Exploring the Potentials of Antioxidants in Retarding Ageing

2017 ◽  
pp. 166-195 ◽  
Author(s):  
Minu Kesheri ◽  
Swarna Kanchan ◽  
Rajeshwar P. Sinha
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Growth And Development ◽  
Aging Process ◽  
Reactive Oxygen ◽  
Normal Growth ◽  
Antioxidant Defenses ◽  
Oxygen Species ◽  
Biotic Stresses ◽  
Living Organisms

In retrospect to the rise in the occurrence of ageing related disorders and the everlasting desire to overcome ageing, exploring the causes, mechanisms and therapies to curb ageing becomes relevant. Reactive Oxygen Species (ROS) are commonly generated during normal growth and development. However abiotic and biotic stresses enhance the level of ROS which in turn pose the threat of oxidative stress. Ability to perceive ROS and to speedily commence antioxidant defenses is crucial for the survival as well as longevity of living cells. Therefore living organisms are bestowed with antioxidants to combat the damages caused by oxidative stress. This chapter aims to elucidate an overview of the process of ageing, generation and enhancement of reactive oxygen species, damages incurred by oxidative stress, its amelioration strategies, therapeutic and biotechnological potentials of antioxidants and various sources of bioactive compounds significant in retardation of aging process.

Exploring the Potentials of Antioxidants in Retarding Ageing

2019 ◽  
pp. 236-259
Author(s):  
Minu Kesheri ◽  
Swarna Kanchan ◽  
Rajeshwar P. Sinha
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Growth And Development ◽  
Aging Process ◽  
Reactive Oxygen ◽  
Normal Growth ◽  
Antioxidant Defenses ◽  
Oxygen Species ◽  
Biotic Stresses ◽  
Living Organisms

In retrospect to the rise in the occurrence of ageing related disorders and the everlasting desire to overcome ageing, exploring the causes, mechanisms and therapies to curb ageing becomes relevant. Reactive Oxygen Species (ROS) are commonly generated during normal growth and development. However abiotic and biotic stresses enhance the level of ROS which in turn pose the threat of oxidative stress. Ability to perceive ROS and to speedily commence antioxidant defenses is crucial for the survival as well as longevity of living cells. Therefore living organisms are bestowed with antioxidants to combat the damages caused by oxidative stress. This chapter aims to elucidate an overview of the process of ageing, generation and enhancement of reactive oxygen species, damages incurred by oxidative stress, its amelioration strategies, therapeutic and biotechnological potentials of antioxidants and various sources of bioactive compounds significant in retardation of aging process.

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

2021 ◽  
Vol 21 ◽  
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.

scholarly journals IP3Receptors, Mitochondria, and Ca2+Signaling: Implications for Aging

2011 ◽  
Vol 2011 ◽  
pp. 1-20 ◽  
Author(s):  
Jean-Paul Decuypere ◽  
Giovanni Monaco ◽  
Ludwig Missiaen ◽  
Humbert De Smedt ◽  
Jan B. Parys ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Endoplasmic Reticulum ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Aging Process ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Intracellular Ca ◽  
Uptake Mechanisms

The tight interplay between endoplasmic-reticulum-(ER-) and mitochondria-mediated Ca2+signaling is a key determinant of cellular health and cellular fate through the control of apoptosis and autophagy. Proteins that prevent or promote apoptosis and autophagy can affect intracellular Ca2+dynamics and homeostasis through binding and modulation of the intracellular Ca2+-release and Ca2+-uptake mechanisms. During aging, oxidative stress becomes an additional factor that affects ER and mitochondrial function and thus their role in Ca2+signaling. Importantly, mitochondrial dysfunction and sustained mitochondrial damage are likely to underlie part of the aging process. In this paper, we will discuss the different mechanisms that control intracellular Ca2+signaling with respect to apoptosis and autophagy and review how these processes are affected during aging through accumulation of reactive oxygen species.

Overproduction of NOX-derived ROS in AML promotes proliferation and is associated with defective oxidative stress signaling

Blood ◽  
2013 ◽  
Vol 122 (19) ◽  
pp. 3322-3330 ◽  
Author(s):  
Paul S. Hole ◽  
Joanna Zabkiewicz ◽  
Chinmay Munje ◽  
Zarabeth Newton ◽  
Lorna Pearn ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Stress Response ◽  
Reactive Oxygen ◽  
Oxidative Stress Response ◽  
Antioxidant Defenses ◽  
Stress Signaling ◽  
Oxygen Species ◽  
Key Points ◽  
P38mapk Signaling

Key Points More than 60% of primary AML blasts constitutively produce high levels of NOX-derived reactive oxygen species (ROS), which drives AML proliferation. High ROS AMLs show depleted antioxidant defenses but evade the oxidative stress response through suppression of p38MAPK signaling.

scholarly journals MELATONIN PROTECTS OVARY FROM DIABETES INDUCED OXIDATIVE DAMAGES IN LABORATORY MICE.

