Antioxidant and Oxidative Stress: A Mutual Interplay in Age-Related Diseases - PubMed (original) (raw)

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Bee Ling Tan et al. Front Pharmacol. 2018.

Abstract

Aging is the progressive loss of organ and tissue function over time. Growing older is positively linked to cognitive and biological degeneration such as physical frailty, psychological impairment, and cognitive decline. Oxidative stress is considered as an imbalance between pro- and antioxidant species, which results in molecular and cellular damage. Oxidative stress plays a crucial role in the development of age-related diseases. Emerging research evidence has suggested that antioxidant can control the autoxidation by interrupting the propagation of free radicals or by inhibiting the formation of free radicals and subsequently reduce oxidative stress, improve immune function, and increase healthy longevity. Indeed, oxidation damage is highly dependent on the inherited or acquired defects in enzymes involved in the redox-mediated signaling pathways. Therefore, the role of molecules with antioxidant activity that promote healthy aging and counteract oxidative stress is worth to discuss further. Of particular interest in this article, we highlighted the molecular mechanisms of antioxidants involved in the prevention of age-related diseases. Taken together, a better understanding of the role of antioxidants involved in redox modulation of inflammation would provide a useful approach for potential interventions, and subsequently promoting healthy longevity.

Keywords: age-related diseases; healthy longevity; inflammation; oxidative damage; oxidative stress.

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Figures

Figure 1

Figure 1

Effect of oxidative stress and the interaction of aging and age-related diseases. Accumulation of reactive oxygen species (ROS) leads to mRNA damage and lipid/protein oxidation and subsequently causes a decrease in mitochondrial function, and ultimately produces more oxidative stress. Mitochondrial function decline and oxidative stress response in aging may subsequently contribute to age-related diseases.

Figure 2

Figure 2

The balance of antioxidants and oxidative stress in aging. An inevitable by-product from aerobic respiration, reactive oxygen species (ROS) at the appropriate level is beneficial and essential for normal cell signaling and cellular immunity. Similarly, reactive nitrogen species (RNS) can be physiologically useful. In a normally functioning cell, antioxidants may adequately neutralize excess ROS/RNS. However, overproduction of reactive species, including superoxide (O2-), hydroxyl radical (•OH), peroxynitrite (ONOO−), hydrogen peroxide (H2O2), hydroperoxides (ROOH), singlet oxygen (1O2), reactive lipid aldehydes, and reactive nitric oxide (NO) coupled with low level of antioxidants in the body may cause oxidative damage to the cellular constituents (protein, lipids, and DNA). This phenomenon is suffered by elderly and thereby promoted abnormal cell death, inflammation and subsequently contributes to age-related diseases. Substantial evidence has demonstrated the importance of antioxidants intake from dietary nutrients to replenish low level of antioxidants (especially endogenous antioxidant such as glutathione and coenzyme Q10) in the body. Antioxidant plays a pivotal role in scavenging ROS/RNS thus protecting the cells from oxidative damage. Administration of exogenous (minerals, organosulfur compounds, vitamins, carotenoids, polyphenols) and endogenous antioxidant (antioxidant cofactor such as coenzyme Q10; and low molecular weight antioxidant: glutathione) have shown to maintain the antioxidant defense and subsequently leads to healthy longevity.

Figure 3

Figure 3

Molecular structures of glutathione, polyphenols (flavonoid, flavonol, flavone, flavanone, anthocyanidin, and isoflavones), and beta-carotene.

Figure 4

Figure 4

Molecular structures of ascorbic acid and vitamin E congeners including tocopherols (α-tocopherol, β-tocopherol, γ-tocopherol, and δ-tocopherol) and tocotrienols (α-tocotrienol, β-tocotrienol, γ-tocotrienol, and δ-tocotrienol).

Figure 5

Figure 5

Molecular structures of ubiquinone and organosulfur compounds (_S-_allylcysteine, diallyl sulfide, diallyl disulfide, and diallyl trisulfide).

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