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Journal ArticleDOI

Controversion on antioxidant administration in elderly

15 May 2018-Vol. 3, Iss: 3
TL;DR: This is the basic of studies that try to evaluate the effectiveness of antioxidant suplementation to inhibit the aging process and to prevent the emergence of degenerative disease so that elongating the life expectancy.
Abstract: There are many theories that try to explain the aging process but have not been satisfying. The theory of free radicals is the only theory closest to the basis of the mechanism of the aging process. This theory states the influences of free radicals will be modified by genetic and environtmental factors. Free radicals are responsible for the cell and tissue destruction due to the oxidation process of biological molecules of fat, protein and nucleic acid. In 1972, it was known that mitochondria were responsible for free radicals reaction in cells. Age is determined by the speed of mitochondria destruction by the free radicals. Mitochondria will continue to produce free radicals in its entire life until its mitochondrial DNA is attacked and destroyed resulting in cell death. Cells always use oxygen but carry the consequences of generating the reactive oxygen species (ROS) free radicals and trigger the formation of endogenous antioxidant to neutralize the oxidant effect.1,2 In aging process, there are seems to be an imbalance of free radical production and antioxidants defences in a large scale. To inhibit this process requires efforts to decreasing the free radicals production and increasing the antioxidants in the body. This is the basic of studies that try to evaluate the effectiveness of antioxidant suplementation to inhibit the aging process and to prevent the emergence of degenerative disease so that elongating the life expectancy. Studies in western countries still get an inconsistent results.3

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References
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Journal ArticleDOI
TL;DR: Dietary supplementation with n-3 PUFA led to a clinically important and statistically significant benefit and vitamin E had no benefit and its effects on fatal cardiovascular events require further exploration.

3,727 citations

Book ChapterDOI
TL;DR: The ferric reducing/antioxidant power (FRAP) assay is a recently developed, direct test of “total antioxidant power” that facilitates experimental and clinical studies investigating the relationship among antioxidant status, dietary habits, and risk of disease.
Abstract: Publisher Summary This chapter discusses ferric reducing/antioxidant power (FRAP) assay. The ferric reducing/antioxidant power (FRAP) assay is a recently developed, direct test of “total antioxidant power.” The FRAP assay is robust, sensitive, simple, and speedy and facilitates experimental and clinical studies investigating the relationship among antioxidant status, dietary habits, and risk of disease. Measurement of the total antioxidant power of fresh biological fluids—such as blood plasma—can be measured directly; the antioxidant content of various dietary agents can be measured objectively and reproducibly and their potential for improving the antioxidant status of the body investigated and compared. The FRAP assay is also sensitive and analytically precise enough to be used in assessing the bioavailability of antioxidants in dietary agents to help monitor longitudinal changes in antioxidant status associated with an increased intake of dietary antioxidants and to investigate the effects of disease on antioxidant status.

3,037 citations

Journal Article
TL;DR: This mini-review deals with the taxonomy, the mechanisms of formation and catabolism of the free radicals, it examines their beneficial and deleterious effects on cellular activities, and it highlights the potential role of the antioxidants in preventing and repairing damages caused by oxidative stress.
Abstract: Free radicals and oxidants play a dual role as both toxic and beneficial compounds, since they can be either harmful or helpful to the body. They are produced either from normal cell metabolisms in situ or from external sources (pollution, cigarette smoke, radiation, medication). When an overload of free radicals cannot gradually be destroyed, their accumulation in the body generates a phenomenon called oxidative stress. This process plays a major part in the development of chronic and degenerative illness such as cancer, autoimmune disorders, aging, cataract, rheumatoid arthritis, cardiovascular and neurodegenerative diseases. The human body has several mechanisms to counteract oxidative stress by producing antioxidants, which are either naturally produced in situ, or externally supplied through foods and/or supplements. This mini-review deals with the taxonomy, the mechanisms of formation and catabolism of the free radicals, it examines their beneficial and deleterious effects on cellular activities, it highlights the potential role of the antioxidants in preventing and repairing damages caused by oxidative stress, and it discusses the antioxidant supplementation in health maintenance.

