The aim of this research was to assess lipid peroxidation (LPO) and antioxidative defense (AOD) changes in adolescent boys with obesity using the integral index. Materials and Methods: We examined 19 adolescent boys with obesity of the first degree (the study group). The control group included 23 healthy adolescent boys. The study included the collection of anamnestic data, physical examination, and anthropometric data analysis (body weight (BW), height, waist circumference (WC), hip circumference (HC), and body mass index (BMI)). Laboratory analysis included an assessment of the blood levels of total cholesterol, triglycerides, HDL, LDL, and glucose, as well as the intensity of LPO and AOD in blood plasma and primary and secondary products of LPO. To measure the intensity of OS, the oxidative stress index (OSi) was calculated (the ratio of the LPO-AOD system indicators in the study group to average indicators in the control group). Results: We found a statistically significant increase in BW, BMI, SDS BMI, WC, and HC in the study group compared to the control group. The obese patients had higher values of blood glucose, total cholesterol, triglycerides and LDL compared to the control group. In the study group, we found a significant decrease in the concentration of diene conjugates and an increase in the level of ketodienes and conjugated trienes. The values of α-tocopherol and retinol, and SOD activity were significantly decreased in the study group compared to the control group. There were no statistically significant changes in total antioxidant activity and glutathione status components. According to the data received, the OSi level in the group of obese patients increased approximately 7 times, which confirms the results on the development of antioxidant insufficiency in this pathology.
The emergence of viral respiratory pathogens with high pandemic potential, such as the SARS-CoV-2, poses a serious public health problem, with a very limited arsenal of effective tools and techniques to prevent and treat a new pandemic infection. The literature on the involvement of reactive oxygen species in the pathogenesis of coronavirus infections and the potential for antioxidant therapy was reviewed. Because of available evidence on the involvement of oxidative stress in the mechanisms of initiation and maintenance of homeostasis disorders in SARS-CoV-2, approaches combining reduction of ROS synthesis, inhibition of virus replication, anti-inflammatory action, reduction of hypoxia, and reduction of the toxic effects of drug therapy may be very effective. The hypothesis of the expediency of treating systemic inflammation aimed at "quenching" the cytokine "storm", caused largely by the production of reactive oxygen species, seems essential. In this connection, it is pathophysiologically justified to use for prophylactic and therapeutic purposes antioxidant drugs, which have proven themselves on the example of other viral respiratory infections. Thus, the high activity of preparations of vitamin C, N-acetylcysteine, melatonin, quercetin, glutathione, astaxanthin, polyphenols, polyunsaturated fatty acids, etc. was noted. In addition, these drugs effectively protect the vascular wall, which has been proven for a number of cardiovascular diseases and that can be effective in developing with COVID-19 vasculitis. There is a more pronounced combined effect of these drugs, which is already used in treatment protocols for patients with SARS-CoV-2. Special attention should also be paid to the use of antioxidant drugs as a means to reduce the toxic manifestations of antiviral therapy. Thus, the use of drugs with antioxidant activity can be justified and will certainly improve the effectiveness of the fight against the pandemic of new coronavirus infection.
The aim of this pilot research was to assess the sleep fragmentation influence on amyloid β42 (Aβ42) plasma levels before and after СPAP in patients with obstructive sleep apnea (OSA). Materials and Methods: The study involved 24 patients (mean age of 52.5±2.7 years) with OSA and 20 persons without OSA (mean age of 49.1±8.2 years). All participants underwent overnight polysomnography, The Aβ42 level was determined in blood plasma by an immunoassay method. Patients with OSA were treated with auto-CPAP for 3 months. Results: The research showed the following results in patients with OSA before CPAP, as compared to control: sleep fragmentation 1-2 times, increases in non-rapid eye movement sleep stage by 60% (P<0.05) and arousal index by 55% (P<0.05), and decreases in slow-wave sleep duration by 40% (P<0.05) and rapid-eye-movement sleep by 43% (P<0.05). After CPAPtherapy, a decrease in arousal index by 40% (P<0.05) and apnea/hypopnea index (P<0.05), and increases in oxygen saturation by 17% (P<0.05), the slow-wave sleep duration by 56% (P<0.05) and rapid-eye-movement sleep by 55% (P<0.05) were found. Aβ42 levels were significantly lower in the group with OSA before CPAP-therapy, as compared to the control group and the group with OSA after CPAP-therapy (P<0.05). There were no differences in Aβ42 levels after treatment between control and main group. Conclusion: Moderate and severe OSA is associated with a decrease in Aβ42 plasma level. CPAP-therapy leads to increase this peptide in blood plasma.
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