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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
Some reactive sulfur species (RSS) are thiyl radical (RS•) and peroxysulfenyl radical (RSOO•). Furthermore, some ROS such as hydrogen peroxide (H2O2), ozone (O3), singlet oxygen (1O2), lipid peroxide (LOOH), and hypochlorous acid (HOCl), are not considered free radicals, and are generally called oxidants because they are more and less stable. It is the same for some RNS like nitrous acid (HNO2), dinitrogen trioxide (N2O3), and some RSS such as sulfite (SO3 –), disulfide (DSSO), and sulfenic acid (RSOH). However, these oxidants can easily lead to free radical reactions in living organisms and can yield reactive species – active free radicals (6, 15, 17–19).
The Role of Altered Glutathione Status in the Development of Parkinson’s Disease
Published in Christopher A. Shaw, Glutathione in the Nervous System, 2018
J. Sian, M. Gerlach, P. Riederer
Alternatively, the GSH deficit in PD may not be a consequence of its protective role, but rather due to the induction of its cytotoxic action. Indeed, glutathione itself can also generate thiyl radicals (GS0) and is involved in toxicity of certain quinones (Butler and Hoey 1992). In vitro studies have shown GSH reacts with quinones to yield quinone–SG glutathione conjugates, GSSG, and semiquinone free radicals (Takahashi, Schreiber, and Fisher 1987; Gant et al. 1988). These products are believed to be formed from the addition of glutathione without any electron transfer (Wardman 1990). However, the thiyl radical is fairly inactive compared to the superoxide and hydroxyl radicals. More importantly, superoxidase dismutase (SOD) is believed to inhibit radical-mediated oxidation of GSH and thereby ameliorate its actions as a physiological antioxidant (Munday and Winterbourn 1989). This notion is supported by the elevation of SOD activity reported in the SN in PD (Martilla, Lorenzo, and Rinne 1988; Saggu et al. 1989).
Treatment of skin with antioxidants
Published in Roger L. McMullen, Antioxidants and the Skin, 2018
Chapter 3 devotes considerable detail to the antioxidant properties of glutathione, a thiol-containing compound. Glutathione works in conjunction with glutathione peroxidase to break down lipid hydroperoxides to their corresponding alcohols, and to rid the cell of H2O2, converting it to H2O. At the cellular level, many thiol-containing compounds play an integral role in maintaining cell homeostasis. They function by a variety of mechanisms, including: (1) quenchers of free radicals, (2) redox reaction substrates, (3) chelating agents, (4) buffer systems, and (5) reductants of disulfide bonds in proteins.93 Given the protective role played by thiol-containing molecules, there is much interest in skin supplementation with similar exogenous species. Some of the best-known examples include derivatives of glutathione, cysteine, N-acetyl cysteine, and lipoic acid. Note, however, that care must be taken to avoid toxic thiols, of which there are many. Often, they become involved in a redox cycling mechanism between the thiol and disulfide, resulting in the formation of thiyl radicals and active oxygen species, which can damage tissue.94
Evaluation of thiol/disulfide homeostasis in patients with pityriasis rosea
Published in Cutaneous and Ocular Toxicology, 2019
Human serum albumin constitutes the largest part of thiol in the plasma. When exposed to the oxidation process, a wide range of thiol products emerge. The oxidation process of thiols may occur in one of the three ways: (1) the thiols form disulfides spontaneously on their own or through the thioredoxin enzyme, (2) the thiols react with two-electron oxidants and form unstable sulfonic acid as the intermediate, which results in the formation of disulfides in the following step, and (3) thiyl radicals are generated through the one-electron oxidation of a single thiol, which leads to the formation of disulfides. Disulfides are transformed back to thiols in the presence of an appropriate reductase6,11. There is a balance between the thiols and their oxidized forms, disulfides, in the organism, which is called thiol-disulfide homeostasis. Abnormal thiol/disulfide homeostasis is considered to be responsible for a number of diseases dominated by chronic inflammation.