2020 ◽  
pp. 1-4
Author(s):  
Anindita Deb ◽  
Sangita Sutradhar ◽  
Shiv Shankar Singh
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Metabolic Disorders ◽  
Reduced Glutathione ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Laboratory Mice ◽  
Oxidative Damages ◽  
Living Organisms ◽  
Dose Dependent

Diabetes is a combination of different metabolic disorders as a result of insulin deficiency and improper action. Improper neutralization of reactive oxygen species produced during metabolism results in oxidative stress in living organisms. Melatonin is a known antioxidant, neutralizes reactive oxygen species in living organisms. We have evaluated the effectiveness of low doses (25µg, 50µg and 100µg/100g B.wt.) of melatonin on diabetes caused oxidative damages in the ovary of mice. The induction of diabetes increased the lipid peroxidation (MDA level) and decreased the antioxidant enzyme (SOD and CAT) activity, reduced glutathione (GSH) level, Nrf2 and HO-1 reactivity in the ovary of mice. Melatonin supplementation suppressed the MDA level and increased the SOD, and CAT activity, GSH levels, Nrf2 and HO-1 reactivity in the ovary of experimental mice in a dose-dependent pattern. Therefore, the present study may suggest that melatonin ameliorates the adverse effects of diabetes by reducing the oxidative stress in the ovary of experimental mice.

scholarly journals Antioxidant potentials of Miyan Kuka (Baobab leaves)

2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Eduitem S. Otong ◽  
Sunday A. Musa
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Free Radicals ◽  
Vitamin C ◽  
Singlet Oxygen ◽  
Nitrosative Stress ◽  
Antioxidant Properties ◽  
Reactive Oxygen ◽  
Antioxidant Defenses ◽  
Oxygen Species

Antioxidant is any substance that directly scavenges reactive oxygen species (ROS) or indirectly acts to up-regulate antioxidant defenses or inhibit ROS production. The review is aimed at highlighting the components of baobab leaves with antioxidant capabilities. Articles were searched from the Directory of Open Access Journals, PubMed, Google Scholar, Science Direct using key words such as composition of baobab leaves, antioxidant properties of baobab leaf, reactive oxygen species, oxidative stress and antioxidant. The result showed that boabab leaves are good sources of food with a lot of antioxidant components such as vitamin C, carotenes, flavonoids, zinc etc. These antioxidant components help to regulate ROS including free radicals such as superoxide anion, hydroxyl radical, as well as non-radical molecules like hydrogen peroxide, singlet oxygen. Baobab leaves carry out the antioxidant activities through the following processes: scavenging and neutralizing free radicals, singlet oxygen quenching, superoxide radical scavenging, hydrogen donation, metal chelating, enzymes inhibition, peroxide decomposing and synergies. They also help in activating antioxidant enzymes, reduce α-tocopherol radicals, reduce nitrosative stress, prevent oxidases, and increase levels of uric acid and low molecular weight molecules which ultimately help to reduce oxidation in the long run. Baobab leaves are rich in phytochemicals with a lot of antioxidant capabilities due to the present of several components like vitamin C, carotenes, flavenoids, etc. These components work in different ways to regulate reactive oxygen species and by extension prevent oxidative stress.

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

scholarly journals 4-Hydroxychalcone Induces Cell Death via Oxidative Stress in MYCN-Amplified Human Neuroblastoma Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Amnah M. Alshangiti ◽  
Eszter Tuboly ◽  
Shane V. Hegarty ◽  
Cathal M. McCarthy ◽  
Aideen M. Sullivan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cytotoxic Effect ◽  
Neuroblastoma Cells ◽  
Reactive Oxygen ◽  
Prognostic Indicator ◽  
Oxygen Species ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma

