Free Radical Theory Research Articles

Modulation of age related protein expression changes by gelam honey in cardiac mitochondrial rats.

Aging is characterized by progressive decline in biochemical and physiological functions. According to the free radical theory of aging, aging results from oxidative damage due to the accumulation of excess reactive oxygen species (ROS). Mitochondria are the main source of ROS production and are also the main target for ROS. Therefore, a diet high in antioxidant such as honey is potentially able to protect the body from ROS and oxidative damage. Gelam honey is higher in flavonoid content and phenolic compounds compared to other local honey. This study was conducted to determine the effects of gelam honey on age related protein expression changes in cardiac mitochondrial rat. A total of 24 Sprague-Dawley male rats were divided into two groups: the young group (2 months old), and aged group (19 months old). Each group were then subdivided into two groups: control group (force-fed with distilled water), and treatment group (force-fed with gelam honey, 2.5 g/kg), and were treated for 8 months. Comparative proteomic analysis of mitochondria from cardiac tissue was then performed by high performance mass spectrometry (Q-TOF LCMS/MS) followed by validation of selected proteins by Western blotting. Proteins were identified using Spectrum Mill software and were subjected to stringent statistical analysis. A total of 286 proteins were identified in the young control group (YC) and 241 proteins were identified in the young gelam group (YG). In the aged group, a total of 243 proteins were identified in control group (OC), and 271 proteins in gelam group (OG). Comparative proteome profiling identified 69 proteins with different abundance (p < 0.05) in OC when compared to YC, and also in YG when compared to YC. On the other hand, 55 proteins were found to be different in abundance when comparing OG with OC. In the aged group, gelam honey supplementation affected the relative abundance of 52 proteins with most of these proteins showing a decrease in the control group. Bioinformatics analysis showed that the majority of the affected proteins were involved in the respiratory chain (OXPHOS) which play an important role in maintaining mitochondrial function.

Population level mitogenomics of long-lived bats reveals dynamic heteroplasmy and challenges the Free Radical Theory of Ageing

Bats are the only mammals capable of true, powered flight, which drives an extremely high metabolic rate. The “Free Radical Theory of Ageing” (FTRA) posits that a high metabolic rate causes mitochondrial heteroplasmy and the progressive ageing phenotype. Contrary to this, bats are the longest-lived order of mammals given their small size and high metabolic rate. To investigate if bats exhibit increased mitochondrial heteroplasmy with age, we performed targeted, deep sequencing of mitogenomes and measured point heteroplasmy in wild, long lived Myotis myotis. Blood was sampled from 195 individuals, aged between <1 and at 6+ years old, and whole mitochondria deep-sequenced, with a subset sampled over multiple years. The majority of heteroplasmies were at a low frequency and were transitions. Oxidative mutations were present in only a small number of individuals, suggesting local oxidative stress events. Cohort data showed no significant increase in heteroplasmy with age, while longitudinal data from recaptured individuals showed heteroplasmy is dynamic, and does not increase uniformly over time. We show that bats do not suffer from the predicted, inevitable increase in heteroplasmy as posited by the FRTA, instead heteroplasmy was found to be dynamic, questioning its presumed role as a primary driver of ageing.

Age- and sex-dependent variation in the activity of antioxidant enzymes in the brown trout (Salmo trutta)

Oxidative stress is defined as the imbalance between pro-oxidant and antioxidant molecules in favor of the former and it represents one of the main driving forces of aging. To counteract the harmful effects of oxidative stress, organisms evolved a complex antioxidant system. According to the free radical theory of aging, while the production of reactive oxygen species (ROS) increases with age, the antioxidant defenses decline. Although this relationship has been investigated in diverse vertebrate taxa, the information in fish is scant and inconsistent, particularly for wild populations. Thus, the aim of the present study was the investigation of age- and sex-related changes of the antioxidant enzymes activity in free-living individuals of the brown trout (Salmo trutta). We measured the activity of the main enzymes involved in antioxidant protection, namely superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione S-transferase (GST), as well as lipid peroxidation, in the gills and the liver dissected from brown trout (1+- to 5+-year-old). A significant age-dependent variation in the activity of antioxidant enzymes was noted, with the exception of CAT. GPx activity followed a significant increasing trend with age in both the organs, while SOD decreased in the liver. Increased GST activity was found in the gills only. Lipid peroxidation levels significantly decreased with age in both the organs. SOD and CAT showed sex-dependent differences in the liver of brown trout, with males showing lower enzymatic activity than females. Our data contribute to improve the knowledge on the relationship between antioxidant enzyme activity, aging, and sex in fish.

