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Free Radicals and Antioxidants
Published in Chuong Pham-Huy, Bruno Pham Huy, Food and Lifestyle in Health and Disease, 2022
Chuong Pham-Huy, Bruno Pham Huy
The widely popular free radical theory of aging states that the age-related degenerative process is to a large extent the consequence of free radical damage (4). The ‘oxidative stress theory’ holds that a progressive and irreversible accumulation of oxidative damage caused by ROS impacts on critical aspects of the aging process and contributes to impaired physiological function, increased incidence of disease, and a reduction in life span (4, 76). Other theories of aging have been proposed, including the free radical and mitochondrial theories of aging (76–78). Both theories speculate that cumulative damage to mitochondria and mitochondrial DNA (mtDNA) caused by reactive oxygen species (ROS) is one of the causes of aging. Oxidative damage affects replication and transcription of mtDNA and results in a decline in mitochondrial function which in turn leads to enhanced ROS production and further damage to mtDNA (76–78).
Mitochondrial Dysfunction in Chronic Disease
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Christopher Newell, Heather Leduc-Pessah, Aneal Khan, Jane Shearer
The free-radical theory of ageing implies that humans age due to a build-up of free radical damage. Initially postulated in the 1950s (46), this theory was further developed in the early 1970s to highlight mitochondrial derived ROS as a primary contributor (47). Since this time, several studies have provided evidence of mitochondrial involvement in the ageing process.
Antioxidant Supplements
Published in David Lightsey, The Myths about Nutrition Science, 2019
In the 1990s, the free radical theory of aging and tissue damage was popularized based upon a limited understanding of the biochemistry of free radicals. At the time, knowledge of their positive roles in cellular metabolism and adaptation to stress was limited at best. This has dramatically changed the last 20 years, which clearly illustrates that free radicals are not only a necessary part of normal cellular metabolism, but the suppression of them can be harmful. The following review of these four misconceptions should clarify why consumers should refrain from ingesting supplemental antioxidants.
Acute and subchronic toxicity studies of rhein in immature and d -galactose-induced aged mice and its potential hepatotoxicity mechanisms
Published in Drug and Chemical Toxicology, 2022
Dong Yang, Wan-Yi Huang, Yan-Qiao Li, Shi-Yu Chen, Si-Yu Su, Yue Gao, Xian-Li Meng, Ping Wang
Aging is a biological phenomenon that causes molecular, cellular, and organic dysfunction, also known as senescence (Shin et al.2003). Among the various theories of aging, Denham Harman’s (1956) free radical theory of aging has received much attention since it was first proposed in the 1950s. Oxidative damage resulting from excess production of reactive oxygen species (ROS) is the most important determinant of aging, and excess ROS formation leads directly to oxidative stress and inflammation. Oxidative stress in turn leads to redox imbalance, which ultimately leads to protein oxidation, lipid peroxidation, and mitochondrial and DNA damage, which can precisely inhibit normal cell function and even lead to apoptosis (Schieber and Chandel 2014, Li et al.2018). Moreover, the content and activities of various antioxidant enzymes such as superoxide dismutase (SOD) are decreased during senescence (van et al.2017).
Etiology of posterior subcapsular cataracts based on a review of risk factors including aging, diabetes, and ionizing radiation
Published in International Journal of Radiation Biology, 2020
Richard B. Richardson, Elizabeth A. Ainsbury, Christina R. Prescott, Frank J. Lovicu
Some PSC risk factors contribute to Stage I alone, while aging affects Stage II alone, yet most factors induce oxidative stress and inflammation that contribute to both stages (Figure 6). Risk factors such as atopy, diabetes, IR, parathyroid disorders and steroid use, principally disrupt lenticular ion/metabolite homeostasis, antioxidant levels and LEC function resulting in Stage I effects. Whereas, PSC risk factors such as atopy, diabetes, and IR (shown in Figure 6 – other risk factors include ocular inflammation, retinal dystrophies and solar radiation) not only produce toxic levels of ROS and inflammation that advance PSC Stage I (Leach et al. 2001; Wright et al. 2006; Bair et al. 2011), but also accelerate systemic aging, ocular aging or inflamm-aging relevant to Stage II. PSC risk factors that exacerbate systemic oxidative stress can be expected to accelerate aging according to the free-radical theory of aging (Harman 2003). Supportive of this premise, atopy (i.e., asthma in children), diabetes and high dose IR have been shown to advance biological age, as assessed by epigenetic markers or the common diseases of aging (Morley 2008; Richardson 2009; Peng et al. 2019).
Effect of black mulberry (Morus nigra) extract treatment on cognitive impairment and oxidative stress status of d -galactose-induced aging mice
Published in Pharmaceutical Biology, 2016
Nergiz Hacer Turgut, Derya Guliz Mert, Haki Kara, Hatice Reyhan Egilmez, Emre Arslanbas, Bektas Tepe, Huseyin Gungor, Nese Yilmaz, Necati Baris Tuncel
Many hypotheses have been introduced to explain the mechanism of the action of d-galactose in aging. One of the mechanisms that has been put forward is that, long-term administration of d-galactose enhances the formation of free radicals which attack lipids and proteins, produces several byproducts and also leads to decrement of antioxidant enzyme activities (Kumar et al. 2011; Li et al. 2012). According to the free radical theory of aging, free radicals play role in mediating accelerating aging and neurodegeneration (Harman 1956). Endogenous antioxidant enzymes such as CAT, SOD, and GSH-Px have an important part to scavenge free radicals or prevent their formation. SOD catalyzes the superoxide anion to hydrogen peroxide and oxygen, and next as electron donor GSH-Px and/or CAT catalyse. These antioxidant enzymes are substantial in fixing memory and learning deficits because there is a strong relation between oxidative stress and cognitive dysfunction (Obrenovich et al. 2011; Campos et al. 2014). The functions of liver, which is an important organ in the detoxification system, diminish due to structure atrophy in aging. Therefore, we detected the enzyme activities and MDA level not only in brain tissue but also in liver tissue and serum. Declined levels of SOD, GSH-Px, and CAT were observed in d-galactose-induced aging mice in serum, brain and liver tissues. Morus nigra improved the antioxidant activity by elevating the activities of SOD, GSH-Px, and CAT significantly in serum, brain, and liver tissues. The increased activities of these enzymes provided reversing d-galactose-induced cognitive deficits produced from oxidative damage by being effective in scavenging free radicals and their products.