Total Oxidant Status Research Articles

Protective effects of hesperidin in gastric damage caused by experimental ischemia-reperfusion injury model in rats.

This study evaluated the protective effect of hesperidin on injury induced by gastric ischemia-reperfusion. Fifty male Sprague Dawley rats (250-300g) were divided into five groups: control (C), sham (S), ischemia (I), ischemia-reperfusion (I/R) and hesperidin + ischemia-reperfusion (Hes + I/R). Hesperidin was injected intraperitoneally at the dose of 100mg/kg one hour before the experimental stomach ischemia-reperfusion. Celiac artery was ligated. After 45minutes ischemia and 60minutes reperfusion period, blood samples were obtained under anesthesia. Then, animals were sacrificed, stomach tissues were excised for biochemical, and histopathological analyses were performed. Malondialdehyde levels and superoxide dismutase, glutathione peroxidase activities and total antioxidant status (TAS), total oxidant status (TOS), protein, total thiol parameters were measured in plasma, and tissue homogenate samples. H + E, periodic acid-Schiff, hypoxia inducible factor, terminal deoxynucleotidyl transferase mediated deoxyuridine triphosphate nick end-labeling (TUNEL), and proliferating cell nuclear antigen (PCNA) for cell proliferation as immunohistochemical parameters were determined. Upon biochemical and histopathological assessment, hesperidin decreased stomach tissue changes in comparison with IR group. Ischemia-reperfusion injury led to a considerably increase in malondialdehyde, protein, and TOS levels (p < 0.001) in stomach tissue. Hesperidin treatment significantly decreased malondialdehyde, protein, and TOS levels (p < 0.001). Hesperidin increased superoxide dismutase, TAS, total thiol and glutathione peroxidase activities in comparison with IR group. Hesperidin reduced damage and also increased TUNEL and PCNA immunoreactivity in stomach tissue. Hesperidin was able to decrease I/R injury of the stomach tissue due to inhibition of lipid peroxidation and protein oxidation, duration of antioxidant, and free radical scavenger properties. Consequently, hesperidin can provide a beneficial therapeutic choice for preventing stomach tissue ischemia-reperfusion injury in clinical application.

Conyza bonariensis (L.) Impact on Carbohydrate Metabolism and Oxidative Stress in a Type 2 Diabetic Rat Model

This study was conducted to assess the possible antidiabetic potential of Conyza bonariensis by employing in vitro as well as in vivo assessments. The dried plant material was extracted in methanol, ethanol, and water. The in vitro results showed that the ethanolic extract (EthCb) was found to have higher antioxidant and antidiabetic potential as compared with the aqueous (AqCb) and methanolic extracts (MthCb) so it was further evaluated in the in vivo trial using a diabetic rat model. Diabetes was induced in male Wistar rats by administering 5% sucrose in drinking water and a cafeteria diet for 8 weeks, followed by nicotinamide and streptozotocin administration. Subsequently, the diabetic rats were divided into 4 groups (n = 8 each): Positive control (no treatment), standard control (Metformin @ 10 mg/kg bw), treatment 1 ( C. bonariensis ethanolic extract @ 200 mg/kg bw), and treatment 2 ( C. bonariensis ethanolic extract @ 400 mg/kg bw). In addition, there was a negative control group of 8 rats without diabetes induction or treatment. After 21 days of treatment, blood samples were collected from all rats. The serum was evaluated through different means for glucose level, lipid profile, oxidative stress, carbohydrate metabolic enzymes and thyroid hormones. ANOVA was used to evaluate the data statistically. Total oxidant status (TOS) and the serum glucose levels of the streptozotocin-treated rats were reduced significantly ( P ⩽ .05) in Conyza bonariensis treated group. Whereas total antioxidant capacity (TAC) along with enzymes like paraoxonase and arylesterase were increased in Conyza bonariensis treated group. The antihyperlipidemic activity was also observed in Conyza bonariensis treated group Interestingly the subnormal levels of T3 and T4 which were observed in the PC group were also normalized in both treatment groups. This study demonstrated the antidiabetic as well as antioxidant activity of different extracts of Conyza bonariensis.

Protective effect of astaxanthin on testis torsion/detorsion injury through modulation of autophagy.