Molecular Mechanisms of Oxidative Stress in Aging

The paper presents a brief overview of the problems in studying the aging under the influence of oxidative reactions in the Human body. The features of the free radical theory of aging were analyzed, the role of antioxidant enzymes was considered. Aging is a complex of processes and phenomena occurring in the Human body under the influence of various factors, the oxidative metabolism has an important role in this process. The study of the mechanisms of aging opens up the prospect of using this knowledge to find methods to prolong human life.

Measurement of white wines resistance against oxidation by Electron Paramagnetic Resonance spectroscopy

Free radical theory of aging hypothesizes that oxygen-derived radicals are responsible for the storage-related flavor instability in wine. In an optimal situation, a balanced-distribution exists between oxidants and antioxidants among wines intrinsic/extrinsic metabolites. Based on the kinetic study of POBN-1-hydroxyethyl spin adduct (POBN-1-HER) formation in wines initiated via the Fenton reaction, a novel tool based on EPR spin trapping methodology was developed to quantify wines resistance against oxidation. Antioxidant capacities of wines were evaluated according to POBN-1-HER maximum signal intensity (Imax POBN-1-HER) and rate formation (rPOBN-1-HER) kinetic parameters. Low Imax POBN-1-HER and rPOBN-1-HER values suggest that endogenous antioxidants in wine are able to quench a substantial amount of radicals capable to take part in deleterious oxidative reactions. This will be very valuable in understanding aging potential and will provide an avenue to better control the process by knowing how it might be possible to change wines resistance against oxidation.

Enhanced expression of thioredoxin-interacting-protein regulates oxidative DNA damage and aging.

The “free radical theory of aging” suggests that reactive oxygen species (ROS) are responsible for age‐related loss of cellular functions and, therefore, represent the main cause of aging. Redox regulation by thioredoxin‐1 (TRX) plays a crucial role in responses to oxidative stress. We show that thioredoxin‐interacting protein (TXNIP), a negative regulator of TRX, plays a major role in maintaining the redox status and, thereby, influences aging processes. This role of TXNIP is conserved from flies to humans. Age‐dependent upregulation of TXNIP results in decreased stress resistance to oxidative challenge in primary human cells and in Drosophila. Experimental overexpression of TXNIP in flies shortens lifespan due to elevated oxidative DNA damage, whereas downregulation of TXNIP enhances oxidative stress resistance and extends lifespan.

Mitochondria and aging: A role for the mitochondrial transition pore?

SummaryThe cellular mechanisms responsible for aging are poorly understood. Aging is considered as a degenerative process induced by the accumulation of cellular lesions leading progressively to organ dysfunction and death. The free radical theory of aging has long been considered the most relevant to explain the mechanisms of aging. As the mitochondrion is an important source of reactive oxygen species (ROS), this organelle is regarded as a key intracellular player in this process and a large amount of data supports the role of mitochondrial ROS production during aging. Thus, mitochondrial ROS, oxidative damage, aging, and aging‐dependent diseases are strongly connected. However, other features of mitochondrial physiology and dysfunction have been recently implicated in the development of the aging process. Here, we examine the potential role of the mitochondrial permeability transition pore (mPTP) in normal aging and in aging‐associated diseases.

Redox Systems, Antioxidants and Sarcopenia.

According to the free-radical theory of aging, oxidative stress is a key contributor to the onset of age-related conditions by inducing structural and functional alterations in several cellular components. Although innate defenses exist for limiting the occurrence of such detrimental effects, their ability to counteract the continuous and large production of reactive oxygen species becomes increasingly inefficient with aging. In this context, interventions aimed at preserving the homeostatic balance between oxidant production and antioxidant protection may be beneficial on the pathophysiological modifications and clinical manifestations featuring the aging process. Sarcopenia is a clinical condition defined as the progressive age-related loss of muscle mass and function. In particular, a reduction of motor units and wasting of muscle fibers occurs during the aging process and negatively affects muscle quality. The biological mechanisms responsible for sarcopenia are complex, multifactorial and closely related to those characterizing the aging process. Among these, a pronounced unbalance between pro-oxidant and antioxidant species may play a major role. This review paper presents and discusses the possible role of the oxidant/antioxidant systems in the determination and development of the sarcopenic phenotype. Special attention will be devoted to the contribution of antioxidant agents in the maintenance of the homeostatic equilibrium for the organismal protection against the onset of age-related conditions. However, despite their popularity as beneficial compounds, there is no clear evidence in the literature about the protective effect of antioxidant supplements usage. Therefore, further research is needed to address and clarify such ambiguity.

