ABSTRACT Background Polycythemia vera (PV), the most common myeloproliferative neoplasm, is driven by JAK2 mutations and frequently coexists with metabolic syndrome (MS), a major cardiovascular risk factor. Despite overlapping mechanisms, few studies have evaluated oxidative stress as a potential link between PV and MS. Research design and methods This observational case – control study was conducted at a tertiary center between 2017 and 2023. Thirty-six patients diagnosed with PV according to the 2016 WHO (World Health Organization) criteria, including 15 with concomitant MS, and 40 healthy volunteers were enrolled. Patients with abnormal hematologic values, impaired renal or hepatic function, elevated CRP, or confounding comorbidities were excluded. Oxidative stress was assessed by measuring total antioxidant status(TAS) and total oxidant status(TOS) using spectrophotometric assays. Results TOS levels were significantly higher in patients with PV and MS compared to those with PV alone (p < 0.05), and oxidative stress markers overall were elevated in PV – MS patients compared to healthy controls (p < 0.05). No significant differences in TAS or TOS were observed between ELN (European LeukemiaNet) high-risk and low-risk patients, nor between those receiving hydroxyurea, aspirin, metformin, or ACE (angiotensin convertase enzyme) inhibitors and untreated patients (p > 0.05). Conclusions Our findings demonstrate that oxidative stress is markedly elevated in patients with concomitant PV and MS, supporting a pathophysiological link between the two conditions. These results underscore the importance of considering oxidative stress in the clinical evaluation of PV patients with metabolic syndrome.

Tartrazine-induced nephrotoxicity via oxidative and genotoxic pathways in rats: Regulatory insights and the nephroprotective role of curcumin.

Oxidative stress is considered to play a role in the etiopathogenesis of bipolar disorder. This study aimed to compare oxidative stress indicators among bipolar disorder patients in different mood states and healthy controls. The sample included 101 bipolar patients (33 euthymic, 36 depressive, and 32 manic) and 29 healthy controls. Total antioxidant status (TAS), total oxidation status (TOS), superoxide dismutase (SOD), glutathione (GSH), thioredoxin reductase 1 (TrxR1), and peroxiredoxin 1 (PRDX1) levels were measured, along with SOD2 rs4880 and GPX3 rs3792797 single nucleotide polymorphisms (SNPs). Compared to controls, bipolar patients had higher TAS (p = 0.031), TrxR1 (p < 0.001), and PRDX1 (p < 0.001) levels, and lower GSH levels (p < 0.001). No significant group differences were found for TOS (p = 0.776), SOD (p = 0.086), or OSI (p = 0.312). Among mood states, TAS, GSH, TrxR1, and PRDX1 levels did not differ significantly. TrxR1 and PRDX1 showed significant diagnostic performance in distinguishing bipolar disorder (p < 0.001 for both). While GPX3 rs3792797 SNP did not differ between patients and controls, a significant difference was found for SOD2 rs4880, with AA allele carriers exhibiting higher SOD levels. This study is among the few investigating oxidative stress markers across different mood episodes in bipolar disorder and the first to examine TrxR1 and PRDX1. Findings suggest TrxR1 and PRDX1 as potential novel biomarkers in the pathophysiology of bipolar disorder. Not applicable.

Rhinitis is a common upper airway disorder, classified as either allergic rhinitis (AR) or non-allergic rhinitis (NAR). While the association between air pollution and AR airway diseases has been well documented, its specific effects on NAR remain poorly understood. This study aimed to evaluate the seasonal impact of air pollution on pulmonary function, oxidative stress biomarkers, and bronchial hyperresponsiveness in patients with AR, patients with NAR, and healthy controls. In this prospective case-control study, 58 participants (23 AR, 22 NAR, 13 controls) were evaluated during periods of low pollution (summer) and high pollution (winter). Assessments included symptom questionnaires, pulmonary function tests, bronchial provocation tests (BPT), serum total antioxidant status (TAS), and total oxidative status. In the high pollution period, the NAR group exhibited significantly lower TAS levels compared to summer (1.51±0.15, 1.60±0.2, P = 0.041), indicating an increased oxidative stress. A significant decrease in post-bronchodilator forced expiratory volume in 1 second (FEV)1 was also observed in the NAR group, suggesting heightened airway reactivity. The AR group demonstrated a higher frequency of BPT reactivity. Pulmonary function declined across all groups in winter, with the greatest reduction observed in AR patients. Within-group analyses revealed seasonal reductions in both FEV1 and post-BPT FEV1 in AR and NAR groups. Seasonal air pollution exerts phenotype-specific effects on oxidative stress and airway reactivity in rhinitis. AR patients exhibited increased bronchial hyperresponsiveness, whereas NAR individuals showed a marked decline in antioxidant capacity. These findings highlight the importance of phenotype-based monitoring and management during periods of high environmental exposure.

