Sources of free radicals and oxidative stress in the oral cavity

Żukowski, Piotr; Maciejczyk, Mateusz; Waszkiel, Danuta

doi:10.1016/j.archoralbio.2018.04.018

Cited by 135 publications

(138 citation statements)

References 118 publications

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“…It is noteworthy that XO catalyzes the oxidation reaction of hypoxanthine to xanthine and uric acid [58], which may also explain increased concentration of UA in our patients. Although UA is considered the most important salivary antioxidant (accounting for 70-80% of salivary antioxidant capacity) [37,59], this compound has also a strong pro-oxidant effect. However, what role does UA play in this scenario?…”

Section: Discussionmentioning

confidence: 99%

“…Salivary antioxidants did not correlate with the content of these substances in plasma/erythrocytes (except UA), which is not surprising because the oral cavity is the only place in the body exposed to numerous pro-oxidant factors. These include: xenobiotics (tobacco smoke, medicines, air pollution), food, dental treatment, and dental materials [37,59]. Thus, the salivary antioxidant barrier does not necessarily reflect the central redox status.…”

Section: Discussionmentioning

confidence: 99%

“…Because the main source of salivary oxidative stress are periodontal disease and dental caries [20,33,37], children with poor oral hygiene (API > 20) and gingivitis (SBI > 0.5, GI > 0.5) were excluded from the experiment. All of the dental examinations were performed by the same dentist (J.S.).…”

Section: Dental Examinationmentioning

confidence: 99%

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A Case-Control Study of Salivary Redox Homeostasis in Hypertensive Children. Can Salivary Uric Acid be a Marker of Hypertension?

Maciejczyk

Taranta-Janusz

Wasilewska

et al. 2020

JCM

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Oxidative stress plays a critical role in the pathogenesis of hypertension; however, there are no data on salivary redox homeostasis and salivary gland function in children with hypertension. A total of 53 children with hypertension and age-and sex-matched controls were classified for the study. The antioxidant barrier and oxidative/nitrosative stress were evaluated in non-stimulated (NWS) and stimulated (SWS) whole saliva, plasma, and erythrocytes, with Student's t-test and Mann-Whitney U-test used for statistical analysis. We demonstrated that the activities of superoxide dismutase, catalase, and peroxidase were significantly higher in NWS, SWS, and erythrocytes of children with hypertension, similar to oxidative damage in proteins (advanced glycation end products) and lipids (malondialdehyde) as well as nitrosative stress markers (peroxynitrite and nitrotyrosine). The level of uric acid (UA) was significantly higher in NWS, SWS, and plasma of children with hypertension. UA concentration in SWS correlated positively with systolic and diastolic blood pressure and UA content in plasma. This parameter differentiates children with hypertension from healthy controls (AUC = 0.98) with a high degree of sensitivity (94%) and specificity (94%). Stimulated salivary flow was significantly lower in the hypertension group, similar to total protein content and salivary amylase activity. In summary, childhood hypertension is associated with hyposalivation as well as disturbances in antioxidant defense and enhanced oxidative/nitrosative damage both in the plasma/erythrocytes as well as saliva. Salivary UA may be a potential biomarker of hypertension in children.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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A Case-Control Study of Salivary Redox Homeostasis in Hypertensive Children. Can Salivary Uric Acid be a Marker of Hypertension?

Maciejczyk

Taranta-Janusz

Wasilewska

et al. 2020

JCM

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“…These changes alter the oxidant–antioxidant status of various clinical stages of oral leukoplakia presumably (Srivastava, Austin, Shrivastava, & Pranavadhyani, ). If oxidative stress and other stresses accumulate in the oral mucosa, intracellular homeostasis might be altered, and autophagy might be impaired (Żukowski, Maciejczyk, & Waszkiel, ).…”

Section: Discussionmentioning

confidence: 99%

Association between p62 expression and clinicopathological characteristics in oral leukoplakia

