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14 pages, 2848 KiB

Open AccessArticle

Astaxanthin Induces Transcriptomic Responses Associated with Lifespan Extension in Caenorhabditis elegans

by Feng Ding and Yan Zhao

Antioxidants 2022, 11(11), 2115; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11112115 - 27 Oct 2022

Cited by 3 | Viewed by 2390

Astaxanthin is a marine xanthophyll carotenoid which effectively prevents intracellular oxidative stress and has beneficial effects against various human diseases. It has been shown that astaxanthin protects Caenorhabditis elegans (C. elegans) from oxidative damages and extends the lifespan of C. elegans [...] Read more.

Astaxanthin is a marine xanthophyll carotenoid which effectively prevents intracellular oxidative stress and has beneficial effects against various human diseases. It has been shown that astaxanthin protects Caenorhabditis elegans (C. elegans) from oxidative damages and extends the lifespan of C. elegans possibly by modulating genes involved in insulin/insulin-like growth factor (IGF) signaling (IIS) and the oxidoreductase system, although the exact mechanisms remain elusive. In this study, RNA sequencing analyses were employed to identify the differentially expressed genes in C. elegans in response to astaxanthin treatment. A total of 190 mRNAs and 6 microRNAs (miRNAs) were significantly changed by astaxanthin treatment in C. elegans. Gene ontology (GO) term and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses indicated that the mRNAs and miRNAs significantly altered by astaxanthin mainly function in innate immunity, lipid metabolism and stress responses, a significant portion of which are related to lifespan regulation in C. elegans. The study revealed novel mRNA and miRNA targets of astaxanthin, providing new insights for understanding the anti-aging mechanisms and the biological function of astaxanthin. Full article

(This article belongs to the Special Issue Oxidative Stress and Antioxidants in Aging)

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16 pages, 3813 KiB

Open AccessArticle

Anti-Oxidant and Anti-Aging Effects of Phlorizin Are Mediated by DAF-16-Induced Stress Response and Autophagy in Caenorhabditis elegans

by Suhyeon Park and Sang-Kyu Park

Antioxidants 2022, 11(10), 1996; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11101996 - 08 Oct 2022

Cited by 14 | Viewed by 2475

Abstract

Phlorizin (phloridzin) is a polyphenolic phytochemical primarily found in unripe Malus (apple). It is a glucoside of phloretin and acts as an inhibitor of renal glucose transport, thus lowering blood glucose. The objective of this study was to determine effects of dietary supplementation [...] Read more.

Phlorizin (phloridzin) is a polyphenolic phytochemical primarily found in unripe Malus (apple). It is a glucoside of phloretin and acts as an inhibitor of renal glucose transport, thus lowering blood glucose. The objective of this study was to determine effects of dietary supplementation with phlorizin on stress response, aging, and age-related diseases using Caenorhabditis elegans as a model system. Survival after oxidative stress or ultraviolet irradiation was significantly increased by pre-treatment of phlorizin. Dietary supplementation with phlorizin also significantly extended lifespans without reducing fertility. Age-related decline of muscle function was delayed by supplementation with phlorizin. Phlorizin induced the expression of stress-responsive genes hsp-16.2 and sod-3 and nuclear localization of DAF-16, a FOXO transcription factor modulating stress response and lifespan in C. elegans. Amyloid-beta-induced toxicity was significantly reduced by phlorizin. This effect was dependent on DAF-16 and SKN-1. Increased mortality induced with a high-glucose diet was partially prevented by phlorizin via SKN-1. Inactivation of dopaminergic neurons observed in a Parkinson’s disease model was completely recovered by supplementation with phlorizin. Genetic analysis suggests that lifespan extension by phlorizin is mediated through oxidative stress response and autophagy. Taken together, these data suggest that phlorizin has strong anti-oxidant and anti-aging activities with potential to be developed as a novel anti-oxidant nutraceutical against aging and age-related diseases. Full article

(This article belongs to the Special Issue Oxidative Stress and Antioxidants in Aging)

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21 pages, 4120 KiB

Open AccessArticle

Preventive Effect of Cocoa Flavonoids via Suppression of Oxidative Stress-Induced Apoptosis in Auditory Senescent Cells

by Luz del Mar Rivas-Chacón, Joaquín Yanes-Díaz, Beatriz de Lucas, Juan Ignacio Riestra-Ayora, Raquel Madrid-García, Ricardo Sanz-Fernández and Carolina Sánchez-Rodríguez

Antioxidants 2022, 11(8), 1450; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11081450 - 26 Jul 2022

Cited by 10 | Viewed by 2118

Abstract

Presbycusis or Age-related hearing loss (ARHL) is a sensorineural hearing loss that affects communication, leading to depression and social isolation. Currently, there are no effective treatments against ARHL. It is known that cocoa products have high levels of polyphenol content (mainly flavonoids), that [...] Read more.

