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Exercise and DNA Damage
Published in James N. Cobley, Gareth W. Davison, Oxidative Eustress in Exercise Physiology, 2022
Josh Williamson, Gareth W. Davison
While the narrative surrounding the sources of RONS attributable to DNA damage following exercise are not well understood, it is known that physiologically relevant levels of superoxide, nitric oxide, hydrogen peroxide, or organic peroxides do not react at appreciable rates (or at all) with any DNA base or deoxyribose sugar. Although the identity of the reactive species generated from Fenton reactions remains equivocal, historically, the hydroxyl free radical () has been linked to exercise-induced DNA damage (Reaction 1 & 2: Cobley et al., 2015; Davison, 2016).
Ozone Therapy in Oncology Patients
Published in Paloma Tejero, Hernán Pinto, Aesthetic Treatments for the Oncology Patient, 2020
The therapeutic properties of ozone are basically conditioned by two independent mechanisms: Direct oxidizing capacity: Its great oxidizing power makes it react directly with microbial walls and exert its germicidal effects or, for example, makes it react directly with mediators of inflammation and pain or cytokine receptors and block biological responses [1,4].Indirect effects: These are related to those that take place after the interaction with O3-biomolecules; in this case, organic peroxides, H2O2, ozonides, aldehydes, and other oxidation products generated in adequate and controlled quantities activate endogenous response mechanisms to the stress, managing to rebalance the redox environment that had been altered by the underlying pathology. While the initial mechanism shows the short-term effects of O3, this second mechanism requires time, which is why the application of a therapeutic cycle is required with several stimuli to achieve most of the effects of O3 [1,4].
Airway Repair and Adaptation to Inhalation Injury
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
S. F. Paul Man, William C. Hulbert
The molecular mechanisms by which oxidizing gases cause cellular injury are not completely understood; however, the formation of free radicals by these agents is postulated to play a pivotal role. These mechanisms have been reviewed (Reck nagel and Glende, 1977; Pryor, 1982; Menzel, 1984). The gases, O3, NO2, and SO2 are strong oxidants that can react with many biochemical moieties to form free radicals. Free radicals formed by these interactions adversely affect the structure and function of cellular components such as proteins, especially enzymes containing sulfhydryl groups (SH), nucleic acids, and, more importantly, the cellular plasma membrane. The plasma membrane provides the containment of all cellular and organelle contents, and its permeability characteristics regulate the molecular species that enter and exit the cell and its organelles. The membrane is composed of lipoproteins rich in polyenoic long-chain fatty acids that are prone to undergo rancid or peroxidation decomposition under certain conditions. Free radicals, once formed, can react readily with molecular oxygen to form organic peroxy free radicals. When a peroxy free radical reacts with a phospholipid fatty acid side chain, it not only denatures the molecule but also produces another new organic free radical; this process is known as linear propagation of lipid hydroperoxide formation. Furthermore, new free radicals can be produced by the decomposition of organic peroxide via a number of cellular biochemical mechanisms (see Recknagel and Glende, 1977, for review).
Emerging drugs for the treatment of acne: a review of phase 2 & 3 trials
Published in Expert Opinion on Emerging Drugs, 2022
Siddharth Bhatt, Rohit Kothari, Durga Madhab Tripathy, Sunmeet Sandhu, Mahsa Babaei, Mohamad Goldust
Benzoyl Peroxide is an organic peroxide derived from coal tar. It is one of the drugs to which no resistance has been detected despite decades of usage. It has antibacterial, oxidative, anti-inflammatory, and keratolytic actions which make it an ideal drug for acne management. Its combination with other drugs is more efficacious than individual use. It helps to prevent resistance to clindamycin when used in combination with it. Combination with retinoids like adapalene provides a synergistic effect. It can cause irritant dermatitis that presents with burning, erythema, peeling, and dryness. This irritation increases with adapalene benzoyl peroxide combination as compared to benzoyl peroxide alone. The chances of true allergy to benzoyl peroxide are rare with an incidence of 0.2 − 1%. It can also bleach the fabric and hair [4].
3,4-Dihydroxybenzaldehyde attenuates pentachlorophenol-induced cytotoxicity, DNA damage and collapse of mitochondrial membrane potential in isolated human blood cells
Published in Drug and Chemical Toxicology, 2022
Nikhil Maheshwari, Riaz Mahmood
SOD converts superoxide radicals to non-radical oxygen and H2O2. SOD activity was inhibited by PCP to 62% while earlier treatment with DHB restored it to 96% of untreated control cells (Table 2). CAT finishes the detoxification started by SOD by converting H2O2 to oxygen and water. The removal of H2O2 also inhibits heme-degradation by preventing its reaction with ferrylHb (Nagababu and Rifkind 2000). PCP alone treatment reduced the CAT activity to 62%. The presence of DHB restored the enzyme activity to that of untreated control cells. GPx catalyzes the elimination of organic peroxides along with H2O2, using GSH and NADPH as the reductant. Thioredoxin reductase (TR) is essential for maintaining protein thiols in their reduced state. GPx activity was increased 2-fold while TR was inhibited to 53% in PCP alone treated groups but DHB treatment normalized these changes. TR was restored to control value while GPx was only 1.4-fold above control. GR converts GSSG to GSH using NADPH as reductant. These enzymes are required in drug metabolism and removal of oxidative species in blood cells. PCP alone lowered the GR activity to 59% but the presence of DHB mitigated PCP-induced changes in enzyme activity, which was 92% of control.
Significance of the coexistence of non-codon 315 katG, inhA, and oxyR-ahpC intergenic gene mutations among isoniazid-resistant and multidrug-resistant isolates of Mycobacterium tuberculosis: a report of novel mutations
Published in Pathogens and Global Health, 2022
Fatemeh Norouzi, Sharareh Moghim, ShimaSadat Farzaneh, Hossein Fazeli, Mahshid Salehi, Bahram Nasr Esfahani
The ACP reductase catalyzes the final reductive step of the mycolic acid elongation cycle; the biosynthesis of fatty acids is crucial for its survival [8]. This enzyme is inhibited by the isonicotinic acyl-NADH adduct, which results in the interruption of mycolic acid biosynthesis and mycobacterial cell death [9]. The main molecular mechanisms of resistance to INH are associated with mutations in katG and InhA genes. A common cause of INH resistance is the katG 315 mutation [10]. Also, mutation of the inhA promoter region is another frequently identified mechanism of resistance [11]. Besides, tolerance for oxidative stress depends on the CP enzyme. In the loss of katG activity, to overcome oxidative stress, the production of alkyl hydroperoxide reductase increases by overexpression of ahpC gene [12]. The ahpC gene mutations act as compensatory alterations for the alkylhydroperoxide reductase upregulation to survive the toxic effects of organic peroxides; consequently, these gene mutations indirectly contribute to INH resistance [13].