Effects of acute carbon monoxide poisoning on liver damage and comparisons of related oxygen therapies in a rat model.

Acute carbon monoxide (CO) poisoning may cause liver damage and liver dysfunction. Therefore, in this study, we aimed to compare the efficiency of normobaric oxygen (NBO) and high-flow nasal cannula oxygen (HFNCO) treatments on liver injury. For that purpose, 28 male Wistar albino rats were divided into four groups (Control, CO, CO + NBO, and 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% NBO 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 anesthesia. Serum liver function tests were measured. Liver tissue total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI) levels, tissue histomorphology and immunoexpression levels of Bax, Caspase 3, TNF-α, IL-1ß, and NF-κB were also examined. Our observations indicated that acute CO poisoning caused significant increases in blood COHb, serum aminotransferase (AST), alanine aminotransferase (ALT0, alkaline phosphatase (ALP), total protein, albumin, and 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-1ß, 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 conclusion, both the NBO and HFNCO treatments were beneficial to alleviate the acute CO poisoning associated with liver injury and dysfunction.

An Examination of the Effects of Propolis and Quercetin in a Rat Model of Streptozotocin-Induced Diabetic Peripheral Neuropathy.

The purpose of this study was to reveal the combined effects of propolis (P) and quercetin (Q) against diabetic peripheral neuropathy developing with streptozotocin-induced diabetes in rats. Sixty-four adult male rats were divided into eight equal groups: control, P (100 mg/kg/day), Q (100 mg/kg/day), P + Q (100 mg/day for both), diabetes mellitus (DM) (single-dose 60 mg/kg streptozotocin), DM + P, DM + Q, and DM + P + Q. The rats were sacrificed, and blood and sciatic nerve tissues were collected. Blood glucose and malondialdehyde (MDA) levels increased, while IL-6 and total antioxidant status decreased in the DM group (p = 0.016 and p = 0.047, respectively). Ultrastructural findings showed degeneration of the axon and myelin sheath. The apoptotic index (AI %), TNF-α, and IL-1ß immunopositivity increased significantly in the DM group (p < 0.001). Morphological structures approaching those of the controls were observed in the DM + P, DM + Q, and DM + P + Q groups. Morphometric measurements increased markedly in all treatment groups (p < 0.001), while blood glucose and MDA levels, AI (%), TNF-α, and IL-1ß immunopositivity decreased. In conclusion, the combined effects of propolis and quercetin in diabetic neuropathy may provide optimal morphological protection with neuroprotective effects by reducing hyperglycemia, and these may represent a key alternative supplement in regenerative medicine.

Biological Markers in Newly Diagnosed Generalized Anxiety Disorder Patients: 8-OHdG, S100B and Oxidative Stress.

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.

Assessment of dynamic thiol-disulfide homeostasis in patients with lipoid proteinosis (Urbach-Wiethe syndrome).

OBJECTIVE: Lipoid proteinosis is a rare autosomal recessive genetic dermatological disease that occurs due to the accumulation of hyaline material in the skin and mucous membranes. This study aimed to investigate whether dynamic thiol-disulfide homeostasis is a new marker of oxidative stress in patients suffering from lipoid proteinosis. METHODS: The study group involved 17 patients with lipoid proteinosis and 17 healthy controls with same gender and age. Native thiol, total thiol, disulfide levels, and thiol-disulfide indexes were measured with the fully automated spectrophotometric method described by Erel and Neselioglu, and the results of the two groups were statistically analyzed. RESULTS: Serum total thiol and native thiol levels were significantly lower in lipoid proteinosis group compared to the control group (p=0.020 and p=0.014, respectively). The disulfide levels were found to be higher in lipoid proteinosis group, but there was no significant difference between two groups. CONCLUSIONS: Impaired dynamic thiol-disulfide homeostasis was observed in lipoid proteinosis patients, suggesting that thiol-disulfide homeostasis may have a role in the pathogenesis of this disease.

Dynamic Thiol Disulphide Homeostasis in the Follow-Up of the Prognosis of Patients Treated for COVID-19 in the Intensive Care Unit.

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.

Nitric oxide synthase activity: A novel potential biomarker for predicting Alopecia areata.

BACKGROUND: Alopecia areata is a dermatological disease characterized by nonscarring type hair loss. The cause of Alopecia areata not known exactly but studies support that it has an autoimmune etiology in which oxidative stress play an important role. AIM: This study was conducted to evaluate the level of nitrosative stress in Alopecia areata and to investigate the predictive power of nitrosative stress parameters for Alopecia areata. PATIENTS/METHODS: Thirty patients diagnosed with Alopecia areata, and 30 healthy controls were included in a prospective, cross-sectional study. In both groups, nitric oxide (NO· ), peroxynitrite (ONOO- ), and nitric oxide synthase (NOS) activity as nitrosative stress markers were measured spectrophotometrically in serum samples. The predictive power of nitrosative stress parameters in Alopecia areata and control groups was compared with binary logistic regression and Receiver Operating Characteristic analysis. RESULTS: NO· , ONOO- , and NOS activity were significantly higher in patients with Alopecia areata than in the control group (p = 0.001; p < 0.001; p < 0.001, respectively). A positive correlation was found between the parameters. Significantly, binary logistic regression modeling suggested that increases in NOS (p = 0.003, OR = 1.305, 95% CI = 1.095-1.556) activity were associated with Alopecia areata. CONCLUSION: According to the data obtained from the present study, patients with Alopecia areata were exposed to potent nitrosative stress. In particular, peroxynitrite, which acts as a bridge between reactive oxygen species and reactive nitrogen species, caused the expansion of the oxidative stress cascade. Nitrosative stress might play a role in the etiopathogenesis of Alopecia areata. Nitrosative stress parameters, particularly NOS activity, may be potential markers for Alopecia areata.

Effects of different-intensity exercise and creatine supplementation on mitochondrial biogenesis and redox status in mice.

Objectives: 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-1α, 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-1α 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.

Assessment of dynamic thiol-disulfide homeostasis in patients with lipoid proteinosis (Urbach-Wiethe syndrome)

SUMMARY OBJECTIVE: Lipoid proteinosis is a rare autosomal recessive genetic dermatological disease that occurs due to the accumulation of hyaline material in the skin and mucous membranes. This study aimed to investigate whether dynamic thiol-disulfide homeostasis is a new marker of oxidative stress in patients suffering from lipoid proteinosis. METHODS: The study group involved 17 patients with lipoid proteinosis and 17 healthy controls with same gender and age. Native thiol, total thiol, disulfide levels, and thiol-disulfide indexes were measured with the fully automated spectrophotometric method described by Erel and Neselioglu, and the results of the two groups were statistically analyzed. RESULTS: Serum total thiol and native thiol levels were significantly lower in lipoid proteinosis group compared to the control group (p=0.020 and p=0.014, respectively). The disulfide levels were found to be higher in lipoid proteinosis group, but there was no significant difference between two groups. CONCLUSIONS: Impaired dynamic thiol-disulfide homeostasis was observed in lipoid proteinosis patients, suggesting that thiol-disulfide homeostasis may have a role in the pathogenesis of this disease.