Exercise as a calorie restriction mimetic. Implications for the treatment of age associated frailty

The free radical theory of aging has provided a theoretical framework for an enormous amount of work leading to advances in our understanding of aging. A critical blow to the free radical theory of aging came from epidemiological studies showing that antioxidant supplementation did not lower the incidence of age-associated diseases. However, work from many laboratories supports the theory, for instance showing that overexpression of antioxidant enzymes results in increases not only in life-span but also in health-span. Improving healthy aging means delaying disability. Disability is often preceded by a state characterized by reduced capacity to respond to stressors, caused by a decline in functional reserves. This condition, frailty, might precede by several years the development of disability. We have recently found that a mouse model with overexpression of G6PD have lower levels of ROS-derived damage and this is accompanied by a protection from frailty. Two interventions with translational potential to improve healthy aging are caloric restriction and exercise training. Both of them share a common protective molecular mechanism, a reduction in oxidative damage through the induction of the antioxidant defense.

New Insight in The Molecular Mechanisms of Neurodegenerative Disease

BACKGROUND: Redox and proteotoxic stress contributes to age-dependent accumulation of dysfunctional mitochondria and protein aggregates, and is associated with neurodegeneration. The free radical theory of aging inspired many studies using reactive species scavengers such as alpha-tocopherol, ascorbate and coenzyme-Q to suppress the initiation of oxidative stress. However, clinical trials have had limited success in the treatment of neurodegenerative diseases (NDDs).CONTENT: The misfolding and aggregation of specific proteins is a seminal occurrence in a remarkable variety of NDDs. In Alzheimer’s disease, the two principal aggregating proteins are β-amyloid (Aβ) and tau. The abnormal assemblies formed by conformational variants of these proteins range in size from small oligomers to the characteristic lesions that are visible by optica lmicroscopy, such as senile plaques and neurofibrillary tangles. Pathologic similarities with prion disease suggest that the formation and spread of these proteinaceous lesions might involve a common molecular mechanism, corruptive protein templating. The accumulation of redox modified proteins or organelles cannot be reversed by oxidant intercepting antioxidants and must then be removed by alternative mechanisms. Autophagy serves this essential function in removing damaged or dysfunctional proteins and organelles thus preserving neuronal function and survival.SUMMARY: Senescent cells and their senescence-associated secretory phenotypes (SASPs) may constitute a novel, understudied, and potentially important contributor to neuro-inflammation and subsequent neurodegeneration. Characterization of cellular senescence in the brain could uncover novel therapeutic targets for the prevention and treatment of chronic age-related NDDs.KEYWORDS: brain, aging, neurodegeneration, DNA damage, senescence, neuro-inflammation, mitochondria, lysosome, proteostasis, prion, amyloidosis

Biology of Aging

With aging, there are multiple internal and external factors that are associated with age-related changes in skin and soft tissue. As Plastic Surgeons, we very commonly evaluate and treat elderly patients, often offering ‘anti-aging’ treatments. An understanding of the science behind aging as well as common patterns of change seen in soft tissue may allow us to refine our treatments. This review provides an overview of mechanisms underlying aging, as well common clinical scenarios with aging regarding anatomic sites commonly treated by Plastic Surgeons including the face, breast, and abdomen. Separately, we discuss aging associated changes to specific tissue types, including skin, fat, muscle, and bone. Knowledge of factors related to aging and concepts related to safe interventions to reverse or mitigate age-related changes and integral to our ability to care for the elderly population. This review contains 9 figures, 3 tables and 69 references Key Words : Cellular senescence, mitochondrial theory, free radical theory, inflammation, protein damage hypothesis, glycation hypothesis, atrophy, lipotoxicity, rhytids, involution

Age‐ and Muscle‐Specific Oxidative Stress Management Strategies in a Long‐Lived Diver, the Weddell Seal