Introduction Symptomatic cerebral vasospasm (CVS) is one of the most severe complications of subarachnoid hemorrhage (SAH) due to ruptured cerebral aneurysms, leading to delayed cerebral ischemia. The pathogenesis of CVS is associated, among other factors, with a deficiency of the endothelial vasorelaxant factor — nitric oxide (NO). Administration of inhaled NO can replenish this deficit and help reduce the severity of CVS; however, clinical data remain limited. Aim To evaluate the feasibility of inhaled nitric oxide (iNO) therapy in patients with signs of symptomatic vasospasm in the acute period of non-traumatic SAH caused by ruptured cerebral aneurysms. Material and methods A case series was carried out involving 9 patients (5 women, 4 men; aged 35–74 years) admitted to the N.V. Sklifosovsky Research Institute for Emergency Medicine in 2022–2024 during the hyperacute period after cerebral aneurysm rupture. The main inclusion criterion was the development of symptomatic CVS resistant to standard therapy (calcium channel blockers, induced hypertension) for at least 1 hour. All the patients underwent microsurgical aneurysm clipping. Inhalation of NO was performed via a face mask using a “Tianox” device at a concentration of 55–80 ppm with FiO₂ 21% until regression of symptoms. Clinical neurological status, jugular venous oximetry, markers of oxidative stress (malondialdehyde (MDA), total antioxidant status (TAS)) and endogenous vascular regulation (nitric oxide metabolites (NOx), angiotensin-converting enzyme (ACE)), video-EEG monitoring and CT perfusion data were assessed. Results Inhalation therapy resulted in regression of symptomatic CVS in 8 of 9 patients, including complete neurological recovery in 5 patients. The mean time to symptom regression ranged from 3 to 21 hours. In 2 patients, premature discontinuation of therapy led to symptom recurrence, requiring resumption of inhalations. CT perfusion on day 7 revealed reversible focal cerebral perfusion deficits in 4 patients. No adverse effects (methemoglobinemia &gt;3.5%, hypotension, toxic NO₂ concentrations) were recorded. Mortality (n=2) was due to extracranial complications. Conclusion Inhaled NO therapy in SAH patients with symptomatic CVS on spontaneous breathing is safe and potentially effective for rapid regression of neurological symptoms and improvement of cerebral perfusion.

The prevalence of diabetes mellitus (DM) is increasing daily worldwide. DM patients suffer from numerous complications, including the development of chronic wounds that can lead to amputation. These complications necessitate innovative approaches. As part of these innovative approaches, this study synthesized four chalcone derivatives and evaluated their activities in an in vitro diabetic wound model. Several spectroscopic techniques, including 1H and 13C NMR and HR-MS, were used to confirm the structures of the newly synthesized compounds. After investigating the inhibition of α-glucosidase in HDF-1 cells treated with D-glucose (50 mM), MTT tests and scratch tests were performed. Tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), total antioxidant status (TAS), and procollagen type-1 were analyzed using an ELISA kit. Additionally, proliferation (Ki67), inflammatory (Nuclear factor kappa B; NFκB), and growth factor (Platelet-derived growth factor subunit A; PDGFA) markers in fibroblasts were assessed by immunohistochemistry. All compounds exhibited strong α-glucosidase inhibitory activity, with IC₅₀ values ranging from 1.115 to 1.612µg/mL. Cytotoxicity analysis demonstrated that all compounds were biocompatible, maintaining over 85% cell viability in HDF-1 cells. Under diabetic conditions, treatment significantly improved cell viability and promoted wound closure, particularly in C4. In addition, the compounds reduced pro-inflammatory cytokines TNF-α and IL-1β while increasing TAS and procollagen type I levels. Immunocytochemical findings revealed enhanced Ki67 and PDGFA expression and decreased NFκB activation in treated groups. Molecular docking analysis supported the experimental findings by demonstrating favorable binding interactions with α-glucosidase. In conclusion, chalcone derivatives-particularly compound C4-promote diabetic wound healing through multitarget mechanisms involving anti-inflammatory, antioxidant, and pro-regenerative effects, highlighting their strong therapeutic potential.