A significant clinical condition known as testicular torsion leads to permanent ischemic damage to the testicular tissue and consequent loss of function in the testicles. In this study, it was aimed to evaluate the protective effects of Astaxanthin (ASTX) on testicular damage in rats with testicular torsion/detorsion in the light of biochemical and histopathological data. Spraque Dawley rats of 21 were randomly divided into three groups; sham, testicular torsion/detorsion (TTD) and astaxanthin + testicular torsion/detorsion (ASTX + TTD). TTD and ASTX + TTD groups underwent testicular torsion for 2 hours and then detorsion for 4 hours. Rats in the ASTX + TTD group were given 1 mg/kg/day astaxanthin by oral gavage for 7 days before torsion. Following the detorsion process, oxidative stress parameters and histopathological changes in testicular tissue were evaluated. Malondialdehyde (MDA) and total oxidant status (TOS) levels were significantly decreased in the ASTX group compared to the TTD group, while superoxide dismutase (SOD), glutathione (GSH) and total antioxidant status (TAS) levels were increased (p < 0.05). Moreover, histopathological changes were significantly reduced in the group given ASTX (p < 0.0001). It was determined that ASTX administration increased Beclin-1 immunoreactivity in ischemic testicular tissue, while decreasing caspase-3 immunoreactivity (p < 0.0001). Our study is the first to investigate the antiautophagic and antiapoptotic properties of astaxanthin after testicular torsion/detorsion based on the close relationship of Beclin-1 and caspase-3 in ischemic tissues. Our results clearly demonstrate the protective effects of ASTX against ischemic damage in testicular tissue. In ischemic testicular tissue, ASTX contributes to the survival of cells by inducing autophagy and inhibiting the apoptosis.

Total antioxidant capacity, total oxidant status, d-dimer and nitric oxide levels in dogs with parvoviral enteritis

Total antioxidant capacity, total oxidant status, d-dimer and nitric oxide levels in dogs with parvoviral enteritis

Identification of biochemical indices for brown spot (Bipolaris oryzae) disease resistance in rice mutants and hybrids.

Brown spot caused by Bipolaris oryzae is a major damaging fungal disease of rice which can decrease the yield and value of produce due to grain discoloration. The objectives of the current study were to investigate and understand the biochemical indices of brown spot disease resistance in rice. A total of 108 genotypes (mutant and hybrid) along with Super Basmati and parent RICF-160 were evaluated against brown spot disease. The genotypes exhibiting resistant and susceptible responses to brown spot disease according to the IRRI standard disease rating scale were screened and selected. To study the biochemical response mechanism, forty five selected genotypes along with Super Basmati and RICF-160 were analyzed using the biochemical markers. The physiological and biochemical analysis provided valuable insights and confirmed the resistance of rice hybrids and mutants against brown spot disease. Positive correlations were observed among stress bio-markers and disease response. Rice genotypes i.e. Mu-AS-8, Mu-AS-19, Mu-AS-20 and Mu-AS-35 exhibited moderate resistant response while Hy-AS-92, Hy-AS-98, Hy-AS-99, Hy-AS-101, Hy-AS-102 and Hy-AS-107 showed resistant response to brown spot disease. Brown spot resistant rice genotypes had lesser values of malondialdehyde and total oxidant status and higher antioxidant activities i.e. superoxide dismutase, peroxidase, total phenolic content and lycopene. The selected resistant rice genotypes had resistance capacity against Bipolaris oryzae stress. In conclusion, identified resistant mutants i.e. Mu-AS-8, Mu-AS-19, Mu-AS-20 and Mu-AS-35 and hybrids i.e. Hy-AS-92, Hy-AS-98, Hy-AS-99, Hy-AS-101, Hy-AS-102 and Hy-AS-107 could be used in rice breeding program to achieve sustainable rice production by coping the emerging challenge of brown spot disease under variable climate conditions.

An analysis of oxidative stress indices and clinical parameters in budgerigars (Melopsittacus undulatus) treated with medetomidine-ketamine and midazolam-ketamine.