The free radical theory of aging purports that the accumulation of cellular oxidative damage leads to aging. While this process is not expected to manifest in wild populations, which can suffer from early predation or injury‐induced mortality, physically active long‐lived mammals are a model in which cellular aging may occur. Air breathing divers such as seals experience repeated bouts of ischemia‐reperfusion, potentially exposing their tissues to oxidative stress and thus damage and accelerated aging. We have previously demonstrated that skeletal muscle cellular morphology “ages” in Weddell seals without a corresponding decrease in diving behavior. This suggests stress response may protect against oxidative damage and functional impairment, providing insight into mechanisms for managing oxidative stress. We studied whether muscular senescence might arise from oxidative damage by comparing muscle from old (age 17–27 years) and young (age 9–16 years) cohorts of adult Weddell seals. Muscle biopsies were collected from healthy, active, non‐reproductive seals and frozen in liquid nitrogen. Apoptosis was examined with a cell‐death ELISA, while markers of oxidative damage to lipids (FOX assay) and proteins (4‐HNE western blot) were contrasted with antioxidant profiles (kinetic activity assays or western blots). These variables were statistically compared between age cohorts with an ANOVA model that included animal sex and biopsy site as cofactors. Old seals exhibited a 43% increase (p = 0.002) in apoptosis over young animals. Lipid peroxidation and oxidative protein damage, however, did not differ with age, suggesting that apoptotic differences were not due to oxidative stress. We also assessed antioxidant profiles and found that glutathione peroxidase (GPx) activity was 22% higher in the old cohort (p = 0.026). GPx reduces lipid hydroperoxides; this enhanced antioxidant protection may limit lipid peroxidation and downstream protein modification in old seals. The locomotory (longissimus dorsi, LD) and maneuvering (pectoralis, P) muscles of Weddell seals are perfused differently from one another during a dive, thus we also considered whether oxidative damage and antioxidant patterns are distinct between muscles using the same ANOVA. Lipid peroxidation was highest in LD (24% increase, p = 0.001), though no difference in protein modification was detected. Antioxidant protein levels revealed increased superoxide dismutase (SOD2, p = 0.009), thioredoxin reductase (TRXR2, p = 0.027) and heat shock protein 70 (HSP70, p = 0.00001) in LD. On the other hand, P exhibited a 14% increase in glutathione S‐transferase (GST, p = 0.004), which is consistent with regionally lower levels of oxidized lipid. Together, these findings illustrate that long‐lived air breathing divers display enhanced antioxidant and stress responses, possibly utilizing the pre‐conditioning effect of repeated diving. Thus, the aging Weddell seal is a compelling model for studying the successful management of oxidative stress.Support or Funding InformationNational Science Foundation Office of Polar ProgramsThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

S-nitrosylation drives cell senescence and aging in mammals by controlling mitochondrial dynamics and mitophagy

S-nitrosylation, a prototypic redox-based posttranslational modification, is frequently dysregulated in disease. S-nitrosoglutathione reductase (GSNOR) regulates protein S-nitrosylation by functioning as a protein denitrosylase. Deficiency of GSNOR results in tumorigenesis and disrupts cellular homeostasis broadly, including metabolic, cardiovascular, and immune function. Here, we demonstrate that GSNOR expression decreases in primary cells undergoing senescence, as well as in mice and humans during their life span. In stark contrast, exceptionally long-lived individuals maintain GSNOR levels. We also show that GSNOR deficiency promotes mitochondrial nitrosative stress, including excessive S-nitrosylation of Drp1 and Parkin, thereby impairing mitochondrial dynamics and mitophagy. Our findings implicate GSNOR in mammalian longevity, suggest a molecular link between protein S-nitrosylation and mitochondria quality control in aging, and provide a redox-based perspective on aging with direct therapeutic implications.

Mitochondria: Central Organelles for Melatonin's Antioxidant and Anti-Aging Actions.

Melatonin, along with its metabolites, have long been known to significantly reduce the oxidative stress burden of aging cells or cells exposed to toxins. Oxidative damage is a result of free radicals produced in cells, especially in mitochondria. When measured, melatonin, a potent antioxidant, was found to be in higher concentrations in mitochondria than in other organelles or subcellular locations. Recent evidence indicates that mitochondrial membranes possess transporters that aid in the rapid uptake of melatonin by these organelles against a gradient. Moreover, we predicted several years ago that, because of their origin from melatonin-producing bacteria, mitochondria likely also synthesize melatonin. Data accumulated within the last year supports this prediction. A high content of melatonin in mitochondria would be fortuitous, since these organelles produce an abundance of free radicals. Thus, melatonin is optimally positioned to scavenge the radicals and reduce the degree of oxidative damage. In light of the “free radical theory of aging”, including all of its iterations, high melatonin levels in mitochondria would be expected to protect against age-related organismal decline. Also, there are many age-associated diseases that have, as a contributing factor, free radical damage. These multiple diseases may likely be deferred in their onset or progression if mitochondrial levels of melatonin can be maintained into advanced age.