Neuroblastoma is an embryonal malignancy that arises from cells of sympathoadrenal lineage during the development of the nervous system. It is the most common pediatric extracranial solid tumor and is responsible for 15% of childhood deaths from cancer. Fifty percent of cases are diagnosed as high-risk metastatic disease with a low overall 5-year survival rate. More than half of patients experience disease recurrence that can be refractory to treatment. Amplification of the MYCN gene is an important prognostic indicator that is associated with rapid disease progression and a poor prognosis, highlighting the need for new therapeutic approaches. In recent years, there has been an increasing focus on identifying anticancer properties of naturally occurring chalcones, which are secondary metabolites with variable phenolic structures. Here, we report that 4-hydroxychalcone is a potent cytotoxin for MYCN-amplified IMR-32 and SK-N-BE (2) neuroblastoma cells, when compared to non-MYCN-amplified SH-SY5Y neuroblastoma cells and to the non-neuroblastoma human embryonic kidney cell line, HEK293t. Moreover, 4-hydroxychalcone treatment significantly decreased cellular levels of the antioxidant glutathione and increased cellular reactive oxygen species. In addition, 4-hydroxychalcone treatment led to impairments in mitochondrial respiratory function, compared to controls. In support of this, the cytotoxic effect of 4-hydroxychalcone was prevented by co-treatment with either the antioxidant N-acetyl-L-cysteine, a pharmacological inhibitor of oxidative stress-induced cell death (IM-54) or the mitochondrial reactive oxygen species scavenger, Mito-TEMPO. When combined with the anticancer drugs cisplatin or doxorubicin, 4-hydroxychalcone led to greater reductions in cell viability than was induced by either anti-cancer agent alone. In summary, this study identifies a cytotoxic effect of 4-hydroxychalcone in MYCN-amplified human neuroblastoma cells, which rationalizes its further study in the development of new therapies for pediatric neuroblastoma.

scholarly journals Protective Effects of Gintonin on Reactive Oxygen Species-Induced HT22 Cell Damages: Involvement of LPA1 Receptor-BDNF-AKT Signaling Pathway

Molecules ◽  
2021 ◽  
Vol 26 (14) ◽  
pp. 4138
Author(s):  
Yeon-Jin Cho ◽  
Sun-Hye Choi ◽  
Ra-Mi Lee ◽  
Han-Sung Cho ◽  
Hyewhon Rhim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Signaling Pathway ◽  
Reactive Oxygen ◽  
Akt Signaling ◽  
Atp Depletion ◽  
Oxygen Species ◽  
Akt Signaling Pathway ◽  
Neuroprotective Effects ◽  
Lpa1 Receptor

Gintonin is a kind of ginseng-derived glycolipoprotein that acts as an exogenous LPA receptor ligand. Gintonin has in vitro and in vivo neuroprotective effects; however, little is known about the cellular mechanisms underlying the neuroprotection. In the present study, we aimed to clarify how gintonin attenuates iodoacetic acid (IAA)-induced oxidative stress. The mouse hippocampal cell line HT22 was used. Gintonin treatment significantly attenuated IAA-induced reactive oxygen species (ROS) overproduction, ATP depletion, and cell death. However, treatment with Ki16425, an LPA1/3 receptor antagonist, suppressed the neuroprotective effects of gintonin. Gintonin elicited [Ca2⁺]i transients in HT22 cells. Gintonin-mediated [Ca2⁺]i transients through the LPA1 receptor-PLC-IP3 signaling pathway were coupled to increase both the expression and release of BDNF. The released BDNF activated the TrkB receptor. Induction of TrkB phosphorylation was further linked to Akt activation. Phosphorylated Akt reduced IAA-induced oxidative stress and increased cell survival. Our results indicate that gintonin attenuated IAA-induced oxidative stress in neuronal cells by activating the LPA1 receptor-BDNF-TrkB-Akt signaling pathway. One of the gintonin-mediated neuroprotective effects may be achieved via anti-oxidative stress in nervous systems.

scholarly journals How to express the antioxidant properties of substances properly?

2021 ◽  
Author(s):  
Małgorzata Olszowy-Tomczyk
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Literature Review ◽  
Antioxidant Activities ◽  
Antioxidant Properties ◽  
Reactive Oxygen ◽  
The Body ◽  
Universal Method ◽  
Oxygen Species ◽  
Good Tool

AbstractOxidative stress, associated with an imbalance between the oxidants (reactive oxygen species) and the antioxidants in the body, contributes to the development of many diseases. The body’s fight against reactive oxygen species is supported by antioxidants. Nowadays, there are too many analytical methods, but there is no one universal technique for assessing antioxidant properties. Moreover, the applied different ways of expressing the results lead to their incompatibility and unreasonable interpretation. The paper is a literature review concerning the most frequent ways of antioxidant activities expression and for an easy and universal method of the obtained results discussion. This paper is an attempt to point out their disadvantages and advantages. The manuscript can support the searching interpretation of the obtained results which will be a good tool for the development of a number of fields, especially medicine what can help in the future detection and treatment of many serious diseases. Graphic abstract

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