Objective(s): Dietary supplementation combined with exercise may potentiate the beneficial effects of exercise by reducing exercise-induced oxidative stress and improving mitochondrial quality and capacity. In this study, the effects of creatine monohydrate (CrM) supplementation with low and high -intensity exercise on mitochondrial biogenesis regulators, Nrf2 anti-oxidant signaling pathway and muscle damage levels were investigated. Materials and Methods: Balb/c male mice were divided into six experimental groups: control, control+CrM, high-intensity exercise, high-intensity exercise+CrM, low-intensity exercise, and low -intensity exercise+CrM. Mice were given CrM supplementation and at the same time, low and high -intensity exercise was applied to the groups on the treadmill at 30min/5day/8week. Then, mitochondrial biogenesis marker (PGC-1 alpha, NRF-1, TFAM), Nrf2 and HO-1 protein expressions, total oxidant -anti-oxidant status level, and histopathological changes were investigated in serum and muscle tissue. Results: Exercise intensity and CrM supplementation were found to be effective factors in mitochondrial biogenesis induction via the PGC-1 alpha signaling pathway. Nrf2 and HO-1 protein levels increased with exercise intensity, and this result was directly related to serum oxidative stress markers. In addition, CrM supplementation was effective in reducing exercise-induced muscle damage. Conclusion: This combination induced skeletal muscle adaptations, including mitochondrial biogenesis and enhanced anti-oxidant reserves. This synergistic effect of dietary supplementation with low-intensity exercise may be valuable as a complement to treatment, especially in diseases caused by mitochondrial dysfunction.

Purpose: Generalized Anxiety Disorder (GAD) is a chronic disease persisting for at least 6 months, characterized by excessive and continuous anxiety, which leads to evident problems and functional disorders. S100B is a glial protein that plays a role in intercellular communication regulating cell growth and differentiation, and intracellular signal transmission. This study aimed to analyze the serum S100B, 8-OHdG, and oxidative stress levels of patients newly diagnosed with GAD who had not started treatment, to better understand the underlying neurobiological basis of the etiology of GAD. Patients and Methods: Forty-four patients diagnosed with GAD according to DSM-5 diagnostic criteria and 44 healthy controls were included in the study. The Beck Anxiety Inventory (BAI) was used to determine the anxiety levels of the GAD patients. The serum S100B, 8-OHdG, total oxidant status (TOS), and total antioxidant status (TAS) levels were measured in the patient and control groups. Results: The 8-OHdG values of the GAD group were determined to be statistically significantly higher than those of the control group (p=0.028). No significant difference was determined between the GAD patients and the control group in respect of the TAS, TOS, and oxidative stress index (OSI) values (p> 0.05). The S100B levels of the GAD group were found to be higher than those of the control group. Conclusion: The results of this study showed that there could be DNA damage because of oxidative stress in GAD patients. There is a need for further studies to confirm the role of S100B protein in GAD etiology and pathogenesis.

Acute carbon monoxide (CO) poisoning may cause liver damage and liver dysfunction. Therefore, in this study, we aimed to compare the efficiency of normobaric (NBO) and high flow nasal cannula oxygen (HFNCO) treatments on liver injury. For that purpose, twenty-eight male Wistar albino rats were divided into four groups (Control, CO, CO + NBO, CO + HFNCO). The control group was allowed to breath room air for 30 min. Acute CO poisoning in CO, CO + NBO, CO + HFNCO was induced by CO exposure for 30 min. Thereafter, NBO group received 100% normobaric oxygen with reservoir mask for 30 min. HFNCO group received high-flow oxygen through nasal cannula for 30 min. At the end of the experiment, all animals were sacrificed by cardiac puncture under anesthasia. Serum liver function tests were measured. Liver tissue TAS, TOS and OSI levels, tissue histomorphology and immunoexpression levels of Bax, Caspase 3, TNF-α, IL-1β, and NF-κB were also examined. Our observations indicated that acute CO poisoning caused significant increases in blood COHb, serum AST, ALT, ALP, total protein, albumin, globulin levels but a decrease in albumin to globulin ratio (all, p < 0.05). Furthermore, acute CO poisoning significantly increased the OSI value, and the immunoexpresssion of Bax, Caspase 3, TNF-α, IL-1β, and NF-κB in liver tissue (all, p < 0.05). These pathological changes in serum and liver tissue were alleviated through both of the treatment methods. In conclussion, both the NBO and HFNCO treatments were beneficial to alleviate the acute CO poisoning associated with liver injury and dysfunction.