The Free Radical Theory of Ageing: Where are We 60 Years Later?

Gerontology & Geriatrics studies The Free Radical Theory of Ageing: Where are We 60 Years Later? Nagba Yendoube Gbandjaba1*, Pakoupati Boyode1, Kafui Kpegba1 and Abdelouahed Khalil2 1Laboratoire de Chimie Organique et des Substances Naturelles, Universite de Lome, Lome, Togo 2Centre de Recherche sur le Vieillissement, Departement de Medecine, Universite de Sherbrooke,Sherbrooke, Quebec, Canada *Corresponding author: Gbandjaba Nagba Yendoube, Laboratoire de Chimie Organique et des Substances Naturelles, Universite de Lome, Lome, Togo Submission: January 18, 2018; Published: January 22, 2018 DOI: 10.31031/GGS.2018.01.000524 ISSN : 2578-0093Volume1 Issue5

Antioxidant Vitamins and Ageing.

The free radical theory of ageing (FRTA), presented by Denham Harman in 1950s, proposed that aerobic organisms age due to reactive oxygen species (ROS)/free radical induced damage that accumulates in cells over time. Since antioxidants can neutralize free radicals by electron donation, the most logical approach was to use them as supplements in order to prevent ageing. In this chapter, we will discuss the inability of antioxidant supplementation to improve health and longevity.Although many antioxidants are efficient free radical quenchers in vitro, their in vivo effects are less clear. Recent evidence from human trials implies that antioxidant supplements do not increase lifespan and can even increase the incidence of diseases. Synthetic antioxidants were unable to consistently prevent ROS-induced damage in vivo, possibly as dietary antioxidants may not act only as ROS scavengers. Antioxidants can have dichotomous roles on ROS production. They are easily oxidized and can act as oxidants to induce damage when present in large concentrations. In appropriate amounts, they can modulate cellular metabolism by induction of cell stress responses and/or activate cell damage repair and maintenance systems. Therefore, the antioxidants' beneficial role may be reversed/prevented by excessive amounts of antioxidant supplements. On the other hand, ROS are also involved in many important physiological processes in humans, such as induction of stress responses, pathogen defence, and systemic signalling. Thus, both "anti-oxidative or reductive stress" (the excess of antioxidants) as well as oxidative stress (the excess of ROS) can be damaging and contribute to the ageing processes.

Mitochondria are an Important Target in the Search for new Drugs for the Treatment of Alzheimer′s Disease and Senile Dementia

The review and summarizes own and literature data about the role of mitochondria as the important target in the search for drugs for the treatment of neurodegenerative diseases. Aging is a major risk factor for sporadic forms of various neurodegenerative diseases, including Alzheimer′s disease. One of the most argued and currently accepted theories is the Mitochondrial Free Radical Theory of Aging. Mitochondrial hypotheses of the development of sporadic forms of neurodegenerative diseases particularly Alzheimer′s disease, are closely connected with it. Impairments of mitochondrial functions lead to a decrease in their ability to regulate calcium homeostasis in the cell and to a decrease in the threshold for the induction of mitochondrial permeability transition (MPT) pores. MPT inhibitors can be considered as a promising approach to the treatment of neurodegenerative diseases, since these drugs can not only exhibit the properties of neuroprotectors, but also can provide normalization of synaptic activity due to increased calcium capacity of mitochondria. The review presents data on the number of MPT inhibitors, including endogenous compounds melatonin and N-acetylserotonin, their bioisosteric analogue Dimebon and a number of other compounds. The use of mitochondria as a basis for the formation of screening strategy for the search for compounds for the treatment of neurodegenerative diseases is of particular interest – both as a test of their potential toxicity, and as a basis for the creation of metabolic stimulants and drugs with neuroprotective and cognitive-stimulating effect.

Role/s of 'Antioxidant' Enzymes in Ageing.

