Despite the proven role of oxidative stress in numerous systemic diseases and in the process of aging, little is still known about the salivary redox balance of healthy children, adults, and the elderly. Our study was the first to assess the antioxidant barrier, redox status, and oxidative damage in nonstimulated (NWS) and stimulated (SWS) saliva as well as blood samples of healthy individuals at different ages. We divided 90 generally healthy people into three equally numbered groups based on age: 2–14 (children and adolescents), 25–45 (adults), and 65–85 (elderly people). Antioxidant enzymes (salivary peroxidase (Px), glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase-1 (SOD)), nonenzymatic antioxidants (reduced glutathione (GSH) and uric acid (UA)), redox status (total antioxidant capacity (TAC), total oxidant status (TOS), and oxidative stress index (OSI)), and oxidative damage products (advanced glycation end products (AGE), advanced oxidation protein products (AOPP), and malondialdehyde (MDA)) were evaluated in NWS and SWS as well as in erythrocyte/plasma samples. We demonstrated that salivary and blood antioxidant defense is most effective in people aged 25–45. In the elderly, we observed a progressive decrease in the efficiency of central antioxidant systems (↓GPx, ↓SOD, ↓GSH, and ↓TAC in erythrocytes and plasma vs. adults) as well as in NWS (↓Px, ↓UA, and ↓TAC vs. adults) and SWS (↓TAC vs. adults). Both local and systemic antioxidant systems were less efficient in children and adolescents than in the group of middle-aged people, which indicates age-related immaturity of antioxidant mechanisms. Oxidative damage to proteins (↑AGE, ↑AOPP) and lipids (↑MDA) was significantly higher in saliva and plasma of elderly people in comparison with adults and children/adolescents. Of all the evaluated biomarkers, only salivary oxidative damage products generally reflected their content in blood plasma. The level of salivary redox biomarkers did not vary based on gender.

This study is the first to assess the diagnostic utility of redox biomarkers in patients with colorectal cancer (CRC). Antioxidant barrier (Cu,Zn-superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), uric acid (UA), reduced glutathione (GSH)), redox status (total antioxidant (TAC)/oxidant status (TOS), ferric reducing ability (FRAP)), and oxidative damage products (advanced glycation end products (AGE), advanced oxidation protein products (AOPP), malondialdehyde (MDA)) were measured in serum/plasma samples of 50 CRC patients. The activity of SOD was significantly higher whereas the activity of CAT, GPx and GR was considerably lower in CRC patients compared to the control group (p < 0.0001). Levels of UA, TOS, and OSI and concentrations of AGE, AOPP, and MDA were significantly higher, and the levels of GSH, TAC, and FRAP were considerably lower in CRC patients compared to the healthy controls (p < 0.0001). AUC for CAT with respect to presence of lymph node metastasis was 0.7450 (p = 0.0036), whereas AUC for MDA according to the depth of tumour invasion was 0.7457 (p = 0.0118). CRC is associated with enzymatic/non-enzymatic redox imbalance as well as increased oxidative damage to proteins and lipids. Redox biomarkers can be potential diagnostic indicators of CRC advancement.

Still little is known about the redox abnormalities in patients with nonalcoholic fatty liver disease (NAFLD). The purpose of the study was to find the relationship between enzymatic and nonenzymatic antioxidants, redox homeostasis and oxidative damage in 67-patients with NAFLD. The study population was divided into patients with nonalcoholic fatty liver (early NAFLD, n = 29) and patients with nonalcoholic steatohepatitis (advanced NAFLD, n = 38). Redox biomarkers: enzymatic antioxidants (Cu−Zn-superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR)); nonenzymatic antioxidants and redox status (reduced glutathione (GSH), total antioxidant capacity (TAC)); and oxidative damage products (total oxidant status (TOS), advanced glycation end products (AGE), malondialdehyde (MDA), and DNA/RNA oxidative damage) were determined in the serum / plasma samples. The activity of SOD, GPx, GR and levels of GSH, TOS, AGE, MDA, and DNA/RNA oxidative damage were significantly elevated in early NAFLD and advanced NAFLD group compared to controls (p < 0.001). There was a positive correlation between AGE, TAC and ALT activity (R = 0.34, p = 0.04; R = 0.36, p = 0.03, respectively) in advanced NAFLD group. Interestingly, ROC analysis for AGE showed good discriminatory ratio for patients with minimal steatosis (BARD score 0–1) vs. moderate steatosis (BARD score 2–4), AUC = 0.76. Plasma AGE can be a potential noninvasive biomarker differentiating NAFLD patients.

