The immediate cause of the occurrence of cataract is unknown, but oxidative damage and effects of reactive oxygen species are considered important in its etiopathogenesis. Our research was aimed at testing the nonenzyme antioxidant power of corticonuclear lens blocks, with different types and different maturity of age-related cataract. Clinical and biochemical researches were carried out in 101 patients with age-related cataract. In corticonuclear lens blocks of the patient, the concentration of nonprotein and total-SH groups and the concentration of total vitamin C and dehydroascorbic acid (DHA) were determined; the current redox balance of dehydroascorbate/ascorbate and total antioxidant power measured by ferric-reducing ability were examined. In corticonuclear lens blocks with incipient cataract a significantly higher concentration of GSH, total SH groups, concentration of total vitamin C and ascorbic acid (AA), and ferric-reducing ability were measured. The measured concentration of DHA is higher than the concentration of AA in the lenses with the incipient and mature cataract. The concentration ratio of redox couple DHA/AA is higher in lenses with mature cataract, where the measured concentration of AA was lower than in the incipient cataract. Timely removal of DHA from the lens is important because of its potential toxicity as an oxidant. An increase of the current concentration of DHA/AA redox balance can be an indicator of oxidative stress.

This study investigated the relationship between serum xanthine oxidase (XOD) activity and the occurrence of diabetic peripheral neuropathy (DPN) in type 2 diabetes mellitus (T2DM) patients. Serum XOD activity, ischemia-modified albumin (IMA), uric acid (UA), albumin, glycated hemoglobin (HbA1c), advanced glycation end products (AGE), total free thiols, atherogenic index of plasma (AIP), and body mass index (BMI) were measured in 80 T2DM patients (29 with and 51 without DPN), and 30 nondiabetic control subjects. Duration of diabetes, hypertension, medication, and microalbuminuria was recorded. Serum XOD activities in controls, non-DPN, and DPN were5.7±2.4 U/L,20.3±8.6 U/L, and27.5±10.6 U/L (p<0.01), respectively. XOD activity was directly correlated to IMA, UA, BMI, HbA1c, and AGE, while inversely correlated to serum total free thiols. A multivariable logistic regression model, which included duration of diabetes, hypertension, AIP, HbA1c, UA, and XOD activity, revealed HbA1c [OR = 1.03 (1.00–1.05);p=0.034] and XOD activity [OR = 1.07 (1.00–1.14);p=0.036] as independent predictors of DPN. Serum XOD activity was well correlated to several other risk factors. These results indicate the role of XOD in the development of DPN among T2DM patients.

Introduction. Reduced compound glutathione (GSH) in the lens has the function to protect the thiol group of lens proteins, and as a substrate of glutathione peroxidase (GPx) and glutathione S-transferase (GST). Protein containing thiol groups is significant for the normal function of lens epithelium, i.e. enzymes Na-K-ATP-ase, thus influencing cell permeability. The relationship GSH/GSSG (oxidized glutathione) is normally high in the lens and other ocular tissue owing to the glutathioneredox cycle, which is localized in the lens epithelium and cortex surface. Objective. The aim of the study was to investigate non-enzymic factors of the antioxidant protection of non-protein and protein tiol, as well as to determine glutathione-dependent enzyme activity in the corticonuclear blocks of lenses in patients with senile cataract. Methods. Biochemical studies of lens were carried on 101 patients with senile cataract. According to cataract maturity degree, the patients were classified into two groups: senile incipient cataract (N=41) and mature senile cataract (N=60). GSH concentration was determined by Ellman?s reagent. GPx activity was assayed with cumene hydroperoxide, and that of glutathione S-transferase by follow-up of glutathione conjugation and 1-chloro-2.4-dinitrobenzene rates. Results. A significantly higher GSH concentration was found in the corticonuclear blocks of lenses with initial as related to mature cataract (p<0.001). The activity of enzyme GPx and GST was considerably higher in the corticonuclear blocks of lenses with initial cataract (p<0.001). With cataract progression, the quantity of available GSH, necessary for GPx and GST functioning, declined, so that the activity of these enzymes was also significantly decreased in mature cataract. Conclusion. The determined lower GSH concentration and antioxidant enzyme activity in corticonuclear blocks of lenses, particularly in cataract with a nuclear component, indicate the weakened antioxidant response of lens tissue during the development of senile cataract.

Oral mucosal repair is a redox-regulated process that may be impaired by diabetes, chronic inflammation, infection, and chemotherapy- or radiotherapy-induced oral mucositis. Reactive oxygen species (ROS) support host defense, epithelial migration, angiogenesis, extracellular matrix remodeling, and adaptive repair when their production is transient and compartmentalized. In contrast, persistent ROS promote lipid, protein, and DNA oxidation, mitochondrial dysfunction, and extracellular matrix damage. Photobiomodulation (PBM) is increasingly used to support oral tissue repair, but its effects should be interpreted as dose- and context-dependent redox modulation rather than as simple antioxidant activity. This narrative review synthesizes oxidative stress biomarkers and redox-sensitive pathways relevant to oral mucosal repair and PBM, including oxidant–antioxidant balance, lipid and protein oxidation, oxidative DNA damage, antioxidant defense, thiol/disulfide homeostasis, mitochondrial and NADPH oxidase-derived ROS, Nrf2/HO-1, NF-κB, HIF-1α/VEGF, MAPK/ERK, PI3K/Akt, and MMP/TIMP signaling. The review emphasizes the distinction between transient mitochondrial ROS/nitric oxide signaling and sustained NADPH oxidase-driven oxi-inflammatory stress. It proposes a practical redox-guided framework for biomarker selection, PBM response interpretation, and future study design, while noting that this framework remains conceptual and is not yet a validated clinical decision algorithm.