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Objective: Obesity involves excessive lipid accumulation in adipose tissue, triggering oxidative stress and DNA damage. This study evaluated the effects of verbascoside doses (50 μM: V50 and 100 μM: V100) on DNA damage and oxidative stress in mature adipocytes.Materials and Methods: 3T3-L1 cells were differentiated into mature adipocytes and treated with V50 or V100. Oil Red O staining quantified the lipid accumulation. DNA damage was evaluated using the Comet assay. We assessed oxidative stress by calculating the oxidative stress index (OSI) based on total oxidant status (TOS) and total antioxidant status (TAS) measurements.Results: V100 reduced lipid accumulation compared with the control group. Furthermore, while V50 increased DNA damage (tail intensity and moment), V100 significantly lowered it compared to V50. Additionally, V100 improved oxidative stress markers (increased TAS, decreased TOS, and OSI), whereas V50 had no significant effect on these parameters.Conclusion: Verbascoside showed dose-dependent effects on mature adipocytes. While V50 increased DNA damage independently of oxidative stress, V100 improved oxidative status and reduced DNA damage. These findings demonstrate that at appropriate doses, verbascoside is a candidate for preventing metabolic disorders, though further molecular studies are needed.

Purpose: Recent studies have shown promising outcomes in the utilization of natural, non-toxic polyphenols with fat-burning properties to combat obesity. The aim of this study was to investigate the changes in the gene expression profile of hypertrophic 3T3-L1 adipocytes in response to Verbascoside (VB) treatment and the mRNA levels of 5' AMP-activated protein kinase (AMPK), peroxisome proliferator-activated receptor gamma (PPAR-γ), hormone-sensitive lipase (HSL), and lipid droplet-associated protein (perilipin1, PLIN1), which play an important role in fat metabolism. Materials and methods: For this purpose, 3T3-L1 preadipocytes were differentiated and hypertrophied. Triglyceride accumulation in the cells was evaluated using Oil Red O staining. The hypertrophic 3T3-L1 cells were incubated with VB for 48 h. Results: Microarray analysis at the end of this period showed that VB increased the mRNA levels of many proteins involved in lipolysis processes, but did not change the expression of PPARγ, AMPK, HSL and PLIN1. Therefore, we confirmed by RT-PCR that PPARγ, AMPK, HSL, and PLIN1 expression levels were altered by VB treatment. Our results showed that VB treatment caused a significant increase in the expression of genes involved in lipolytic processes compared to the control. Conclusion: The findings of this study suggest that VB may play an active role through important intracellular proteins involved in lipolytic processes.

Purpose: The purpose of this study was to ascertain how radioactive iodine therapy (RAIT). affected the DNA damage in the lymphocytes of differentiated thyroid cancer (DTC) patients. Materials and Methods: Our study included 21 DTC patients in total, with a mean age of 45.09±10.02 years. Six (28.6%) of the 21 patients had a low dose of RAIT (≤30 mCi), eleven (52.4%) received a moderate dose of ablation (31 to 100 mCi), and four (%19) received a high dose (>100 mCi). Before, one week, and six months following treatment, venous blood samples were obtained from each patient. DNA damage was evaluated using the COMET assay. For a quantitative analysis of DNA damage, a number of characteristics were assessed, including head length, tail length, head intensity, tail intensity, and tail moment. Results: Compared to before treatment (23.83±9.82), tail intensity levels were considerably lower after treatment (1st week and 6th months) (18.30±6.48 vs. 18.06±5.58). Following therapy (1st week and 6th months), the head intensity values were statistically substantially higher (81.69±6.48 vs. 81.93±5.58) than they were prior to treatment (76.16±9.82). Six months after therapy, the tail moment was lower than it was before treatment (5.24±2.51 vs. 8.04±3.86). Conclusion: Treatment has a beneficial effect on peripheral blood cells, as seen by the increase in head intensity and decrease in tail intensity and moment after treatment. By triggering repair mechanisms, RAIT may have activated protective effects on the DNA of lymphocytes.