The aim of this study was to investigate the relationship between oxidative stress parameters [total oxidant status (TOS), total antioxidant status (TAS), thiol/disulfide homeostasis, ischemia-modified albumin (IMA)] and serum copper levels in women who use oral contraceptives (OCs) compared to those who do not. This single-center, prospective case-control study included a total of 154 women aged 18 to 45 years (72OC users and 82 non-users) who presented to the gynecology outpatient clinic of a tertiary care training and research hospital. After obtaining written informed consent, demographic data and information regarding OC use were collected. Venous blood samples were drawn and serum samples were stored at -80°C until analysis. Serum levels of TOS, TAS, total thiol, native thiol, disulfide, IMA and copper were measured. A p-value of < 0.05 was considered statistically significant. In OC users, serum levels of copper, TOS, oxidative stress index (OSI), disulfide and IMA were significantly elevated, whereas TAS and native thiol levels were significantly reduced compared to non-users (p < 0.05). Serum copper levels showed a positive correlation with oxidative stress markers and a negative correlation with antioxidant capacity indicators. OC use is associated with increased serum copper levels, which in turn have a significant impact on oxidative stress biomarkers. These findings suggest that OC use elevates systemic oxidative stress while compromising antioxidant defense mechanisms. Moreover, elevated copper levels may independently contribute to oxidative stress regardless of OC use.

The standard method for transporting tissues during limb transplantation and replantation is cold ischemic transport (CIT). However, CIT cannot completely prevent ischemia-reperfusion injury (IRI). As an alternative, extracorporeal perfusion (ECP) methods that provide an adequate metabolic environment for ischemic tissues could be considered. In this study, we investigated the differences between CIT and ECP in terms of their effects on IRI. An ischemia-reperfusion model was used to compare the CIT and ECP groups. This model includes a 6-hour ischemia period followed by a one-hour reperfusion period. Superoxide dismutase, catalase, total antioxidant status, total oxidant status, and total thiol levels in muscle and blood samples were biochemically analyzed to determine oxidative damage levels. TNF-α, NF-κB, and IL-10 levels were measured in the same samples to evaluate the degree of inflammation. Apoptosis was evaluated by measuring the levels of Bax and Bcl-2 proteins in muscle samples. Histopathologic examination was performed for tissue damage and mitochondria were evaluated by Cox staining. It was found that the ECP causes less oxidative and inflammatory damage than the CIT. Bax and bcl-2 levels did not differ between the 2 groups. Biochemical parameters were found to be higher in the CIT group. More mitochondrial damage was observed in the CIT system. ECP caused less inflammatory and oxidative damage compared with CIT. The promising results of our experimental study suggest that the clinical use of extracorporeal circulation machines for extremity transport may reduce histopathologic damage.

Evaluation of biological properties of the light-cured, CAD/CAM milled, and 3D printed dental composites after artificial aging - an in vitro study.

The study aimed to determine the efficacy of quercetin, catechin and genistein in restoring plasma hepatic biomarkers, oxidative indices and histopathological alterations in the liver following cisplatin (cDDP) exposure in Wistar rats. Administration of cDDP (12 mg/kg, IP) significantly (p < 0.05) increased activities of AST, ALT, indirect bilirubin, LDH, and ALP, indicating acute hepatic injury in exposed rats. It reduced (p < 0.05) the hepatic levels of total antioxidant status, total thiols (TTH), and activities of glutathione reductase (GR), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase whereas it increased (p < 0.05) the levels of malondialdehyde and advanced oxidation protein product. These observations were further corroborated by the intensity of histopathological changes in the liver of treated animals as compared to controls. Increased levels of TTH and restored hepatic GPx, GR, and SOD activities following treatment with quercetin, catechin, and genistein indicated restoration of antioxidant biomarkers in cDDP-induced hepatotoxicity. Concurrent exposure to quercetin (100 mg/kg), catechin (100 mg/kg) and genistein (15 mg/kg) along with cDDP led to a significant (p < 0.05) reduction of hepatic tissue damage as indicated by reduced oxidation of membrane lipids and proteins and the restoration of plasma hepatic biomarkers and histopathological alterations. Overall, quercetin showed better ameliorative efficacy followed by genistein and catechin.

