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      Measurement of oxidative stress and total antioxidant capacity in hyperthyroid patients following treatment with carbimazole and antioxidant

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          Abstract

          Hyperthyroidism is a common endocrine disorder in which the thyroid produces too many hormones, resulting in the metabolism speed up. The present study was designed to measure oxidative stress and total antioxidant capacity in hyperthyroid patients following treatment with carbimazole and antioxidants supplements. This randomized clinical trial study was conducted to compare Malondialdehyde (MDA) and total antioxidant capacity (TAC) among 25 newly diagnosed hyperthyroid patients (Group A), 25 hyperthyroid patients treated with carbimazole (Group B) and 25 hyperthyroid patients treated with carbimazole and antioxidants supplement (Group C) of both sexes. In this study, the mean serum malondialdehyde (MDA) of the three groups were 4.60 ± 1.08 μmol/L (Group A), 2.79 ± 0.58 μmol/L (Group B), and 1.57 ± 0.29 μmol/L (Group C). We found the mean MDA level was significantly higher in Group A than Group B and Group C. This study found the MDA level was significantly higher in hyperthyroid patients treated with carbimazole alone (Group B, 2.79 ± 0.58 umol/L) than hyperthyroid patients treated with carbimazole and antioxidant combined (Group C, 1.57 ± 0.29 umol/L) among the study groups (p < 0.001). The results showed that the mean serum TAC was significantly lower in newly diagnosed hyperthyroid (Group A, 527.8 ± 78.44 umol/L] patients compared to carbimazole treated alone (Group B, 951.80 ± 99.67 umol/L) and combination with the antithyroid drug (carbimazole) and antioxidant treated (Group C, 1113.56 ± 121.69 umol/L). There was more improvement found in the treatment combined with the antithyroid drug (carbimazole) and antioxidant (Group C).

          Conventional treatment of hyperthyroid patients significantly reduced oxidative stress and elevated serum TAC but not up to normal level. Therefore, the supplementation of antioxidants could be utilized to improve thyroid function in hyperthyroid patients by boosting antioxidants and restoring oxidant-antioxidant balance. However, further studies are required to determine the optimal dosage, route of administration, and timing of antioxidant therapy needed before this supplementation could be officially recommended as adjuvant therapy.

          Highlights

          • Antioxidant boosting with conventional treatment enhanced of thyroid function in hyperthyroidism.

          • Treating antioxidants and carbimazole enhanced thyroid function more than carbimazole alone.

          • MDA level was normalized along with improved TAC by treating antioxidants with the antithyroid drug.

          • Serum T4 significantly reduces and TSH significantly improves boosting antioxidant with carbimazole.

          • Antioxidant adding helps to improve thyroid hormone and oxidative damage of hyperthyroidism.

          Abstract

          Hyperthyroidism, Oxidative stress, Malondialdehyde, Total antioxidant capacity, Antioxidant, Carbimazole.

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          Most cited references33

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          The ferric reducing ability of plasma (FRAP) as a measure of "antioxidant power": the FRAP assay.

          A simple, automated test measuring the ferric reducing ability of plasma, the FRAP assay, is presented as a novel method for assessing "antioxidant power." Ferric to ferrous ion reduction at low pH causes a colored ferrous-tripyridyltriazine complex to form. FRAP values are obtained by comparing the absorbance change at 593 nm in test reaction mixtures with those containing ferrous ions in known concentration. Absorbance changes are linear over a wide concentration range with antioxidant mixtures, including plasma, and with solutions containing one antioxidant in purified form. There is no apparent interaction between antioxidants. Measured stoichiometric factors of Trolox, alpha-tocopherol, ascorbic acid, and uric acid are all 2.0; that of bilirubin is 4.0. Activity of albumin is very low. Within- and between-run CVs are <1.0 and <3.0%, respectively, at 100-1000 micromol/liter. FRAP values of fresh plasma of healthy Chinese adults: 612-1634 micromol/liter (mean, 1017; SD, 206; n = 141). The FRAP assay is inexpensive, reagents are simple to prepare, results are highly reproducible, and the procedure is straightforward and speedy. The FRAP assay offers a putative index of antioxidant, or reducing, potential of biological fluids within the technological reach of every laboratory and researcher interested in oxidative stress and its effects.
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            Free radicals and antioxidants in normal physiological functions and human disease.