Previous studies reported that WBV can increase peripheral blood flow and oxygenation. Investigating the acute effects of a single WBV exercise session on hemorheological parameters, blood glucose levels, balance, flexibility, and oxidative stress markers (total oxidant status [TOS], total antioxidant status [TAS], and oxidative stress index [OSI]) was the goal of this study. All participants engaged in a WBV exercise program consisting of nine exercises, each lasting 60 seconds, for a total of 13 minutes. Flexibility, balance, visual analog pain scale (VAS) scores, heart rate, blood pressure, capillary blood glucose levels, hemorheological parameters, and TOS/TAS were assessed before and immediately after the WBV session. Twelve healthy active male volunteers (mean age: 20.83±2.59 years; mean height: 174.79±5.26 cm; mean weight: 79.21±14.87 kg) participated in the study. Hematocrit values and heart rate significantly increased, while blood glucose levels decreased following the WBV protocol (p

Purpose: S-sulfocysteine (SSC), a toxic byproduct of sulfur-containing amino acid metabolism, accumulates in conditions such as molybdenum cofactor deficiency (MoCD) and isolated sulfite oxidase deficiency (iSOD), leading to severe neurodegeneration. Despite evidence of SSC's neurotoxicity, the apoptotic mechanisms it triggers remain unclear, particularly in different brain regions. This study aimed to investigate the region-specific apoptotic pathways induced by SSC in hippocampal HT-22 and primary cortical neurons, focusing on caspase-dependent and -independent mechanisms. Materials and methods: Neuronal cells were treated with increasing doses of SSC, and cell viability, glutathione (GSH) levels, and apoptosis-related proteins (AIF, calpain, cytochrome c, caspase-3) were assessed using CCK-8 assay, GSH enzymatic assay, and ELISA. The protective effects of specific inhibitors targeting AIF, calpain, and cytochrome c were also evaluated. Results: SSC reduced cell viability in both neuronal types with half-maximal lethal dose (LD50) values of 150 μM (HT-22) and 155 μM (cortical neurons). In both models, SSC elevated AIF and calpain levels, whereas cytochrome c and caspase-3 were significantly increased only in cortical neurons. GSH levels initially rose at 2–8 hours and declined by 16 hours. Inhibitors of AIF, calpain, and cytochrome c partially restored viability, with combined administration offering the most robust protection. Conclusion: SSC induces both caspase-independent and caspase-dependent apoptosis in a region-specific manner: HT-22 cells predominantly activate AIF and calpain, while cortical neurons engage additional cytochrome c and caspase-3 pathways. These findings suggest distinct molecular vulnerabilities and offer potential targets for therapeutic intervention in sulfite-related neurodegenerative diseases.

Purpose: The present study evaluates the levels of oxidative stress and DNA damage in patients diagnosed with acute myeloid leukemia (AML; newly diagnosed patients and patients in remission) compared to healthy controls. Materials and methods: A total of 96 participants were enrolled into this study in three groups: 32 newly diagnosed AML patients, 32 patients in remission, and 32 age- and sex-matched healthy individuals. Various laboratory analyses were conducted to measure biochemical parameters, total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), and DNA damage using the comet assay. Results: We showed that while TOS levels did not differ significantly between the groups, both the newly diagnosed and remission groups exhibited higher OSI levels compared to controls. TAS levels were notably lower in the remission group, suggesting decreased antioxidant capacity. The comet assay demonstrated significantly elevated DNA damage in the newly diagnosed AML group, followed by the remission group, relative to healthy controls. These findings highlight an increased oxidative stress burden and genotoxicity in AML patients, which may contribute to disease pathophysiology. Furthermore, the results suggest that the oxidative stress and DNA damage are more pronounced in newly diagnosed patients compared to those in remission. Conclusion: The study showed that the oxidative stress and DNA damage observed in AML patients, particularly at diagnosis, could play a role in the progression and recurrence of the disease, suggesting potential prognostic value for oxidative stress markers in AML management.

Objective: Obesity disrupts the homeostasis of adipose tissue, leading to an increase in the number and size of adipose cells. Many positive effects of quercetin polyphenol on health through various mechanisms are known in the literature. The aim of our study was to investigate the effects of quercetin on lipid accumulation and adiponectin levels in mature and hypertrophic adipocytes. Materials and methods: In this study, differentiated preadipocyte cells were exposed to high glucose media for 8 days to generate mature adipocytes, then for 18 days to produce hypertrophic adipocytes. Quercetin (40 and 80 µM) was administered to mature adipocytes for 24 hours and to hypertrophic adipocytes for 48 hours. Lipid content was visualized by Oil-Red-O staining method. Lipid accumulation and adiponectin level were measured by ELISA method. For statistical analysis; one-way analysis of variance (post hoc: Tukey test) was used for independent group comparisons and Wilcoxon paired two-sample test was used for dependent group comparisons. p≤0.05 was considered statistically significant. Results: The administration of quercetin to mature adipocytes significantly reduced lipid accumulation (p≤0.05). The administration administration of 80 µM quercetin in mature adipocytes caused a significant increase in adiponectin levels (p≤0.05). Administration of quercetin to hypertrophic adipocytes caused a significant decrease in adiponectin levels (p≤0.05). Conclusion: Our study revealed that quercetin decreased lipid accumulation and increased adiponectin levels in mature adipocytes. However, in hypertrophic adipocytes, quercetin had no significant effect on lipid accumulation and decreased adiponectin levels. These findings suggest that quercetin has protective effects on health in the early stages of obesity, but its efficacy is limited in the later stages of obesity.