Presbycusis or Age-related hearing loss (ARHL) is a sensorineural hearing loss that affects communication, leading to depression and social isolation. Currently, there are no effective treatments against ARHL. It is known that cocoa products have high levels of polyphenol content (mainly flavonoids), that are potent anti-inflammatory and antioxidant agents with proven benefits for health. The objective is to determine the protective effect of cocoa at the cellular and molecular levels in Presbycusis. For in vitro study, we used House Ear Institute-Organ of Corti 1 (HEI-OC1), stria vascularis (SV-k1), and organ of Corti (OC-k3) cells (derived from the auditory organ of a transgenic mouse). Each cell line was divided into a control group (CTR) and an H₂O₂ group (induction of senescence by an oxygen radical). Additionally, every group of every cell line was treated with the cocoa polyphenolic extract (CPE), measuring different markers of apoptosis, viability, the activity of antioxidant enzymes, and oxidative/nitrosative stress. The data show an increase of reactive oxidative and nitrogen species (ROS and RNS, respectively) in senescent cells compared to control ones. CPE treatment effectively reduced these high levels and correlated with a significant reduction in apoptosis cells by inhibiting the mitochondrial-apoptotic pathway. Furthermore, in senescence cells, the activity of antioxidant enzymes (Superoxide dismutase, SOD; Catalase, CAT; and Glutathione peroxidase, GPx) was recovered after CPE treatment. Administration of CPE also decreased oxidative DNA damage in the auditory senescent cells. In conclusion, CPE inhibits the activation of senescence-related apoptotic signaling by decreasing oxidative stress in auditory senescent cells. Full article

(This article belongs to the Special Issue Oxidative Stress and Antioxidants in Aging)

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16 pages, 3841 KiB

Open AccessArticle

SOD3 Suppresses the Expression of MMP-1 and Increases the Integrity of Extracellular Matrix in Fibroblasts

by Jin Hyung Kim, Hae Dong Jeong, Min Ji Song, Dong Hun Lee, Jin Ho Chung and Seung-Taek Lee

Antioxidants 2022, 11(5), 928; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11050928 - 09 May 2022

Cited by 16 | Viewed by 2696

Abstract

The superoxide dismutase (SOD) family functions as a reactive oxygen species (ROS)-scavenging system by converting superoxide anions into hydrogen peroxide in the cytosol (SOD1), mitochondria (SOD2), and extracellular matrix (SOD3). In this study, we examined the potential roles of SOD family members in [...] Read more.

The superoxide dismutase (SOD) family functions as a reactive oxygen species (ROS)-scavenging system by converting superoxide anions into hydrogen peroxide in the cytosol (SOD1), mitochondria (SOD2), and extracellular matrix (SOD3). In this study, we examined the potential roles of SOD family members in skin aging. We found that SOD3 expression levels were significantly more reduced in the skin tissues of old mice and humans than in young counterparts, but SOD1 and SOD2 expression levels remained unchanged with aging. Accordingly, we analyzed the effects of SOD3 on intracellular ROS levels and the integrity of the extracellular matrix in fibroblasts. The treatment of foreskin fibroblasts with recombinant SOD3 reduced the intracellular ROS levels and secretion of MMP-1 while increasing the secretion of type I collagen. The effects of SOD3 were greater in fibroblasts treated with the TNF-α. SOD3 treatment also decreased the mRNA levels and promoter activity of MMP-1 while increasing the mRNA levels and promoter activities of COL1A1 and COL1A2. SOD3 treatment reduced the phosphorylation of NF-κB, p38 MAPK, ERK, and JNK, which are essential for MMP-1 transactivation. In a three-dimensional culture of fibroblasts, SOD3 decreased the amount of type I collagen fragments produced by MMP-1 and increased the amount of nascent type I procollagen. These results demonstrate that SOD3 reduces intracellular ROS levels, suppresses MMP-1 expression, and induces type I collagen expression in fibroblasts. Therefore, SOD3 may play a role in delaying or preventing skin aging. Full article