Various companion birds, including budgerigars, are anesthetized with injectable anesthesia.The current study aimed to evaluate oxidative stress indices including malondialdehyde (MDA), total antioxidant capacity (TAC), total oxidant status (TOS), and oxidative stress index (OSI) along with clinical parameters such as the time required to induce, maintain and recover from medetomidine-ketamine anesthesia and midazolam-ketamine anesthesia in budgerigars.Among 20 mature and healthy budgerigars, three groups were assigned as follows: Control (n = 4) to determine baseline oxidative stress indices medetomidine + ketamine (n = 8) anesthetized by intramuscular injections of medetomidine (0.04 mg kg-1) and ketamine (30.00 mg kg-1) in the pectoral muscles, midazolam + ketamine (n = 8) anesthetized by intramuscular injections of midazolam (1.00 mg kg-1) and ketamine (50.00 mg kg-1). Half of birds (n = 4) in the second and third groups were euthanized by cervical dislocation 1 hr after anesthesia induction, blood samples were collected directly from the heart, and sera were extracted. Additionally, the remaining birds were euthanized 24 hr later, and their serum was analyzed for oxidative stress indices. Clinical parameters were recorded during the study.Compared to the medetomidine + ketamine group, the midazolam + ketamine group experienced shorter induction, anesthetic, and recovery times. Administering medetomidine and ketamine elevated TOS levels compared with midazolam + ketamine. No significant difference was found between the test groups for TAC, MDA, or OSI.Therefore, the midazolam + ketamine regimen appears superior to medetomidine + ketamine when performing minor surgeries on budgerigars.

Evaluations of Oxidative Stress, Thiol/Disulphide Homeostasis, and Nitric Oxide in Patients with Aneurysmal Subarachnoid Hemorrhage.

To investigate changes in nitric oxide (NO) levels, oxidative stress, and dynamic thiol/disulphide homeostasis in the serum and cerebrospinal fluid (CSF) of patients with aneurysmal subarachnoid hemorrhages (aSAH). This prospective study included a total of 40 consecutive patients suffering from aSAH, who were operated on within the first 48 hours from onset of symptoms; CSF and blood samples were collected from these patients during their operations. To create a control group, blood samples and cerebrospinal fluid were taken from patients (n=40) without neurologic disorders who had undergone lumbar puncture for spinal anesthesia. We observed that the serum total antioxidant status had decreased markedly (p=0.0143) but that no change was evident in the oxidative stress index and total oxidant status in aSAH patients when compared to the controls. While total thiol (p=0.0014) and native thiol (p < 0.0001) levels had decreased in the aSAH patients, disulphide levels (p < 0.0001) had increased significantly. Although the native thiol/total thiol ratio declined (p < 0.0001), the dynamic disulphide/total thiol ratio (p < 0.0001) and dynamic disulphide/native thiol ratio (p < 0.0001) increased markedly in serum samples from the patient group. Patient serum NO levels were also significantly elevated (p < 0.0001). There were no marked changes in CSF for all measured parameters (p > 0.05). This study demonstrated that serum NO levels and oxidative stress parameters increased markedly in the patients. These results may help to understand the underlying mechanisms behind early tissue damage due to aSAH and to monitor disease progression and improve the early detection of disease severity.

The effects of topical aloe vera on an experimentally designed penile fracture model in rats.

This study assessed the histopathological and oxidative effects of topical Aloe Vera (AV) on penile fractures (PF) formed experimentally in a rat model. Forty Wistar albino rats (220-250 g) were used. The PF model was created experimentally with a number 15 lancet. Then, the rats were randomly and equally divided into five groups. In the first group (C), no incision was formed. In the second group (P), an incision was formed. In the third group (PR), the incision line was closed primarily. In the fourth group (PA), AV was locally applied onto the incision without suturing for three days. In the last group (PRA), AV was applied to the primary repair region for three days. All groups were compared to each other according to histopathological and biochemical data. Hyperemia-bleeding was observed to be suppressed in the PRA group compared to the other groups (p<0.001). Inflammation was observed only in Groups PR and PRA (p<0.001). Significant fibrosis was observed in the PA and PRA groups compared to the other groups (p<0.001). Superoxide Dismutase (SOD) and Glutathione (GSH) values increased in favor of Group PRA (p=0.009 and p=0.035, respectively). Total Oxidative Status (TOS) and Malondialdehyde (MDA) values decreased in favor of Group PA (p=0.036 and p=0.026, respectively). Tumor Necrosis Factor-alpha (TNF-α) and Interleukin-1 beta (IL-1ß) levels decreased mostly in the PRA group, but these changes did not reach statistical significance (p>0.05). Topical AV application reduces tissue inflammation and oxidative stress but appears to increase the development of fibrosis after PF.

Effect of humic acid on oxidative stress and neuroprotection in traumatic spinal cord injury: an experimental study.