Purpose: Metabolic syndrome (MetS) is a health condition characterized by obesity, insulin resistance, dyslipidemia and type 2 diabetes (T2DM). This study aimed to assess the effects of quercetin, a natural flavonoid on MetS induced by fructose in Sprague Dawley rats. Materials and methods: The rats, aged 8-10 weeks, were divided into 4 groups: control (C) group, metabolic syndrome (MetS) group, control+quercetin (C+Q) group, and metabolic syndrome+quercetin (MetS+Q) group. The MetS groups received a 20% fructose solution in drinking water for a duration of 10 weeks. For the last 4 weeks of the study, rats in the Q groups were administered 50 mg/kg/body weight quercetin. After 10 weeks, serum samples were tested using ELISA for Triglycerides (TG), High-Density Lipoprotein (HDL), fasting insulin, resistin, (Interleukin 6) IL6, Tumor Necrosis Factor-alpha (TNF-α), leptin, C-Reactive Protein (CRP) and, adiponectin (ADP). The body weights, Lee index and HOMA-IR scores were also measured. Results: Fructose-fed rats showed significant increases in body weight, Lee index, HOMA-IR scores and, fasting insulin with significant decrease in HDL compared to controls. In MetS group, ADP levels were significantly lower compared to control group. In MetS+Q group, there was a tendency for reduced levels of resistin, IL-6, and leptin compared to the untreated MetS group. Conclusion: These findings suggest that quercetin may be beneficial in managing MetS, though further research is needed to explore its mechanisms and effectiveness.

Objective: Chronic Obstructive Pulmonary Disease (COPD) is a common, preventable, curable disease characterized by persistent airflow limitation, respiratory symptoms due to airway and/or alveolar abnormalities caused by severe exposure to harmful particles, gases. During the endobronchial coil treatment (EBCT) process, the volume of the lung parenchyma is reduced by shrinking the elastic recoil. Although there are studies showing worsening of hemorheological parameters in COPD exacerbations, no study investigated whether hemorheological parameters are improved after coil. The aim of this study was to assess the effects of coil therapy on erythrocyte deformability, whole blood viscosity (WBV) measured at autologous, standard (40%) hematocrit and plasma viscosity (PV) in COPD patients. Material and methods: Venous blood samples were taken once from the healthy control group (n=17) and before and 1 month after the treatment from the COPD patients who had been indicated for coil according to GOLD guidelines (n=20). To assess erythrocyte deformability, shear-dependent erythrocyte elongation was measured at 0.3-3.0 Pa by an ektacytometer (LORCA), while WBV, PV were measured using a rotational viscometer. Results: Erythrocyte deformability measured at shear stresses between 0.3-5.33 Pa were found to be higher following treatment compared to pre-coil values. EBCT did not have a statistically significant effect on WBV measured at autologous, 40% hematocrit, PV and oxidative stress indices. Conclusion: Increased erythrocyte deformability determined following EBCT at the shear stresses observed at the pulmonary level is a favourable finding, showing that the procedure may positively affect the hemodynamics of COPD patients as well as causing clinical improvement.

Purpose: Chronic lymphocytic leukemia (CLL) is the most seen type of leukemia in adults. There are few biomarkes that are used for better understanding how oxidative stress is involved in the pathophysiology of hematologic malignency.We aimed to oxidative stress, DNA damage and erythrocyte membrane lipid profile in CLL patients in this study. The study is included 38 CLL patients and 38 age-sex matched controls. Materials and method: Total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), DNA damage examination with Comet assay, serum 8-OHdG measurement and gas chromatographic analysis were performed between the case and control groups. Results: It was observed that TOS and OSI values were higher in the case group than in the control group (p=0.014 and p=0.022, respectively). DNA damage measured by Comet method was found to be increased in the case group (p0.05). Conclusion: It has been shown that CLL patients had higher oxidant capasity as consequence. Oxidative stress and DNA damage are increased in CLL patients in this study. It is early to evaulate on erythrocyte membrane lipid profile in CLL patients. However, the study can be ligthed the way future studies on the subject.