Oxidative stress is a key pathogenic factor in both neurogenerative and metabolic diseases. However, its contribution in the brain complications of insulin resistance is still not well understood. Therefore, the aim of this study was the evaluation of redox homeostasis and oxidative damage in the hypothalamus and cerebral cortex of insulin‐resistant and control rats. 16 male Wistar rats were divided into two equal groups (n = 8): the control and high fat diet group (HFD). Prooxidant enzymes (xanthine oxidase and NADPH oxidase); enzymatic and nonenzymatic antioxidants [glutathione peroxidase (GPx), glutathione reductase (GR), catalase (CAT), superoxide dismutase‐1 (SOD‐1), and uric acid (UA)]; and oxidative damage products [advanced glycation end products (AGE), 4‐hydroxynonenal (4‐HNE), malondialdehyde (MDA), and 8‐hydroxy‐2 ^′‐deoxyguanosine (8‐OHdG)] as well as the total antioxidant capacity (TAC), total oxidant status (TOS), oxidative stress index (OSI), and total ferric reducing ability of sample (FRAP) were evaluated in the hypothalamus and cerebral cortex as well as serum/plasma of HFD‐fed and control rats. The activity of prooxidant enzymes was significantly increased in the cerebral cortex and hypothalamus of HFD‐fed rats vs. control rats. Additionally, we have showed enhanced antioxidant efficiency in the hypothalamus (↑CAT, ↑UA, ↑TAC, and ↑FRAP) and cerebral cortex (↑GPx, ↑CAT, ↑SOD‐1, ↑UA, ↑TAC, and ↑FRAP) of HFD‐fed rats. All of the oxidative damage markers (AGE, 4‐HNE, MDA, 8‐OHdG, and OSI) were significantly increased in the cerebral cortex of insulin‐resistant rats, while only 4‐HNE and MDA were markedly higher in the hypothalamus of the HFD group. Summarizing, the results of our study indicate an adaptive brain response to the increased production of free radicals under insulin resistance conditions. Despite the increase in antioxidative defense systems, this mechanism does not protect both brain structures from oxidative damages. However, the cerebral cortex is more susceptible to oxidative stress caused by HFD.

Periodontitis is inextricably linked to oxidative-reductive (redox) imbalance. However, little is still known about the resultant ability to scavenge oxygen free radicals in saliva and gingival crevicular fluid in patients with periodontitis. The multitude of enzymatic and non-enzymatic antioxidants and their synergistic effects cause an interest in the evaluation of the total antioxidative capacity. Thus, our study aimed to evaluate the total oxidative and antioxidative activity of gingival crevicular fluid and saliva in the periodontitis, as well as to relate these biomarkers to clinical indices of periodontopathy. Additionally, by calculating the oxidative stress index (OSI), the intensity of redox disturbances was also evaluated. Fifty-eight periodontitis patients were included in the study and divided into two subgroups depending on the severity of the disease. In the non-stimulated/stimulated saliva as well as a gingival crevicular fluid of the study group, we found significantly higher OSI and total oxidant status (TOS) as well as lower total antioxidant capacity (TAC). However, the ability to reduce iron ions (FRAP) was significantly lower only in stimulated and non-stimulated saliva of patients with periodontitis. The examined parameters correlated with the periodontium’s clinical condition, which indicates the exacerbation of the inflammatory process. However, TAC, TOS, OSI, and FRAP did not differentiate individual stages of periodontitis.

This study is the first to assess redox homeostasis in patients with colorectal cancer (CRC) in respect to histopathological parameters associated with the tumour microenvironment such as tumour budding and inflammatory infiltration. Pro-oxidant enzymes (NADPH oxidase (NOX), xanthine oxidase (XO)), antioxidant barrier (Cu,Zn-superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), reduced glutathione (GSH)), redox status (total antioxidant (TAC)/oxidant status (TOS)) and oxidative damage products (advanced glycation end products (AGE), advanced oxidation protein products (AOPP), malondialdehyde (MDA) and 8-hydroxydeoxyguanosine (8-OHdG)) were determined in both the normal and cancerous tissue of 29 CRC patients. The activity of NOX (p < 0.01) and XO (p = 0.01), as well as SOD (p < 0.0001), CAT (p < 0.0001) and TAC level (p < 0.01) were significantly higher in tumour tissue than in normal colon mucosa. Oxidative damage products (AGE—p < 0.01, AOPP—p < 0.001, MDA—p < 0.001, 8-OHdG—p < 0.0001) were also higher in cancerous colon tissue. Furthermore, we observed that CAT (p < 0.05) and XO (p < 0.05) activity depends on the intensity of inflammatory infiltration. Oxidative stress index (OSI) (p < 0.05) and MDA (p < 0.01) values were significantly higher in patients with tumour budding (TB) > 5 versus cases with TB < 5. However, OSI level did not differ significantly between cancer and normal tissue. Our results confirm that CRC is associated with enzymatic/non-enzymatic redox imbalance and increased oxidative damage to proteins, lipids and DNA. The determination of these biomarkers could be useful for the evaluation of the tumour progression.