The administration of SkQ1 to rats at the dose of 50 nmol/kg for five days significantly increased the mRNA levels of transcription factor Nrf2 and of Nrf2-controlled genes encoding antioxidant enzymes SOD1, SOD2, CAT, and GPx4, whereas changes in the level of mRNA of SOD3 in the cerebral cortex of the rat brain were not significant. This was accompanied by activation of antioxidant enzymes (SOD, CAT, GPx, and GST) and increase in reduced glutathione concentration. Under oxidative stress induced by hyperoxia (0.5 MPa for 90 min), the mRNA level of transcription factor Nrf2 decreased, whereas changes in the transcriptional activity of Nrf2-induced genes (SOD1-3, CAT, GPx4) encoding antioxidant enzymes in the cortex of the rat brain hemispheres were insignificant. Under conditions of hyperoxia, lipid peroxidation intensity was increased, CAT was inhibited, and GST activity was moderately increased, whereas SOD and GPx activities in the rat brain cerebral cortex remained at the stationary level. Pretreatment with SkQ1 before the exposure to hyperbaric oxygenation led to an increase in mRNA level of transcription factor Nrf2 and of Nrf2-induced genes (SOD1-2, CAT, and GPx4) encoding antioxidant enzymes, whereas SOD3 expression in the cerebral cortex of the rat brain under oxidative stress was not changed. Concurrently, we observed an increase in activities of these antioxidant enzymes (SOD, CAT, GPx, and GST) and in level of reduced glutathione. We hypothesize that the protective effect of SkQ1 under hyperoxia-induced oxidative stress could be realized via direct antioxidant activity and through stimulation of the signaling defense system Keap1/Nrf2/ARE.

This work aimed to study the toxic implications of zinc oxide nanoparticles (ZnO NPs) on the physio-biochemical responses of spring barley (Hordeum sativum L.). The experiments were designed in a hydroponic system, and H. sativum was treated with two concentrations of ZnO NPs, namely 300 and 2000 mg/L. The findings demonstrated that ZnO NPs prevent the growth of H. sativum through the modulation of the degree of oxidative stress and the metabolism of antioxidant enzymes. The results showed increased malondialdehyde (MDA) by 1.17- and 1.69-fold, proline by 1.03- and 1.09-fold, and catalase (CAT) by 1.4- and 1.6-fold in shoots for ZnO NPs at 300 and 2000 mg/L, respectively. The activity of superoxide dismutase (SOD) increased by 2 and 3.3 times, ascorbate peroxidase (APOX) by 1.2 and 1.3 times, glutathione-s-transferase (GST) by 1.2 and 2.5 times, and glutathione reductase (GR) by 1.8 and 1.3 times in roots at 300 and 2000 mg/L, respectively. However, the level of δ-aminolevulinic acid (ALA) decreased by 1.4 and 1.3 times in roots and by 1.1 times in both treatments (nano-300 and nano-2000), respectively, indicating changes in the chlorophyll metabolic pathway. The outcomes can be utilized to create a plan of action for plants to withstand the stress brought on by the presence of NPs.

The identification of biomarkers of post-traumatic osteoarthritis (PTOA) progression is of clinical importance. The aims of this study were: (1) to assess the abilities of various soluble proinflammatory mediators in plasma to distinguish patients with knee PTOA from controls; (2) to determine the correlations between the mediators in plasma and those mediators in synovial fluid (SF); and (3) to explore the associations of the mediators with radiographic PTOA severity. The concentrations of IL-1β, IL-6, IL-18, TNFα, and leptin were measured using ELISA. Nitric oxide was determined as nitrite/nitrate (NO x ) using the Griess reaction. We included 171 subjects (134 PTOA patients and 37 controls) and excluded patients with rheumatoid arthritis or gout. The ROC curve of plasma NO x had the highest AUC, a specificity of 100%, and a sensitivity of 84.4%. The combination of IL-6 and leptin proved to be the most discriminatory, with an AUC value of 0.933, a specificity of 96.7%, and a sensitivity of 85.7%. The levels of NO x , IL-6, IL-18, and leptin in plasma were significantly correlated with their levels in SF. Leptin levels in both plasma (p = 0.036) and SF (p = 0.041) and the synovial IL-18 level (p = 0.045) were correlated with the Kellgren–Lawrence (KL) grade. Early-stage PTOA (KL 1–2) was associated with a high concentration of IL-1β in plasma before and after (OR 6.235, 95% CI 1.362 to 28.552, p = 0.018) adjusting for age, gender, and BMI. Circulating NO x level and a combination of IL-6 and leptin permitted the strongest discrimination of patients with PTOA from controls. PTOA severity was correlated with leptin levels in plasma and SF and with the synovial IL-18 level. Early PTOA was associated with the circulating level of IL-1β. III (case–control study).

The study demonstrated that oxidative stress induced by hyperoxia (0.5 MPa for 90 min) resulted in reduction of mRNA levels of transcription factor Nrf2 and Nrf2-induced genes encoding antioxidant enzymes (SOD1, CAT, GPx4) in peripheral blood leukocytes of rats. The changes in gene expression profiles under hyperoxia were accompanied by disbalance of activity of antioxidant enzymes in the leukocytes, namely activation of superoxide dismutase and inhibition of catalase, glutathione peroxidase, and glutathione-S-transferase. Pretreatment of rats with SkQ1 (50 nmol/kg for five days) significantly increased mRNA levels of transcription factor Nrf2 and Nrf2-induced genes encoding antioxidant enzymes SOD2 and GPx4 and normalized the transcriptional activity of the SOD1 and CAT genes in the leukocytes in hyperoxia-induced oxidative stress. At the same time, the activity of catalase and glutathione peroxidase was increased, and the activity of superoxide dismutase and glutathione-S-transferase returned to the control level. It is hypothesized that protective effect of SkQ1 in hyperoxia-induced oxidative stress can be realized via a direct antioxidant property and the stimulation of the Keap1/Nrf2 redox-sensitive signaling system.

ЦЕЛЬ ИССЛЕДОВАНИЯ Изучение связи показателей окислительного стресса и клинических изменений у пациентов с нейродегенеративным паркинсонизмом и выделение клинико-биохимических подтипов заболевания. МАТЕРИАЛ И МЕТОДЫ В исследование включены 109 человек, из них 91 пациент с нейродегенеративным паркинсонизмом (72 пациента с болезнью Паркинсона (БП), 10 — с мультисистемной атрофией (МСА), 9 — с кортикобазальной дегенерацией; средний возраст — 61,1±7,2 года) и 18 клинически здоровых людей, средний возраст — 55,1±9,2 года. Для оценки редокс-статуса в периферической крови пациентов с БП и здоровых лиц определяли показатели окислительного стресса. Определение биохимических показателей проводили в эритроцитах и мононуклеарной фракции крови. Оценивалась активность глутатионредуктазы (GR) и миелопероксидазы (MPO), содержание восстановленного глутатиона. РЕЗУЛЬТАТЫ И ЗАКЛЮЧЕНИЕ Окислительный стресс является универсальным механизмом и наблюдается при многих нейродегенеративных заболеваниях. Тем не менее возможно выявить достаточно характерные изменения редокс-баланса с выделением групп и их корреляций с определенными подтипами и течением БП, что дает возможность проводить дифференциальный диагноз с атипичным паркинсонизмом.