Cisplatin is a potent chemotherapeutic agent whose clinical application is frequently limited by severe nephrotoxicity. N-acetylserotonin (NAS), a precursor of melatonin and a selective agonist of the TrkB receptor, has demonstrated significant antioxidant and neuroprotective properties. This study aimed to evaluate the potential renoprotective effects of NAS against cisplatin-induced acute kidney injury (AKI) in a rat model. Thirty-five Wistar Albino rats were divided into five groups: Control, Sham, NAS (5 mg/kg), Cisplatin (CP; 7.5 mg/kg), and CP + NAS. NAS was administered daily for seven days, while cisplatin was given as a single dose on the fourth day. Renal function was assessed via serum urea and creatinine. Oxidative stress markers, including Malondialdehyde (MDA), Superoxide Dismutase (SOD), Total Antioxidant Status (TAS), and Total Oxidant Status (TOS), were measured in kidney tissue. Comprehensive histopathological evaluations were performed to assess tubular and glomerular damage. Cisplatin administration significantly increased serum creatinine levels and induced severe histopathological damage (p < 0.05). While cisplatin reduced SOD and TAS levels, NAS treatment showed a trend toward biochemical recovery without reaching statistical significance in oxidative markers. Notably, NAS administration significantly ameliorated cisplatin-induced histopathological lesions, specifically reducing tubular epithelial loss, glomerular degeneration, interstitial inflammation, and vacuolization (p < 0.05). Our findings indicate that NAS exerts a profound structural protective effect against cisplatin-induced renal injury. The preservation of renal parenchyma, despite modest systemic biochemical shifts, suggests that NAS-mediated protection may involve localized TrkB-dependent pro-survival signaling and stabilization of mitochondrial integrity. NAS represents a promising therapeutic candidate for mitigating chemotherapy-induced nephrotoxicity.

Context: Sirtuin-2 (SIRT2) is a longevity-related protein implicated in apoptosis, metabolic regulation and oxidative stress; however, its role in ageing pancreas remains unclear. Objective: This study investigated the effects of the selective SIRT2 inhibitor, Arabidopsis guanylate kinases-2 (AGK-2) on oxidative stress and apoptosis in aged rat pancreatic tissue. Methods: Young (3-month) and aged (22-month) Wistar albino rats were divided into control and AGK-2-treated groups (10 μM, 30 days). Total oxidant status (TOS) and total antioxidant status (TAS) used commercial kits, then calculated Oxidative stress index (OSI). For detecting nitrosative stress, we determined nitrite-nitrate levels using the Griess test. SIRT2 and caspase-3 were evaluated by ELISA and Western blot. Discussion and conclussion: Our findings showed that ageing increased SIRT2 expression, oxidative stress and caspase-3 protein compared to young rats. AGK-2 treatment reduced SIRT2, TOS, OSI and caspase-3, and increased TAS particularly in aged rats. AGK-2 reverses ageing-associated changes in pancreatic oxidative stress and apoptosis. SIRT2 modulation may represent a potential therapeutic target against age-related pancreatic degeneration.