Traumatic spinal cord injury (TSCI) is an important health problem, especially in developing countries with additional socioeconomic loss. Humic acid (HA) usually has antioxidant, antiinflammatory, blood circulating, and antiviral effects. Hence, it was aimed herein to show the effect of HA on neuroprotection in a TSCI model. A TSCI model was used, in which 24 Wistar albino rats were divided into 4 groups: control group: subjected to only laminectomy; sham group: subjected to laminectomy + TSCI; HA 5 mg/kg group: subjected to laminectomy + TSCI + intraperitoneal (IP) injection of 5 mg/kg of HA; and HA 10 mg/kg group: subjected to laminectomy + TSCI + IP injection of 10 mg/kg of HA. Intracardiac blood samples were obtained preoperatively (preop), and at 1 and 24 h postoperatively (postop). The total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI) levels were evaluated in the serum. The motor functions were evaluated using the Modified Tarlov Score at 24 h postop. There were no significant changes in the TAS values between the sham and HA 5 mg/kg and HA 10 mg/kg groups (p = 0.77/0.21). However there was a significant decrease in the TOS values at 24 h postop when comparing the sham and HA 5 mg/kg groups (p = 0.02). The pathological evaluation showed a significant decrease in the severity of edema, hemorrhage, polymorphonuclear leucocyte (PNL) infiltration, and mononuclear leucocyte (MNL)/macrophage/microglia infiltration when compared with the control group (p < 0.05). There was a significant recovery at the paraplegia level when the HA 5 mg/kg and HA 10 mg/kg groups were compared with the control group (p < 0.001). The effects of HA in the early stages of TSCI on oxidative stress, histopathological changes, and neurological improvement were investigated herein. It is thought to be a potential therapeutic agent in acute TSCI but needs to be further evaluated to determine the extent of its effect on other neuroprotective pathways in larger series.

The Role of Different Antioxidant Pathways Like AKT, SIRT-1, NRF2 and HO-1 in Cardiac Damage After Subarachnoid Hemorrhage.

To explore the pathophysiological mechanism of subarachnoid haemorrhage (SAH) using cellular oxidative stress mechanisms and inflammation. A total of 20 Wistar Albino rats were divided into two groups, namely sham and SAH. On day 0, 0.3 mL of saline in the sham group and 0.3 ml of autologous blood in the SAH group were applied in the cisterna magna of the animals. After sacrification on the 7th day of the procedure, brain, blood and heart tissues were collected. In different tissues, total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), creatin kinase MB (CKMB) and lactate dehydrogenase (LDH) levels were detected biochemically. AKT, sirtuin-1 (SIRT-1), NF-E2-related factor 2 (NRF2), heme oxygenase-1 (HO-1) genes and glutathione peroxidase-4 expression were examined genetically. Moreover, histopathological analyses were conducted both in heart and brain tissues. Enhanced TOS, OSI levels in all tissues and glial fibrillary acidic protein (GFAP) expressions in brain tissue and NFkβ, IL-6 and Cox-1 expressions in heart tissues; it was observed that levels of TAS in blood and AKT, SIRT-1, NRF2 and HO-1 gene expressions in brain tissue were decreased. In the oxidative stress and inflammation situation that takes place following SAH, AKT, SIRT-1, NRF2 and HO-1 pathways, which are antioxidant mechanisms, are suppressed and GFAP, NFkβ, IL-6, Cox-1 expressions, which trigger inflammation, are enhanced. Treatment of SAH necessitates studies on the inhibition or activation of such pathways.

Dehydroepiandrosterone modulates the PTEN/PI3K/AKT signaling pathway to alleviate 4-vinylcyclohexene diepoxide-induced premature ovarian insufficiency in rats.

Dehydroepiandrosterone (DHEA) is frequently integrated as an adjuvant in over a quarter of controlled ovarian hyperstimulation (COH) protocols, despite the ongoing debate regarding its impact. This study aimed to evaluate the efficacy and mechanism of action of DHEA on ovarian follicular development and ovarian response in rats with varying ovarian reserves. The study involved 75 rats categorized into 15 distinct groups. The ovarian tissues of rats in both the normal ovarian reserve group and the premature ovarian insufficiency (POI) group, induced by 4-vinylcyclohexene diepoxide (VCD) injection, were subjected to histomorphological and biochemical analyses following the administration of DHEA, either alone or in combination with COH. Follicle counting was performed on histological sections obtained from various tissues. Serum concentrations of anti-Müllerian hormone (AMH) and the quantification of specific proteins in ovarian tissue, including phosphatase and tensin homolog of chromosome 10 (PTEN), phosphoinositide 3-kinase (PI3K), phosphorylated protein kinase B (pAKT), cyclooxygenase 2 (COX-2), caspase-3, as well as assessments of total antioxidant status and total oxidant status, were conducted employing the ELISA method. The impact of DHEA exhibited variability based on ovarian reserve. In the POI model, DHEA augmented follicular development and ovarian response to the COH protocol by upregulating the PTEN/PI3K/AKT signaling pathway, mitigating apoptosis, inflammation, and oxidative stress, contrary to its effects in the normal ovarian reserve group. In conclusion, it has been determined that DHEA may exert beneficial effects on ovarian stimulation response by enhancing the initiation of primordial follicles and supporting antral follicle populations.