(This article belongs to the Special Issue Oxidative Stress and Antioxidants in Aging)

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17 pages, 2745 KiB

Open AccessArticle

Angiotensin Type-1 Receptor Inhibition Reduces NLRP3 Inflammasome Upregulation Induced by Aging and Neurodegeneration in the Substantia Nigra of Male Rodents and Primary Mesencephalic Cultures

by Aloia Quijano, Carmen Diaz-Ruiz, Andrea Lopez-Lopez, Begoña Villar-Cheda, Ana Muñoz, Ana I. Rodriguez-Perez and Jose L. Labandeira-Garcia

Antioxidants 2022, 11(2), 329; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11020329 - 08 Feb 2022

Cited by 7 | Viewed by 2188

Abstract

The tissue renin–angiotensin system (RAS) has been shown to be involved in prooxidative and proinflammatory changes observed in aging and aging-related diseases such as dopaminergic degeneration in Parkinson’s disease (PD). We studied the activation of the NLRP3 inflammasome in the substantia nigra with [...] Read more.

The tissue renin–angiotensin system (RAS) has been shown to be involved in prooxidative and proinflammatory changes observed in aging and aging-related diseases such as dopaminergic degeneration in Parkinson’s disease (PD). We studied the activation of the NLRP3 inflammasome in the substantia nigra with aging and early stages of dopaminergic degeneration in PD models and, particularly, if the brain RAS, via its prooxidative proinflammatory angiotensin II (AngII) type 1 (AT1) receptors, mediates the inflammasome activation. Nigras from aged rats and mice and 6-hydroxydopamine PD models showed upregulation in transcription of inflammasome-related components (NLRP3, pro-IL1β and pro-IL18) and IL1β and IL18 protein levels, which was inhibited by the AT1 receptor antagonist candesartan. The role of the AngII/AT1 axis in inflammasome activation was further confirmed in rats intraventricularly injected with AngII, and in primary mesencephalic cultures treated with 6-hydroxydopamine, which showed inflammasome activation that was blocked by candesartan. Observations in the nigra of young and aged AT1 and AT2 knockout mice confirmed the major role of AT1 receptors in nigral inflammasome activation. In conclusion, the inflammasome is upregulated by aging and dopaminergic degeneration in the substantia nigra, possibly related with a decrease in dopamine levels, and it is mediated by the AngII/AT1 axis. Full article

(This article belongs to the Special Issue Oxidative Stress and Antioxidants in Aging)

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21 pages, 7190 KiB

Open AccessArticle

Na/H Exchange Regulatory Factor 1 Deficient Mice Show Evidence of Oxidative Stress and Altered Cisplatin Pharmacokinetics

by Adrienne M. Bushau-Sprinkle, Michelle T. Barati, Yuxuan Zheng, Walter H. Watson, Kenneth B. Gagnon, Syed Jalal Khundmiri, Kathleen T. Kitterman, Barbara J. Clark, Leah J. Siskind, Mark A. Doll, Michael E. Brier, Susan Coventry and Eleanor D. Lederer

Antioxidants 2021, 10(7), 1036; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox10071036 - 28 Jun 2021

Cited by 1 | Viewed by 2292

Abstract

(1) Background: One third of patients who receive cisplatin develop an acute kidney injury. We previously demonstrated the Na/H Exchange Regulatory Factor 1 (NHERF1) loss resulted in increased kidney enzyme activity of the pentose phosphate pathway and was associated with more severe cisplatin [...] Read more.