Background: Hypothyroidism and type 2 diabetes are common conditions worldwide, with hypothyroidism affecting 4–10% of the population and type 2 diabetes affecting approximately 10% of adults globally. The increasing co-occurrence of these two conditions may contribute to increased oxidative stress and associated complications. Low levels of antioxidants are linked to hypothyroidism with type II diabetes because of the growth and production of free radicals, which makes patients more susceptible to oxidative stress. Objective: It was to assess how low antioxidants may exacerbate the pathogenic state of type 2 diabetic hypothyroid patients. Methods: 140 hypothyroid individuals with type 2 diabetes, ages 25 to 60, were assigned to take supplements every day with either intervention group before Eltroxin,( n = 50) (intervention group after Eltroxin, n=50) ( placebo group, n=40) for twelve weeks, take two capsules of vitamin E (268 mg, 400 IU), and one pill of selenium (200 mcg). Serum malondialdehyde (MDA), total antioxidant status (TAS), glycated haemoglobin (HbA1c), and fasting serum glucose (FSG) were measured using laboratory kits. Meanwhile, thyroid hormones were measured using (ELISA) technique. Estimates of selenium) Se) and vitamin E were obtained using atomic absorption spectroscopy and high-performance liquid chromatography (HPLC), respectively. Results: The levels of MDA, TAS, thyroid stimulating hormone (TSH), triiodothyronine (T3), thyroxine (T4), FSG, HbA1c, and oxidative stress index (OSI) did not differ significantly (p&gt;0.05) between the patient group and placebo participants, according to this study. Vit E and Se levels in the placebo group are not markedly distinct from those in the sick team (p&gt;0.05). Increased degrees of MDA, TAS, OSI, and TSH noticeably (p&lt;0.05) were observed in the placebo group. After taking the medicine, the T4 level was lower noticeably (p&lt;0.05 than that of the patients after taking the medicine. Conclusion: Individuals with hypothyroidism with type 2 diabetes may prevent hypothyroidism by consuming dietary supplements containing antioxidants, which reduce oxidative stress and promote overall health. Graphical Abstract

Cardiovascular diseases are among the most common health problems worldwide. Inflammation plays a critical role in the pathogenesis of various heart diseases. Lipopolysaccharides (LPS) trigger inflammatory mechanisms, leading to an inflammatory response. Fluvoxamine (FLV) is a selective serotonin reuptake inhibitor with anti-inflammatory and antioxidative properties. This study investigated the potential protective effects of FLV on sepsis-induced cardiac inflammation and injury. Thirty-two female Wistar Albino rats were divided into four groups: control, LPS (5 mg·kg-1 intraperitoneally), LPS + FLV, and FLV (50 mg·kg-1·day-1 orally for 3days). Thirty minutes after the final FLV administration, LPS was administered, and animals were killed 6 h later. Cardiac tissues were evaluated by histopathological analysis, immunohistochemical assessment of caspase-3, TNF-α, interleukin-1 beta (IL-1β), interleukin-6 receptor (IL-6R), IL-10, and NF-κB; biochemical determination of total oxidant status (TOS), total antioxidant status (TAS), and oxidative stress index (OSI); and gene expression analysis by real-time quantitative polymerase chain reaction (RT-qPCR) of sirtuin-1 (SIRT-1), nuclear factor erythroid 2-related factor 2 (NRF-2), peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α), and p53. LPS administration significantly increased TOS, OSI, caspase-3, TNF-α, IL-1β, IL-6R, NF-κB, and p53, while decreasing IL-10, SIRT-1, NRF-2, and PGC-1α, accompanied by marked inflammatory and structural cardiac damage. FLV treatment markedly reversed these alterations, attenuating inflammation, oxidative stress, and apoptosis. These findings suggest that FLV may confer cardioprotection against LPS-induced inflammatory and apoptotic cardiac injury, potentially through modulation of IL-6R/NF-κB-mediated inflammatory signalling and the SIRT-1-NRF-2-PGC-1α axis.

The widespread use of glyphosate-based herbicides (GBHs), including formulations such as Roundup, has raised toxicological concern due to their capacity to induce oxidative stress, inflammatory signaling, and mitochondrial dysfunction leading to hepatocellular injury. The present study investigated whether coenzyme Q10 (CoQ10) confers hepatoprotection against GBH exposure through modulation of oxidative stress-driven P2X7/NLRP3 inflammasome signaling and downstream inflammatory and apoptotic pathways. Fifty male ICR mice were randomly assigned to five groups (control, sham, CoQ10, GBH, and GBH + CoQ10) and treated by oral gavage for 49days with Roundup (500mg/kg/day), CoQ10 (200mg/kg/day), or their combination. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP) levels were assessed along with hepatic oxidative stress markers malondialdehyde (MDA), glutathione (GSH), total antioxidant status (TAS), total oxidant status (TOS), and oxidative stress index (OSI). Liver injury was evaluated histologically, while proliferative and inflammatory responses were analyzed by immunohistochemistry. Hepatic expression of inflammasome- and apoptosis-related genes (P2X7, NLRP3, caspase-1, IL-1β, NF-κB, TNF-α, caspase-3, and Bcl-2) was quantified by RT-qPCR. GBH exposure markedly increased serum liver enzymes, disrupted oxidative balance, and induced necroinflammatory liver injury with Kupffer cell activation and hepatocellular nuclear alterations. These changes were associated with increased PCNA and COX-2 immunoreactivity, activation of the P2X7-NLRP3 inflammasome axis, and a proapoptotic transcriptional profile. CoQ10 coadministration attenuated biochemical, histopathological, inflammatory, and apoptotic alterations, although several parameters remained incompletely normalized. In conclusion, CoQ10 provides partial but meaningful hepatoprotection against GBH-induced liver injury, highlighting P2X7-NLRP3-linked oxidative inflammation as a key mechanism in GBH hepatotoxicity.