Yoshida

Terabe

Nagai

et al. 2019

Clinical & Exp Dental Res

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Objective Oral leukoplakia is keratinized lesions in the buccal mucosa, tongue, and gingiva. It is the most common oral precancerous lesion; oxidative stresses and irrelevant autophagy have been reported to be the cause of oncogenesis. p62, a cytoplasmic protein induced by oxidative stress, is an adaptor protein involved in the formation of protein aggregates and induction and inhibition of autophagy. The inhibition of autophagy induces p62 overexpression and promotes oncogenesis via the oncogenic signaling pathway. The aim of the present study was to elucidate the involvement of intracellular expression of p62 in oral leukoplakia and to address its potential clinical implementation as a biomarker to predict malignant transformation. Material and Methods Fifty samples from subjects with confirmed oral leukoplakia were evaluated by immunohistochemical staining for the expression of p62, 8‐hydroxy‐2′‐deoxyguanosine (8‐OHdG), Ki67, and p53. Univariate and multivariate logistic regression analyses were performed to evaluate the association between p62, 8‐OHdG, Ki67, and p53 and clinical characteristics, including epithelial dysplasia. Results Significant associations were observed between p62 expression in the nucleus, p62 aggregation, and epithelial dysplasia (adjusted odds ratio [OR] = 5.75; 95% confidence interval [CI]: [1.28, 26.2]; .024 and OR = 6.16; 95% CI: [1.01, 37.4]; .048, respectively). The expression of p62 in the cytoplasm and the levels of 8‐OHdG, Ki67, and p53 were not significantly associated with epithelial dysplasia. A significant relationship was found between p62 expression in the nucleus and p53 expression (OR = 3.94; 95% CI: [1.14, 13.6]; .031). Conclusions The results suggested that p62 expression in the nucleus and p62 aggregation can be potential markers to predict the malignant transformation of oral leukoplakia.

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“…Physiological metabolism is the main source of free radicals [15], and saliva and its antioxidants are considered regulators of oral cavity redox status under physiological and pathological conditions [16]. Salivary redox status, however, may alter the integrity of oral structures, as normal saliva is exposed to a variety of antioxidants [17,18] and oxidants which are of extrinsic origin, such as diet and oral bacteria, as well as exposure to ionizing and ultraviolet radiation, smoking, and alcohol [15]. Other sources of reactive oxidative species (ROS) may also include dental materials, restorative treatments [15,19], and medication use [15].…”

Section: Introductionmentioning

confidence: 99%

Carious Lesion Severity Induces Higher Antioxidant System Activity and Consequently Reduces Oxidative Damage in Children’s Saliva

Araujo

Nakamune

Garcia

et al. 2020

Oxidative Medicine and Cellular Longevity

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Oxidative stress biomarkers can be found at detectable concentrations in saliva. These salivary biomarkers reflect specific oxidation pathways associated with caries and periodontitis. Our study evaluated the influence of dental caries severity (assessed using the ICCMS™ criteria) on the levels of oxidative stress biomarkers in saliva from children. Unstimulated saliva samples were collected from patients (from one to three years old) in a day care center in Birigui, SP, Brazil, two hours after fasting. Children were divided into four groups (n=30/group), according to caries severity: caries free (group A), early carious lesions (group B), moderate carious lesions (group C), and advanced carious lesions (group D). The following salivary biomarkers were determined: total proteins (TP), measured by the Lowry method; oxidative damage, measured by the TBARS method; total antioxidant capacity (TAC); superoxide dismutase (SOD) enzymatic antioxidant activity; and uric acid (UA) non-enzymatic antioxidant activity. Data were analyzed by ANOVA, followed by the Student-Newman-Keuls test, Pearson and Spearman correlation coefficients, and multivariable linear regression (p<0.05). TP, TAC, SOD enzymatic antioxidant activity, and UA non-enzymatic antioxidant activity increased with caries severity, consequently reducing salivary oxidative damage. It was concluded that higher caries severity increases salivary antioxidant system activity, with consequent reduction in salivary oxidative damage.

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Sources of free radicals and oxidative stress in the oral cavity

Cited by 135 publications

References 118 publications

A Case-Control Study of Salivary Redox Homeostasis in Hypertensive Children. Can Salivary Uric Acid be a Marker of Hypertension?

A Case-Control Study of Salivary Redox Homeostasis in Hypertensive Children. Can Salivary Uric Acid be a Marker of Hypertension?

Association between p62 expression and clinicopathological characteristics in oral leukoplakia

Carious Lesion Severity Induces Higher Antioxidant System Activity and Consequently Reduces Oxidative Damage in Children’s Saliva

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