Reactive oxygen species (ROS), generated externally and during aerobic metabolism, are a potent cause of cell damage. Oxidative damage is a feature of many diseases and ageing, including age-associated diseases, such as diabetes, cancer, cardiovascular and neurodegenerative diseases. Indeed, this association helped lead to the widely expounded 'Free Radical Theory of Aging', proposing that the accumulation of ROS-induced damage is the underlying cause of ageing. In the last decade, it has become apparent that ROS play more complex roles in ageing than simply causing damage. This includes the induction of signalling pathways that protect against/repair cell damage. Cells encode a variety of enzymes that metabolise ROS, some of which reduce them to less reactive species. In this chapter, we review the evidence that manipulating the levels of these enzymes has any effect/s on ageing. We will also highlight a few examples illustrating why it is an over-simplification to describe the activities of some of these enzymes as 'antioxidants'. We discuss how these studies have helped refine our view of how ROS and ROS-metabolising enzymes contribute to the ageing process.

Free Radical and Functional Group Reaction and Index Gas CO Emission during Coal Spontaneous Combustion

ABSTRACTTo explore the reaction mechanism of the low-temperature oxidation of coal and the law of active groups producing CO through oxygenolysis, this article analyzed the reaction characteristics of free radicals and functional groups during low-temperature oxidation by using electron spin resonance and Fourier transform infrared technologies. Based on gas chromatograph analysis, the index gas CO produced by active groups during coal spontaneous combustion was analyzed by studying the reaction of free radicals and oxygen-containing functional groups. The experiments showed that, with rising oxidizing temperatures from 30°C to 230°C, the g-value increased first and then decreased, while the concentration of free radicals constantly rose by 48.3%. When the oxidation temperatures rose to 100°C, the maximum g-value occurred, and the concentration of free radicals changed from slowly increasing by 10.2% to dramatically rising by 31.7%. Moreover, the relative intensities of various oxygen-containing functional groups, including –OH, C=O, C–O, and –COOH, exhibited different change laws with rising temperatures. The –OH constantly declined by 67.0% and began to slowly decrease when the temperatures reached 100°C, while C=O declined first, then increased, and began a rapidly rising stage after the temperatures increased to 80°C. The C–O was nearly unchanged below 180°C, while the growth was accelerated after reaching 180°C, and –COOH decreased at first, then rapidly increased after 80°C. Based on the free radical theory of coal spontaneous combustion, it was revealed that carbonyl radicals are the important active groups to produce CO. It can be assumed that a C=O functional group can also produce CO by taking phenylacetaldehyde as an example. A C–O functional group can produce CO by generating carbonyl radicals, so carbonyl radicals are the direct active groups to produce CO during low-temperature oxidation. CO concentration sharply increased after the oxidizing temperatures reached 100°C, which is consistent with the change of concentration of free radicals. There is a significant inflection point of oxygen-containing functional groups at 80°C, so 80–100°C (especially 100°C) is the allowable maximum temperature of the low-temperature oxidation of coal mass.

Aging and anti-gerontological effects of algae

Today, a new urban living, chemicals that are being used in working conditions and anthropogenic activity has brought environmental pollution. It is known that chemicals cause metabolismal, cytotoxic and mutagenic damage on living things. There is a relationship between the mutagenic and carcinogenic chemicals activities. The most common cause of death, heart disease and cancer in Turkey, this situation creates obstacles to people's complete genetic life. Aging, leading to progressive and irreversible decrease in body functions and meanwhile remodeling, is defined as a natural part of the complex life cycle between birth and death. There are many theories trying to explain the aging process of living organisms in gerontology science. Somatic mutation theory, telomerase activity theory, the theory of free radicals, the theory of genetic aging, immunology and endocrine theory, calorie restriction theory are some of them. Nowadays, the view which explains the aging with chronic and cumulative effects of the free oxygen radicals is one of the leading theories. According to this theory, small but all imperfections in antioxidant system during the period of life cause aging. Free radicals are atoms or groups of atoms with an odd (unpaired) number of electrons and can be formed when oxygen interacts with certain molecules during the respiration in the cell. Once formed, these highly reactive radicals, such as dominoes, can damage cellular molecules such as DNA by chain reactions. The accumulation of these damages can lead to diseases such as cancer and accelerate aging. Antioxidants are closely related to the prevention of cellular damage, which is a common pathway to cancer, aging and various diseases. In addition to the body's own antioxidant defense system, antioxidants must also be taken with foods to prevent free radical damage. Therefore, some varieties of algae growing in importance every day and antioxidant compounds obtained from them by the technology have been offered to commercial enterprises by the market as nutritional supplements. It is known that some algae contain valuable antioxidants and the anti-gerontological role of these algae rich in antioxidants is an important issue. Some positive results were obtained on animal model species about longevity by dietary addition of antioxidants derived from the algae. The purpose of this study is to draw attention to the future anti-gerontological potentials of algae because of their rich antioxidant content.