Biochanin A restored the blood-brain barrier in cerebral ischemia-reperfusion in rats.

Blood-brain barrier is a protective layer that regulates the influx and efflux of biological materials for cerebral tissue. The aim of this study was to investigate the effects of Biochanin A on cerebral histopathology and blood-brain barrier immunohistochemically. A total of 24 rats were assigned to three groups: sham, ischemia-reperfusion, and ischemia-reperfusion+Biochanin A. Ischemia-reperfusion was performed by occluding the left carotid artery for 2/24 h. Notably, 20 mg/kg Biochanin A was administered to rats for 7 days after ischemia-reperfusion. Blood was collected for malondialdehyde and total oxidant/antioxidant status analysis. Cerebral tissues were processed for histopathology and further for immunohistochemical analysis. Malondialdehyde content with total oxidant status value was significantly increased and total antioxidant status values were significantly decreased in the ischemia-reperfusion group compared with the sham group. Biochanin A treatment significantly improved scores in the ischemia-reperfusion+Biochanin A group. The normal histological appearance was recorded in the cerebral sections of the sham group. Degenerated neurons and vascular structures with disrupted integrity of the cerebral cortex were observed after ischemia-reperfusion. Biochanin A alleviated the histopathology in the cerebrum in the ischemia-reperfusion+Biochanin A group. Ischemia-reperfusion injury decreased the expression of blood-brain barrier in the ischemia-reperfusion group compared to the sham group. Administration of Biochanin A upregulated the blood-brain barrier immunoreactivity in the cerebrum by restoring blood-brain barrier. Cerebral ischemia-reperfusion caused an increase in oxidative stress and pathological lesions in the cerebrum. Biochanin A treatment restored the adverse effects of ischemia-reperfusion injury by restoring blood-brain barrier.

Dexpanthenol ameliorates lipopolysaccharide-induced cardiovascular toxicity by regulating the IL-6/HIF1α/VEGF pathway

IntroductionLipopolysaccharide (Lps) is an essential component responsible for the virulence of gram-negative bacteria. Lps can cause damage to many organs, including the heart, kidneys, and lungs. Dexpanthenol (Dex) is an agent that exhibits anti-oxidative and anti-inflammatory effects and stimulates epithelialization. In this study, we aimed to investigate the effects of Dex on Lps-induced cardiovascular toxicity. MethodsRats were divided into four groups: control, Lps (5 mg/kg, intraperitoneal), Dex (500 mg/kg, intraperitoneal), and Lps + Dex. The control group received saline intraperitoneally (i.p.) once daily for three days. The Lps group received saline i.p. once daily for three days and a single dose of Lps i.p. was administered on the third day. The Dex group received Dex i.p. once daily for three days and saline on the third day. The Lps + Dex group received Dex i.p. once daily for three days and a single dose of Lps i.p. on the third day. Heart and aortic tissues were taken for biochemical, histopathological, immunohistochemical, and genetic analysis. ResultsLps injection caused histopathological changes in both heart and aortic tissues and significantly increased total oxidant status and oxidative stress index levels. Interleukin-6, and Tumor necrosis factor-α mRNA expressions were significantly altered in heart and aorta, likely do to the anti-inflammatory and antioxidative effects of Dex. Furthermore, Dex affected Caspase-3 and Hypoxia-inducible factor 1-α staining patterns. ConclusionsOur results show that Dex treatment has a protective effect on Lps-induced cardiac and endothelial damage in rats by reducing inflammation, oxidative stress, and apoptosis.

