive oxygen species in visceral fat depots of aging male C57Bl/6 mice. Interestingly, aging visceral fat depots were observed to have significantly less change in the expression of genes involved in redox regulation compared with aging subcutaneous fat tissue. Exposure of 3T3-L1 adipocytes to the levels of hypoxia observed in aging adipose tissue was sufficient to alter multiple aspects of adipose biology inducing increased levels of in insulin-stimulated glucose uptake and decreased lipid content. Taken together, these data demonstrate that hypoxia and increased levels of reactive oxygen species occur in aging adipose tissue, highlighting the potential for these two stressors as potential modulators of adipose dysfunction during aging.

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Manipulation of plasma uric acid in broiler chicks and its effect on leukocyte oxidative activity

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00437.2001 ◽

2002 ◽

Vol 282 (3) ◽

pp. R791-R796 ◽

Cited By ~ 47

Author(s):

Melvin F. Simoyi ◽

Knox Van Dyke ◽

Hillar Klandorf

Keyword(s):

Oxidative Stress ◽

Uric Acid ◽

Plasma Glucose ◽

Shear Force ◽

Oxidative Activity ◽

Broiler Chicks ◽

Metabolic Rates ◽

Body Temperatures ◽

Plasma Uric Acid ◽

Tissue Aging

Birds have high metabolic rates, body temperatures, and plasma glucose concentrations yet physiologically age at a rate slower than comparably sized mammals. These studies were designed to test the hypothesis that the antioxidant uric acid protects birds against oxidative stress. Mixed sex broiler chicks (3 wk old) were fed diets supplemented or not with purines (0.6 mol hypoxanthine or inosine). Study 1 consisted of 18 female Cobb × Cobb broilers that were fed purines for 7 days, whereas study 2 consisted of 12 males in a 21-day trial. Study 3involved 30 mixed sex broilers that were fed 40 or 50 mg allopurinol/kg body mass (BM) for 21 days, a drug that lowers plasma uric acid (PUA). PUA and leukocyte oxidative activity (LOA) were determined weekly for all studies. For study 2, pectoralis major shear force, relative kidney and liver sizes (RKS and RLS), and plasma glucose concentrations were also determined. In study 1, PUA concentration was increased three- and twofold ( P < 0.001) in birds fed inosine or hypoxanthine, respectively, compared with control birds. LOA of birds supplemented with inosine was lower ( P < 0.05) than that of control or hypoxanthine birds. In study 2, PUA concentrations were increased fivefold ( P < 0.001) in birds fed inosine and twofold ( P < 0.001) in birds fed hypoxanthine compared with control birds at day 21. RKS (g/kg BM) was greater ( P < 0.001) for chicks fed purine diets compared with control chicks. Muscle shear value was lower ( P < 0.05) in chicks fed purine diets. PUA concentration was decreased ( P < 0.001) in birds consuming allopurinol diets, whereas LOA was increased ( P < 0.01) in study 3. These studies show that PUA concentrations can be related to oxidative stress in birds, which can be linked to tissue aging.

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Anti-Aging Effect of the Ketone Metabolite β-Hydroxybutyrate in Drosophila Intestinal Stem Cells

International Journal of Molecular Sciences ◽

10.3390/ijms21103497 ◽

2020 ◽

Vol 21 (10) ◽

pp. 3497 ◽

Cited By ~ 1

Author(s):

Joung-Sun Park ◽

Yung-Jin Kim

Keyword(s):

Oxidative Stress ◽

Stem Cells ◽

Stem Cell ◽

Adult Stem Cells ◽

Intestinal Stem Cells ◽

Aging Effects ◽

Age Related ◽

Tissue Aging ◽

And Oxidative Stress ◽

Age Related Changes

Age-related changes in tissue-resident adult stem cells may be closely linked to tissue aging and age-related diseases, such as cancer. β-Hydroxybutyrate is emerging as an important molecule for exhibiting the anti-aging effects of caloric restriction and fasting, which are generally considered to be beneficial for stem cell maintenance and tissue regeneration. The effects of β-hydroxybutyrate on adult stem cells remain largely unknown. Therefore, this study was undertaken to investigate whether β-hydroxybutyrate supplementation exerts beneficial effects on age-related changes in intestinal stem cells that were derived from the Drosophila midgut. Our results indicate that β-hydroxybutyrate inhibits age- and oxidative stress-induced changes in midgut intestinal stem cells, including centrosome amplification (a hallmark of cancers), hyperproliferation, and DNA damage accumulation. Additionally, β-hydroxybutyrate inhibits age- and oxidative stress-induced heterochromatin instability in enterocytes, an intestinal stem cells niche cells. Our results suggest that β-hydroxybutyrate exerts both intrinsic as well as extrinsic influence in order to maintain stem cell homeostasis.

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Oxidative Stress and Human Skin Connective Tissue Aging

Cosmetics ◽

10.3390/cosmetics3030028 ◽

2016 ◽

Vol 3 (3) ◽

pp. 28 ◽

Cited By ~ 17

Author(s):

Yidong Tu ◽

Taihao Quan

Keyword(s):

Oxidative Stress ◽

Connective Tissue ◽

Human Skin ◽

Tissue Aging

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