Abstract Alzheimer’s disease (AD) is a progressive neurodegenerative disorder that is characterized by memory loss, cognitive decline, and behavioral disturbances. Given the limited efficacy of current treatments, there is an urgent need for new neuroprotective strategies. In this study, the therapeutic potential of curcumin and resveratrol was evaluated in a rat AD model induced by intracerebroventricular (ICV) administration of streptozotocin (STZ) (3 mg/kg). Subsequent to model induction, rats were administered curcumin, resveratrol, or a combination of both. The behavioral analyses, which included the Morris water maze, open field, and passive avoidance tests, revealed that both compounds significantly improved learning and memory performance. The histological and immunohistochemical findings demonstrated a decrease in caspase-3 and GFAP immunoreactivity, suggesting reduced neuronal apoptosis and astrocyte activation. The behavioral analyses, which included the Morris water maze, open field, and passive avoidance tests, revealed that both compounds significantly improved learning and memory performance. The histological and immunohistochemical findings demonstrated a decrease in caspase-3 and GFAP immunoreactivity, suggesting reduced neuronal apoptosis and astrocyte activation. Biochemical results showed an increase in total antioxidant status (TAS) and superoxide dismutase (SOD) activity, along with a decrease in total oxidative status (TOS) and TNF-α levels. Stereological evaluation also confirmed partial restoration of hippocampal volume. While curcumin and resveratrol exhibited potent neuroprotective effects when used separately, no synergistic interaction was observed when used in combination. These findings suggest that curcumin and resveratrol may serve as promising therapeutic agents for reducing oxidative stress, neuroinflammation, and neuronal degeneration associated with Alzheimer’s disease.

Objective: Maraş powder is a smokeless tobacco product made by combining dried Nicotiana rustica leaves with wood ash and is used by placing it in the lower lip. In addition to nicotine’s local and systemic effects, excess free radicals contribute to oxidative injury. This study aimed to compare the oxidative stress markers and antioxidant vitamin levels among Maraş powder users, smokers, and healthy controlsMethod: We enrolled 32 male Maraş powder users ( 1–2 grams, 3–6 times/day for at least one year), 32 male cigarette smokers (≥1 pack/day for at least one year), and 32 healthy male controls from Kahramanmaraş and nearby villages. After fasting (12 h) and abstaining from tobacco use for 8 h, venous blood samples were collected in the morning (08:00–10:00). Serum was stored at −80 °C. Using commercial colorimetric kits, Total Oxidant Status (TOS), Total Antioxidant Status (TAS), total thiol, and native thiol levels were measured. Vitamin A, C, and E levels were measured by ELISA. Statistical tests included Shapiro–Wilk, one-way analysis of variance (ANOVA), and Kruskal–Wallis tests, with significance set at p &amp;lt; 0.05.Results: No significant differences were observed in the TAS, TOS, total thiol, or native thiol levels among the three groups (all p &amp;gt; 0.05). In contrast, vitamin A, C, and E levels differed significantly among the groups (p = 0.01 for vitamin A; p = 0.05 for vitamin C; p = 0.02 for vitamin E). Vitamin A levels were highest among Maraş powder users, and vitamin C and E levels were lowest among cigarette smokers.Conclusion: Although Maraş powder and cigarette smoking did not significantly affect global oxidative stress markers or thiol levels in this sample, smoking was associated with lower vitamin C and E levels. Maraş powder users exhibited elevated vitamin A levels. Findings suggest that different forms of tobacco exposure may exert distinct effects on the antioxidant vitamin status. Future studies with larger sample sizes and dietary controls are required.

