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      The Relationship between the Concentration of Salivary Tyrosine and Antioxidants in Patients with Oral Lichen Planus

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          Abstract

          The diagnosis of oral lichen planus (OLP) is based on clinical examination and histopathological criteria. Noninvasive diagnostics of saliva may be considered as a confirmation of OLP diagnosis and a potential alternative to an invasive method. The objective of the present study was to evaluate the relationship between the level of tyrosine (Tyr) as well as antioxidants like uric acid (UA) and glutathione peroxidase (GPx) activity in the saliva of patients with OLP in comparison with the control group (healthy subjects without any oral changes). A total of 40 patients with OLP and 40 healthy volunteers were selected for the study based on the modified WHO diagnostic (clinical and histopathological) criteria. High-performance liquid chromatography (HPLC) was performed for Tyr concentration, while GPx activity and uric acid levels were determined by a colorimetric method. The concentrations of Tyr, UA, and GPx activity were statistically lowered in OLP patients compared to the control group. All examined parameters correlated strongly and positively with each other. Mean values of salivary UA concentrations differed between the groups of OLP patients (reticular and erosive forms) and controls (206.66 vs. 196.54 vs. 218.49  μmol/L, respectively, p = 0.001). A similar trend was demonstrated in salivary Tyr concentration which differed statistically between the study and control groups (0.08 vs. 0.07 vs. 0.13  μmol/L, respectively, p = 0.001). Determining of a relationship between the concentrations of Tyr, UA, and GPx activity may be useful in the prognosis of OLP. The HPLC method may be employed, as an additional noninvasive diagnostic procedure to screen OLP patients, during the routine diagnostics of salivary biochemical parameters such as aromatic amino acids.

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          Most cited references39

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          Antioxidant responses and cellular adjustments to oxidative stress

          Redox biological reactions are now accepted to bear the Janus faceted feature of promoting both physiological signaling responses and pathophysiological cues. Endogenous antioxidant molecules participate in both scenarios. This review focuses on the role of crucial cellular nucleophiles, such as glutathione, and their capacity to interact with oxidants and to establish networks with other critical enzymes such as peroxiredoxins. We discuss the importance of the Nrf2-Keap1 pathway as an example of a transcriptional antioxidant response and we summarize transcriptional routes related to redox activation. As examples of pathophysiological cellular and tissular settings where antioxidant responses are major players we highlight endoplasmic reticulum stress and ischemia reperfusion. Topologically confined redox-mediated post-translational modifications of thiols are considered important molecular mechanisms mediating many antioxidant responses, whereas redox-sensitive microRNAs have emerged as key players in the posttranscriptional regulation of redox-mediated gene expression. Understanding such mechanisms may provide the basis for antioxidant-based therapeutic interventions in redox-related diseases.
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            The antioxidant capacity of saliva.

            Saliva, a heterogeneous fluid comprising proteins, glycoproteins, electrolytes, small organic molecules and compounds transported from the blood, constantly bathes the teeth and oral mucosa. It acts as a cleansing solution, an ion reservoir, a lubricant and a buffer. In addition to its other host-protective properties, saliva could constitute a first line of defence against free radical-mediated oxidative stress, since the process of mastication and digestion of ingested foods promotes a variety of reactions, including lipid peroxidation. Moreover, during gingival inflammation, gingival crevicular fluid flow increases the change of saliva composition with products from the inflammatory response; this, in turn, could have some rôle in controlling and/or modulating oxidative damages in the oral cavity. This is the reason why the antioxidant capacity of saliva has led to increasing interest, and the development of techniques suitable for saliva antioxidant evaluation. Here, we review the current peer-reviewed literature concerning the nature and characteristics of free radicals, reactive oxygen species, oxidants, pro-oxidants and antioxidants in saliva, especially pro-oxidant and antioxidant features, as well as current methods for assessing the antioxidant capacity of saliva. In the last decade, several methods have been developed for assaying the antioxidant activity of saliva, indicating an increasing interest of researchers and clinicians. Unfortunately, systematic studies of saliva are still lacking, even in healthy populations.
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              Inactivation of nitric oxide by uric acid.

              The 1980 identification of nitric oxide (NO) as an endothelial cell-derived relaxing factor resulted in an unprecedented biomedical research of NO and established NO as one of the most important cardiovascular, nervous and immune system regulatory molecule. A reduction in endothelial cell NO levels leading to "endothelial dysfunction" has been identified as a key pathogenic event preceding the development of hypertension, metabolic syndrome, and cardiovascular disease. The reduction in endothelial NO in cardiovascular disease has been attributed to the action of oxidants that either directly react with NO or uncouple its substrate enzyme. In this report, we demonstrate that uric acid (UA), the most abundant antioxidant in plasma, reacts directly with NO in a rapid irreversible reaction resulting in the formation of 6-aminouracil and depletion of NO. We further show that this reaction occurs preferentially with NO even in the presence of oxidants peroxynitrite and hydrogen peroxide and that the reaction is at least partially blocked by glutathione. This study shows a potential mechanism by which UA may deplete NO and cause endothelial dysfunction, particularly under conditions of oxidative stress in which UA is elevated and intracellular glutathione is depleted.
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                Author and article information

                Contributors
                Journal
                Oxid Med Cell Longev
                Oxid Med Cell Longev
                OMCL
                Oxidative Medicine and Cellular Longevity
                Hindawi
                1942-0900
                1942-0994
                2019
                29 November 2019
                : 2019
                : 5801570
                Affiliations
                1Chair of Periodontology and Clinical Oral Pathology, Jagiellonian University Medical College, Montelupich 4, 31–155 Krakow, Poland
                2Department of Medical Diagnostics, Jagiellonian University Medical College, Medyczna 9, 30–688 Krakow, Poland
                3Department of Toxicology, Chair of Toxicology, Jagiellonian University Medical College, Medyczna 9, 30–688 Krakow, Poland
                4Department of Periodontology and Oral Medicine, Jagiellonian University Medical College, Montelupich 4 31–155 Krakow, Poland
                5Department of Pediatric Dentistry, Institute of Dentistry, Jagiellonian University Medical College, Montelupich 4, 31–155 Krakow, Poland
                6Department of Oral Surgery, Jagiellonian University Medical College, Montelupich 4, 31–155 Krakow, Poland
                Author notes

                Guest Editor: Anna Zalewska

                Author information
                https://orcid.org/0000-0003-0452-295X
                Article
                10.1155/2019/5801570
                6906868
                87b852c6-fac8-455f-9e8b-b6e55d331f0e
                Copyright © 2019 Dagmara Darczuk et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 12 September 2019
                : 30 October 2019
                : 5 November 2019
                Funding
                Funded by: Uniwersytet Jagielloński Collegium Medicum
                Award ID: K/ZDS/007935
                Award ID: K/ZDS/005515
                Categories
                Research Article

                Molecular medicine
                Molecular medicine

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