Identification and characterization of protein cross-links induced by oxidative reactions
Published in Expert Review of Proteomics, 2018
Per Hägglund, Michele Mariotti, Michael J. Davies
The extent of dimer formation is dependent on the reactivity of the species concerned (i.e. their lifetimes) and how readily these species undergo alternative reactions. Many carbon-centered radicals, ., such as those generated from oxidation of aliphatic side chains (e.g. Leu, Ile, Val, Pro) undergo rapid reaction with molecular oxygen, O2, to give peroxyl radicals ROO. at diffusion controlled rates (k ~ 109 M−1s−1) [20]. Although these reactions are very fast, the concentration of O2 is low in most cells, tissues, and biological samples (5–100 μM) which can limit ROO. formation and allow formation of R-R dimers when the flux of R. is high [49]. In contrast, the rate constants for reaction of Cys-derived thiyl radicals, RS., Tyr phenoxyl radicals, and Trp indolyl radicals with O2 are much lower (k < 107 M−1s−1 for RS. and ≪ 105 M−1s−1 for the Tyr and Trp species [50–52]). This results in a much higher yield of radical-radical (dimer) products. Thus, reaction of two Cys-derived thiyl radicals gives cystine, two Tyr phenoxyl radicals give di-Tyr, and reaction of two Trp indolyl radicals gives di-Trp. Crossed dimers such as Tyr-Trp are also known (see below).
N-acetyl-cysteine reduces the risk for mechanical ventilation and mortality in patients with COVID-19 pneumonia: a two-center retrospective cohort study
Published in Infectious Diseases, 2021
Stelios F. Assimakopoulos, Diamanto Aretha, Dimitris Komninos, Dimitra Dimitropoulou, Maria Lagadinou, Lydia Leonidou, Ioanna Oikonomou, Athanasia Mouzaki, Markos Marangos
Despite the pathophysiological rationale for the potential value of NAC in COVID-19, there is very limited data regarding its clinical impact in this disease. To the best of our knowledge, there is only one double-blind, placebo-controlled randomised unicentric trial, conducted in Brazil, where 135 patients diagnosed with severe COVID-19 beyond standard of care were assigned 1:1 to either 21 g of IV NAC (14 g in the first 4 h and 7 g in the next 16 h) or placebo [19]. This study found no difference regarding the progression to severe respiratory failure requiring invasive or non-invasive mechanical ventilation, admission to ICU and mortality. However, in accordance with our positive results, previous case reports and series of patients with COVID-19 have shown that NAC administered at 1200 mg/d induced a positive clinical impact [20,21]. A potential explanation for these contradictory results might have been the short treatment duration with NAC (20 h) in the Brazilian study, as compared to its repeated daily administration for 14 days in the present study. It has been previously shown that early NAC discontinuation in COVID-19 was associated with relapse of laboratory indices of inflammation [21]. An additional explanation might have been the significantly different doses of NAC used in the present and the Brazilian study (1.2 vs. 21 g). Very higher doses of intravenous NAC (200 mg/kg/d) have been used clinically for the treatment of ARDS and a meta-analysis of randomised clinical trials on this field failed to demonstrate a survival benefit by high NAC dose administration, although length of ICU stay was decreased [22]. It should not be neglected that it has been previously shown that high doses of other free radical scavengers like beta-carotene, vitamin E, and vitamin C have led to enhanced oxidative stress [23]. Regarding thiol containing compounds, the interaction of thiols with reactive radicals can generate thiyl radicals, depending on the baseline levels of oxidative stress [24]. Previous in vitro and experimental animal studies have shown that higher doses of NAC may exert a prooxidant action, depending on the nature of the radicals generated by the biological system [24–26]. Specifically, high NAC doses have been shown to enhance the Fe2+/H2O2-dependent oxidative stress and increase superoxide radical formation [24,25].