1,991 citations

Journal ArticleDOI
Dean P. Jones1
TL;DR: Data is summarized supporting a complementary hypothesis for oxidative stress in disease that can occur without free radicals, which is that oxidative stress occurs as a consequence of disruption of thiol redox circuits, which normally function in cell signaling and physiological regulation.
Abstract: Free radical-induced macromolecular damage has been studied extensively as a mechanism of oxidative stress, but large-scale intervention trials with free radical scavenging antioxidant supplements show little benefit in humans. The present review summarizes data supporting a complementary hypothesis for oxidative stress in disease that can occur without free radicals. This hypothesis, which is termed the “redox hypothesis,” is that oxidative stress occurs as a consequence of disruption of thiol redox circuits, which normally function in cell signaling and physiological regulation. The redox states of thiol systems are sensitive to two-electron oxidants and controlled by the thioredoxins (Trx), glutathione (GSH), and cysteine (Cys). Trx and GSH systems are maintained under stable, but nonequilibrium conditions, due to a continuous oxidation of cell thiols at a rate of about 0.5% of the total thiol pool per minute. Redox-sensitive thiols are critical for signal transduction (e.g., H-Ras, PTP-1B), transcription factor binding to DNA (e.g., Nrf-2, nuclear factor-κB), receptor activation (e.g., αIIbβ3 integrin in platelet activation), and other processes. Nonradical oxidants, including peroxides, aldehydes, quinones, and epoxides, are generated enzymatically from both endogenous and exogenous precursors and do not require free radicals as intermediates to oxidize or modify these thiols. Because of the nonequilibrium conditions in the thiol pathways, aberrant generation of nonradical oxidants at rates comparable to normal oxidation may be sufficient to disrupt function. Considerable opportunity exists to elucidate specific thiol control pathways and develop interventional strategies to restore normal redox control and protect against oxidative stress in aging and age-related disease.

1,067 citations

Journal ArticleDOI
TL;DR: Antioxidant-specific gene induction, involved in xenobiotic metabolism, is mediated by the "ant antioxidant responsive element" (ARE) commonly found in the promoter region of such genes, but has not been found in plant Gst genes.
Abstract: Molecular oxygen (O2) is the premier biological electron acceptor that serves vital roles in fundamental cellular functions. However, with the beneficial properties of O2 comes the inadvertent formation of reactive oxygen species (ROS) such as superoxide (O2*-), hydrogen peroxide, and hydroxyl radical (OH*). If unabated, ROS pose a serious threat to or cause the death of aerobic cells. To minimize the damaging effects of ROS, aerobic organisms evolved non-enzymatic and enzymatic antioxidant defenses. The latter include catalases, peroxidases, superoxide dismutases, and glutathione S-transferases (GST). Cellular ROS-sensing mechanisms are not well understood, but a number of transcription factors that regulate the expression of antioxidant genes are well characterized in prokaryotes and in yeast. In higher eukaryotes, oxidative stress responses are more complex and modulated by several regulators. In mammalian systems, two classes of transcription factors, nuclear factor kB and activator protein-1, are involved in the oxidative stress response. Antioxidant-specific gene induction, involved in xenobiotic metabolism, is mediated by the "antioxidant responsive element" (ARE) commonly found in the promoter region of such genes. ARE is present in mammalian GST, metallothioneine-I and MnSod genes, but has not been found in plant Gst genes. However, ARE is present in the promoter region of the three maize catalase (Cat) genes. In plants, ROS have been implicated in the damaging effects of various environmental stress conditions. Many plant defense genes are activated in response to these conditions, including the three maize Cat and some of the superoxide dismutase (Sod) genes.

1,057 citations

Trending Questions (1)
How does the free radical ageing theory explain the ageing process?

The free radical aging theory states that free radicals, produced during the oxidation process, cause cell and tissue destruction, leading to aging.