Background and Objectives: Migraine is a leading cause of disability worldwide, with complex pathophysiological mechanisms involving oxidative and nitrosative stress. Recent research suggests that Indole-3-Propionic Acid (IPA) may have a neuroprotective role in reducing nitrosative stress. This study aims to elucidate the roles of IPA and nitrosative stress biomarkers in migraine patients, focusing on their potential as therapeutic targets. Materials and Methods: This cross-sectional, case-control study included 57 migraine patients and 30 healthy controls. Patients were categorized into episodic migraine (EM) and chronic migraine (CM) groups. Socio-demographic and clinical characteristics were documented through structured interviews. Validated scales such as the Visual Analog Score (VAS), Headache Impact Test 6 (HIT-6), Migraine Disability Assessment Test (MIDAS), Migraine 24 h Quality of Life Scale (24 h QoL), Mini-Mental State Examination (MMSE), and Migraine Attacks–Subjective Cognitive Impairments Scale (Mig-SCog) were administered. Venous blood samples were collected, and serum levels of IPA, Nitric Oxide (NO), Nitric Oxide Synthase (NOS), and Peroxynitrite (ONOO⁻) were measured using ELISA and spectrophotometric methods. Results: Significant differences in serum IPA and NO levels were observed between migraine patients and controls. Specifically, higher serum IPA levels were found in the EM group, while higher serum NO levels were observed in the CM group. Elevated NO levels correlated with increased migraine attack frequency. Conversely, serum IPA levels showed a negative correlation with attack frequency, suggesting a protective role. Specifically, NO levels were positively correlated with the number of painful days, NSAID usage, VAS scores, HIT-6 scores, and MIDAS scores, while negatively correlated with 24 h QoL scores. Conclusions: The study highlights the significant involvement of IPA and nitrosative stress in migraine pathophysiology. Elevated IPA levels, particularly in EM patients, suggest its potential neuroprotective role. These findings underscore the importance of targeting oxidative and nitrosative stress pathways in developing effective migraine therapies.

Introduction: Evaluation of the prognosis in the early period of intensive care patients and arranging the treatment accordingly is of vital importance. In the present study, we investigated whether serum thiol/disulphide concentration can be used in the follow-up of prognosis in the early period in patients with COVID-19 under intensive care. Methods: The study included 25 patients [their ages were between 19 and 92; 10 (40%) were male and 15 (60%) were female] who were diagnosed with COVID-19 and treated in the intensive care unit (ICU). The patients were followed for four weeks. On the first, third, and fifth days of intensive care treatment, venous blood samples were taken from the patients to analyze the thiol/disulphide parameters, and coma scores were calculated. Statistical analyses were conducted to evaluate the relationship between thiol/disulphide levels and the prognosis of COVID-19 patients. Results: At the end of the four-week follow-up of the patients included in the study, 9 were discharged and 16 died. In patients who died, the relationship between thiol/disulphide homeostasis parameters and coma scores was not statistically significant. Meanwhile, in discharged patients, the relationship between disulphide concentration, total thiol, and coma scores was statistically significant. Conclusion: The relationship between thiol/disulphide homeostasis and coma scores in COVID-19 patients treated in the intensive care unit may help to evaluate the prognosis of the disease in the early period, thus the effectiveness of medical intervention.

Purpose: A combination of antiepileptic drugs and antioxidants may be an effective treatment by restoring the disrupted redox balance and reducing oxidative stress exposure to neurons. This study aims to evaluate the effects of valproate and vitamin B12 on oxidative stress in an experimental epilepsy model induced by penicillin when administered alone or in combination. Patients and Methods: 35 male Wistar rats were used in this study. The rats were divided into five groups, which were saline group, 1 mg/kg, 2 mg/kg Vit B12 groups and Sodium valproate group Sodium valproate + Vit B12 group. The epileptic activity was induced by 500 IU of penicillin injection. Sodium valproate and Vitamin B12 were administered 30 min after penicillin administration. Electrocorticogram recordings were taken for 2 hours post-treatment and serum parameters were assessed for oxidative stress markers using spectrophotometric method. Results: There is statistically significant difference between the groups in total antioxidant status, total oxidant status, and oxidative stress index value (p=0.013; p˂0.001; p˂0.001, respectively). The valproate+vitamin B12 group showed elevated total thiol and native thiol levels, along with reduced disulphide levels, resulting in the lowest OSI value. Conclusion: These findings suggest the combined treatment effectively reduces oxidative stress. This study provides valuable insights into the antioxidant properties of valproate and vitamin B12, positioning them as potential agents for managing epilepsy. Understanding the efficacy and reliability of antioxidant strategies in epilepsy management could contribute significantly to advancements in epilepsy therapeutics.