            Reactive oxygen species (ROS) and reactive nitrogen species (RNS, e.g. nitric oxide, NO(*)) are well recognised for playing a dual role as both deleterious and beneficial species. ROS and RNS are normally generated by tightly regulated enzymes, such as NO synthase (NOS) and NAD(P)H oxidase isoforms, respectively. Overproduction of ROS (arising either from mitochondrial electron-transport chain or excessive stimulation of NAD(P)H) results in oxidative stress, a deleterious process that can be an important mediator of damage to cell structures, including lipids and membranes, proteins, and DNA. In contrast, beneficial effects of ROS/RNS (e.g. superoxide radical and nitric oxide) occur at low/moderate concentrations and involve physiological roles in cellular responses to noxia, as for example in defence against infectious agents, in the function of a number of cellular signalling pathways, and the induction of a mitogenic response. Ironically, various ROS-mediated actions in fact protect cells against ROS-induced oxidative stress and re-establish or maintain "redox balance" termed also "redox homeostasis". The "two-faced" character of ROS is clearly substantiated. For example, a growing body of evidence shows that ROS within cells act as secondary messengers in intracellular signalling cascades which induce and maintain the oncogenic phenotype of cancer cells, however, ROS can also induce cellular senescence and apoptosis and can therefore function as anti-tumourigenic species. This review will describe the: (i) chemistry and biochemistry of ROS/RNS and sources of free radical generation; (ii) damage to DNA, to proteins, and to lipids by free radicals; (iii) role of antioxidants (e.g. glutathione) in the maintenance of cellular "redox homeostasis"; (iv) overview of ROS-induced signaling pathways; (v) role of ROS in redox regulation of normal physiological functions, as well as (vi) role of ROS in pathophysiological implications of altered redox regulation (human diseases and ageing). Attention is focussed on the ROS/RNS-linked pathogenesis of cancer, cardiovascular disease, atherosclerosis, hypertension, ischemia/reperfusion injury, diabetes mellitus, neurodegenerative diseases (Alzheimer's disease and Parkinson's disease), rheumatoid arthritis, and ageing. Topics of current debate are also reviewed such as the question whether excessive formation of free radicals is a primary cause or a downstream consequence of tissue injury.
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              Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal

              Lipid peroxidation can be described generally as a process under which oxidants such as free radicals attack lipids containing carbon-carbon double bond(s), especially polyunsaturated fatty acids (PUFAs). Over the last four decades, an extensive body of literature regarding lipid peroxidation has shown its important role in cell biology and human health. Since the early 1970s, the total published research articles on the topic of lipid peroxidation was 98 (1970–1974) and has been increasing at almost 135-fold, by up to 13165 in last 4 years (2010–2013). New discoveries about the involvement in cellular physiology and pathology, as well as the control of lipid peroxidation, continue to emerge every day. Given the enormity of this field, this review focuses on biochemical concepts of lipid peroxidation, production, metabolism, and signaling mechanisms of two main omega-6 fatty acids lipid peroxidation products: malondialdehyde (MDA) and, in particular, 4-hydroxy-2-nonenal (4-HNE), summarizing not only its physiological and protective function as signaling molecule stimulating gene expression and cell survival, but also its cytotoxic role inhibiting gene expression and promoting cell death. Finally, overviews of in vivo mammalian model systems used to study the lipid peroxidation process, and common pathological processes linked to MDA and 4-HNE are shown.
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                Author and article information

                Contributors
                Journal
                Heliyon
                Heliyon
                Heliyon
                Elsevier
                2405-8440
                30 December 2021
                January 2022
                30 December 2021
                : 8
                : 1
                : e08651
                Affiliations
                [a ]Department of Pharmacology and Therapeutics, Rajshahi Medical College, Rajshahi, Bangladesh
                [b ]Department of Community Medicine, Rajshahi Medical College, Rajshahi, Bangladesh
                Author notes
                []Corresponding author. drrazia28@ 123456gmail.com
                Article
                S2405-8440(21)02754-7 e08651
                10.1016/j.heliyon.2021.e08651
                8741446
                35028444
                4a0c8df9-7380-462c-8717-bb8a32d380fb
                © 2021 The Author(s)

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 13 September 2021
                : 12 November 2021
                : 17 December 2021
                Categories
                Research Article

                hyperthyroidism,oxidative stress,malondialdehyde,total antioxidant capacity,antioxidant,carbimazole

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