Ageing – the biology of growing old
David Beales, Michael Denham, Alistair Tulloch in Community Care of Older People, 2018
The cell is protected against free-radical damage by several mechanisms. A peptide, glutathione, protects against the toxic effects of oxygen. Hydrogen peroxide can be removed by enzymes such as catalases and peroxidases, while superoxide dismutase specifically removes the superoxide radical. Several ‘scavenging’ systems are also present to protect the cell from lipid peroxides. Vitamin E is incorporated into membrane structure and may trap free radicals. There are age-associated reductions in glutathione, glutathione reductase and superoxide dismutase in some tissues, but no correlation has been found between the maximum lifespan potential and levels of superoxide dismutase in primates. Thus, no linkage has been found yet between the length of lifespan and the level of protective antioxidant mechanisms in an organism. Attempts to extend animal survival by feeding antioxidants throughout the lifespan have been inconclusive but results in these animals are difficult to interpret.
Dietary supplements and food fortification
Geoffrey P. Webb in Nutrition, 2019
The following circumstances might be predicted to increase the risk of disease due to free radical damage of cellular components. These circumstances would theoretically justify the use of antioxidant supplements or antioxidant-rich foods: Increased generation of free radicals beyond the capacity of the mechanisms for their safe disposal and repair of the damage that they induce. This might be due to exposure to noxious environmental stimuli like ionising radiation (including sunlight), cigarette smoke, high oxygen concentration, certain toxic chemicals. It might also be caused by any infection or injury that leads to inflammation and the generation of excess free radicals by neutrophils that infiltrate the diseased or injured area. Impaired capacity of the disposal mechanisms to handle any free radicals that are generated e.g. due to dietary deficiency of a key antioxidant nutrient. Thus it seems highly probable that severe deficiency of vitamin E, vitamin C or selenium e.g. would slow down the rate of free radical disposal and increase the cellular damage that they cause. The severe effects of genetic or induced deficiency of some of the key enzymes involved in free radical disposal were discussed earlier.
The Use of Brain Slices in the Study of Free Radical Actions
Avital Schurr, Benjamin M. Rigor in BRAIN SLICES in BASIC and CLINICAL RESEARCH, 2020
Long-term potentiation (LTP) is a sustained increase in synaptic efficacy that occurs following tetanic stimulation of an orthodromic pathway. The brain slice preparation provides an integrated network that allows us to evaluate LTP, a process that many investigators associate with memory and learning. Peroxide at concentrations that have no direct effect on synaptic potentials (0.002%) interferes with LTP.76,77 Following treatment with peroxide, high-frequency orthodromic stimulation causes potentiation of the synaptic potential, but the response decays back to its pretetanus amplitude within an hour. In contrast, untreated tissue sustains the potentiation for hours without decrement (Figure 4). Peroxide must be present at the time of the high-frequency stimulation to be effective, suggesting that free radicals interfere with the induction of LTP.77 The finding that LTP is sensitive to free radical damage begins to address possible mechanisms underlying some of the symptoms associated with free radical-induced pathologies.
Protective effect of raisin (currant) against spatial memory impairment and oxidative stress in Alzheimer disease model
Published in Nutritional Neuroscience, 2019
Mohammad Gol, Davoud Ghorbanian, Nabiollah Soltanpour, Jamshid Faraji, Mohsen Pourghasem
Al is a proxidant and produces free radicals which increase LPO and consequently, results in oxidative damage and severe neurotoxicity.46 Under oxidative stress situations, antioxidants are the first line of protection against free radical damage.18 Therefore, the investigation of the endogenous antioxidant enzymes status is in high demand. Raisin contains polyphenol and phenolic acid compounds, which have antioxidant properties. The role of natural polyphenols in the body is to remove the free radicals, chelate metal catalysts, activate antioxidant enzymes, reduce α-tocopherol radicals, and inhibit oxidases.47 Biochemical inspection results showed that the oxidation was reduced and inferred that raisins prevent oxidative damages to the brain tissue. Raisin treatment during Al exposure showed a significant decrease of LPO and increase in FRAP compared with the Al-treated group. This could be mainly due to the antioxidant and free radical scavenging properties of the raisin.48 Antioxidants prevent oxidative stress as they have a tenancy to remove metal ions involved in neuronal plaque formation. Furthermore, in post-oxidative stress scenarios, antioxidant therapy has proven to be vital in hunting down free radicals and ROS therefor preventing neuronal degeneration.38
The effects of long-term doppler ultrasound exposure in the prenatal period on renal tissue physiology in rats
Published in Electromagnetic Biology and Medicine, 2022
Fatma Beyazal Celiker, Levent Tümkaya, Tolga Mercantepe, Ertan Zengin, Mehmet Beyazal, Arzu Turan, Hatice Beyazal Polat, Zehra Topal Suzan, Adnan Yılmaz
USG and DUSG have been shown to inactivate various enzymes and to cause free radical production, both of which can initiate cellular damage (Chapman et al. 1980). Changes in antioxidant enzyme concentrations occur in the face of induced free radical damage (Feril and Kondo 2004). Reactive oxygen species (ROS) generated by DUSG-dependent oxidative stress can cause tissue damage. ROS are directly involved in oxidative damage to cellular biomolecules such as lipids, DNA, and proteins in tissues. ROS can trigger lipid peroxidation and alter low GSH and MDA levels. MDA is a major degradation product of chain reactions triggering the oxidation of polyunsaturated fatty acids and therefore serves as a reliable marker for oxidative stress in tissues, while GSH serves as a good anti-oxidant marker (Riesz and Kondo 1992). The results of the present study also support this idea. MDA and GSH levels increased significantly in the DUSG groups compared to the control group. Although MDA and GSH levels in the DUSG group differed, this was not statistically significant.
Surrogate Markers of Subclinical Atherosclerosis and Its Associated Factors in Patients with β-Thalassemia Major
Published in Hemoglobin, 2021
Danesh Soltani, Hossein Fakhrzadeh, Farshad Sharifi, Mohammad Jafar Mahmoudi, Elham Mahmoudi, Ali Vasheghani-Farahani
β-Thalassemia major (β-TM) is a severe genetic hemoglobin (Hb) disorder characterized by severe anemia requiring regular red blood cell (RBC) transfusions to survive. Iron overload is the most critical complication of regular transfusions, which can be associated with increased risk of cardiovascular morbidity and mortality, especially in the absence of chelation therapy [1-3]. Free radical damage resulting from iron toxicity is responsible for cardiovascular disorders such as early atherosclerosis and other vascular abnormalities [4,5]. In patients without iron overload, some other mechanisms, such as increasing the expression of cytokines and adhesion molecules, have been proposed for cardiovascular complications [6,7]. An increase in procoagulant activity due to oxidative stress and abnormal erythrocytes has also been found to increase cardiovascular disease risk in β-TM patients [8-10].
Related Knowledge Centers
- DNA
- Hydroxyl Radical
- Ionizing Radiation
- Melanoma
- Nucleic Acid
- Nucleobase
- Radiolysis
- Radical
- Indirect DNA Damage
- Hydrogen Atom Abstraction