(1) Background: One third of patients who receive cisplatin develop an acute kidney injury. We previously demonstrated the Na/H Exchange Regulatory Factor 1 (NHERF1) loss resulted in increased kidney enzyme activity of the pentose phosphate pathway and was associated with more severe cisplatin nephrotoxicity. We hypothesized that changes in proximal tubule biochemical pathways associated with NHERF1 loss alters renal metabolism of cisplatin or response to cisplatin, resulting in exacerbated nephrotoxicity. (2) Methods: 2–4 month-old male wild-type and NHERF1 knock out littermate mice were treated with either vehicle or cisplatin (20 mg/kg dose IP), with samples taken at either 4, 24, or 72 h. Kidney injury was determined by urinary neutrophil gelatinase-associated lipocalin and histology. Glutathione metabolites were measured by HPLC and genes involved in glutathione synthesis were measured by qPCR. Kidney handling of cisplatin was assessed by a kidney cortex measurement of γ-glutamyl transferase activity, Western blot for γ-glutamyl transferase and cysteine S-conjugate beta lyase, and ICP-MS for platinum content. (3) Results: At 24 h knock out kidneys show evidence of greater tubular injury after cisplatin and exhibit a decreased reduced/oxidized glutathione ratio under baseline conditions in comparison to wild-type. KO kidneys fail to show an increase in γ-glutamyl transferase activity and experience a more rapid decline in tissue platinum when compared to wild-type. (4) Conclusions: Knock out kidneys show evidence of greater oxidative stress than wild-type accompanied by a greater degree of early injury in response to cisplatin. NHERF1 loss has no effect on the initial accumulation of cisplatin in the kidney cortex but is associated with an altered redox status which may alter the activity of enzymes involved in cisplatin metabolism. Full article

(This article belongs to the Special Issue Oxidative Stress and Antioxidants in Aging)

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28 pages, 2030 KiB

Open AccessReview

Oxidative Stress and Antioxidants in Age-Related Macular Degeneration

by Neetu Kushwah, Kiran Bora, Meenakshi Maurya, Madeline C. Pavlovich and Jing Chen

Antioxidants 2023, 12(7), 1379; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox12071379 - 03 Jul 2023

Cited by 11 | Viewed by 4681

Abstract

Oxidative stress plays a crucial role in aging-related eye diseases, including age-related macular degeneration (AMD), cataracts, and glaucoma. With age, antioxidant reparative capacity decreases, and excess levels of reactive oxygen species produce oxidative damage in many ocular cell types underling age-related pathologies. In [...] Read more.

Oxidative stress plays a crucial role in aging-related eye diseases, including age-related macular degeneration (AMD), cataracts, and glaucoma. With age, antioxidant reparative capacity decreases, and excess levels of reactive oxygen species produce oxidative damage in many ocular cell types underling age-related pathologies. In AMD, loss of central vision in the elderly is caused primarily by retinal pigment epithelium (RPE) dysfunction and degeneration and/or choroidal neovascularization that trigger malfunction and loss of photo-sensing photoreceptor cells. Along with various genetic and environmental factors that contribute to AMD, aging and age-related oxidative damage have critical involvement in AMD pathogenesis. To this end, dietary intake of antioxidants is a proven way to scavenge free radicals and to prevent or slow AMD progression. This review focuses on AMD and highlights the pathogenic role of oxidative stress in AMD from both clinical and experimental studies. The beneficial roles of antioxidants and dietary micronutrients in AMD are also summarized. Full article

(This article belongs to the Special Issue Oxidative Stress and Antioxidants in Aging)

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16 pages, 1076 KiB

Open AccessReview

Redox Mechanisms of Platelet Activation in Aging

by Sean X. Gu and Sanjana Dayal

Antioxidants 2022, 11(5), 995; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox11050995 - 19 May 2022

Cited by 4 | Viewed by 2360

Abstract

Aging is intrinsically linked with physiologic decline and is a major risk factor for a broad range of diseases. The deleterious effects of advancing age on the vascular system are evidenced by the high incidence and prevalence of cardiovascular disease in the elderly. [...] Read more.

Aging is intrinsically linked with physiologic decline and is a major risk factor for a broad range of diseases. The deleterious effects of advancing age on the vascular system are evidenced by the high incidence and prevalence of cardiovascular disease in the elderly. Reactive oxygen species are critical mediators of normal vascular physiology and have been shown to gradually increase in the vasculature with age. There is a growing appreciation for the complexity of oxidant and antioxidant systems at the cellular and molecular levels, and accumulating evidence indicates a causal association between oxidative stress and age-related vascular disease. Herein, we review the current understanding of mechanistic links between oxidative stress and thrombotic vascular disease and the changes that occur with aging. While several vascular cells are key contributors, we focus on oxidative changes that occur in platelets and their mediation in disease progression. Additionally, we discuss the impact of comorbid conditions (i.e., diabetes, atherosclerosis, obesity, cancer, etc.) that have been associated with platelet redox dysregulation and vascular disease pathogenesis. As we continue to unravel the fundamental redox mechanisms of the vascular system, we will be able to develop more targeted therapeutic strategies for the prevention and management of age-associated vascular disease. Full article

(This article belongs to the Special Issue Oxidative Stress and Antioxidants in Aging)

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