Objective: This randomized controlled study examined the potential antioxidant effects of a three-dimensional (3D) film prepared for anxiety management in children hospitalized in pediatric surgery clinics. The study aimed to determine whether virtual reality (VR)-based distraction could influence oxidative stress markers associated with preoperative anxiety.Method: 50 children aged 5–12 years were randomly assigned to either a VR group or a control group. After exclusions due to insufficient or hemolyzed samples, 38 participants (18 VR, 20 control) were included in the final analysis. The VR group watched a 3D hospital-themed film using VR goggles before intravenous cannulation. Blood samples taken before and after the intervention were analyzed for total oxidant status (TOS), total antioxidant status (TAS), oxidative stress index (OSI), glutathione (GSH), and cortisol levels. Results: Compared with the control group, the VR group showed significantly lower TOS, OSI, and cortisol levels, and higher TAS and GSH levels (p &amp;lt; 0.001). These results indicate that VR exposure reduced oxidative stress and helped maintain antioxidant balance.Conclusion: The use of 3D VR films prior to minor surgical procedures has been associated with reduced biochemical stress markers in children. In addition to potential psychological benefits, VR intervention resulted in measurable biochemical improvements. These findings suggest that the method could be used as an adjunct non-pharmacological approach in pediatric surgical settings.

The need to increase agricultural productivity due to population growth and rising food demand has led to the widespread use of pesticides, which are significant environmental pollutants that contribute to bioaccumulation in the food chain. Among pesticides, insecticides have effects not only on insecticides but also on non-target organisms. One of the insecticides, diflubenzuron, is a chitin synthesis inhibitor that is effective against both agricultural pests and public health pests such as mosquitoes. The present study aimed to investigate the biochemical effects of diflubenzuron on non-target organisms, scorpion (Aegaeobuthus gibbosus). After exposure to 1 and 10 mg/L diflubenzuron for 96 h, the hemolymph fluid and muscles (femur and telson) were sampled to analyze oxidative stress parameters. Total antioxidant status and total oxidative stress levels in the hemolymph fluid were altered significantly (p < 0.05). In telson muscles, superoxide dismutase activity was significantly reduced after 10 mg/L diflubenzuron exposure, while catalase and glutathione peroxidase activities increased (p < 0.05). A significant increase in catalase and glutathione peroxidase activities was observed in femur muscle tissue (p < 0.05). This study demonstrates that diflubenzuron, a chitin synthesis inhibitor, has strong metabolic and oxidative toxic effects on scorpions. These effects suggest that diflubenzuron may pose a significant toxicity risk to non-target arthropods and that its use in pest control should be re-evaluated in terms of potential side effects on the ecosystem.

Objectives: Acute peritonitis remains a critical condition with high mortality rates, further complicated by the rising antibiotic resistance. This study aimed to investigate the therapeutic potential of Chlorella vulgaris (CHL), both alone and in combination with standard antibiotic therapy (SFT), in a rat model of cecal ligation and puncture (CLP)-induced peritonitis. Methods: Seventy (70) male Wistar albino rats were divided into seven groups (n = 10): Control, Peritonitis Control, Low-dose CHL (CHL I) (150 mg/kg), High-dose CHL (CHL II) (300 mg/kg), the standard first-line therapy group (SFT) (Ceftriaxone + Metronidazole), SFT + CHL I, and SFT + CHL II. Following CLP-induced peritonitis, treatments were administered for 7 days. Peritoneal tissues were evaluated histopathologically and immunohistochemically for TNF-α, IL-1β, IL-10, and iNOS expression. Total Antioxidant Status (TAS) and Total Oxidant Stress (TOS) were measured to assess the oxidative stress. Results: Histopathological analysis showed that CLP-induced severe inflammatory damage was significantly reduced in all treatment groups, with the most prominent recovery observed in the SFT + CHL II group. CHL treatment led to a significant decrease in pro-inflammatory markers (TNF-α, IL-1β, iNOS) compared to the peritonitis control group (PC) (p < 0.05). Furthermore, CHL administration significantly improved the oxidative balance by increasing TAS and reducing TOS levels. Conclusions: Chlorella vulgaris exhibits significant anti-inflammatory, antioxidant, and immunomodulatory properties in experimental peritonitis. When used as an adjunct to standard antibiotic therapy, high-dose CHL provides synergistic effects that contribute to limiting tissue damage and controlling systemic inflammation. These findings suggest that CHL may be a promising supportive agent in the clinical management of acute peritonitis.