Aspir Yağının Japon Bıldırcınlarında Büyüme Performansı, Et Kalitesi, Karkas Kompozisyonu ve Oksidatif Stres Üzerine Etkileri

This study was conducted to investigate the effects of the addition of SFO (Chartamus tinctorius L.) to dietary of Japanese quail on growth performance, meat quality, carcass composition, and oxidative stress. A total of 40 Japanese quails at ten days of age were used as material and divided into four groups comprising ten birds. The experiment was continued for 35 days. The control group was fed with a diet including no additives, while 0.1%, 0.2%, and 0.3% SFO were added to the feed of the other groups. For this purpose, the effects of SFO on body weight and average daily weight gain of quails, feed consumption (FC) and feed conversion ratio (FCR) of quails, slaughter and carcass piece weights of quails, breast meat quality characteristics, breast meat color characteristics and stress parameters were investigated. There was no significant (P&gt;0.05) difference between the groups in terms of body weight (BW), daily body weight gain (DBWG), daily feed consumption (DFC), FCR, carcass, and slaughter characteristics, color, and pH values. It was found that the addition of SFO significantly reduced total oxidative status (TOS) (P

Investigation of the Protective Role of Quercetin on Oxidative Stress and Endoplasmic Stress Pathway in 4-aminopyridine-induced Neuronal Damage

Quercetin (QU) is a flavonoid found in different fruits and vegetables. Studies report that QU may have positive effects on neurological diseases. However, the effect of QU on 4-aminopyridine (4-AP)-induced neurodegeneration in neuronal cells is still not fully elucidated. In this study, the effects of QU on 4-AP-induced hippocampal neuron damage in vitro and the possible role of oxidative stress and endoplasmic reticulum stress in this effect were investigated. The study was carried out using the HT-22 hippocampal neuronal cell line. The effect of pre-treatment with QU on cell viability after 4-AP-induced neuronal damage was determined by the XTT test. Cells were evaluated histopathologically for apoptotic nuclear change (ANC) using DAPI staining. The effects of QU on oxidative stress (total oxidant state (TOS) and total antioxidant status (TAS)) occurring after neuronal damage were evaluated with colorimetric commercial kits and endoplasmic reticulum stress markers (activating transcription factor 4 (ATF-4) and C/EBP homologous protein). (CHOP) was measured with the ELISA kits. While the cell viability rate decreased in the cells treated with 4-AP, it was determined that pre-treatment with QU reversed this situation. In terms of histopathology, treatment with 4-AP increased the number of ANC, while QU pre-treatment reduced it. In addition, in terms of biochemical evaluations, TOS, ATF-4, and CHOP increased in neuronal cells after 4-AP, and QU was determined to suppress this increase. In addition, QU normalized the decreased TAS levels following the 4-AP application. As a result, in the HT-22 cell line, it was found that QU treatment had a neuroprotective effect by suppressing oxidative stress and endoplasmic reticulum stress in 4-AP-induced neuronal damage.

Investigation of the Effect of Pumpkin (Cucurbita pepo L.) Seed Oil on Pentylenetetrazole-induced Neuronal Damage in HT-22 Cell Line

Recent studies have shown the positive effects of Cucurbita pepo L. (pumpkin) seed oil (PSO) in different disease models. However, the effect of PSO on neurological diseases has not been clarified yet. Therefore, this study aims to elucidate the effects of BBS on pentylenetetrazole (PTZ)-induced neuronal damage and the possible roles of oxidative and nitrosative stress in this effect in vitro. The HT-22 hippocampal neuronal cell line was used in the study. Cell survival after PTZ-induced neuronal damage was evaluated with the XTT test in the groups. While the effects of BBS on total antioxidant status (TAS) and total oxidant status (TOS) after PTZ were measured with colorimetric commercial kits, its effects on neuronal nitric oxide synthase (nNOS) and nitric oxide (NO) levels were also determined by ELISA kits. In light of the data obtained, it was found that pre-treatment with PSO prevented the decrease in cell survival after exposure to PTZ. In addition, it has been found that PSO normalizes the increase in TOS, nNOS, and NO in neuronal cells after PTZ. As a result, it was determined that the treatment of neuronal cells with PSO prevented neuronal damage caused by PTZ and showed neuroprotective properties. It is thought that PSO may achieve these effects through oxidative and nitrosative systems. Enrichment of a daily diet with PSO might be beneficial in reducing the risks of neurological diseases.

Investigation of the Effect of Indatraline on Oxidative Damage Induced by Hydrogen Peroxide in C6 Glioma Cell Line

Oxidative stress is defined as an imbalance between the generation of reactive oxygen species (ROS) and their scavenging. Indatralin, which has serotonin reuptake inhibitory activity, has not yet been studied for its ability to prevent oxidative damage. Our research's objective was to find out how indatraline defends against oxidative damage. C6 cells were used in the study and four different cell groups were created. The control group received no therapy at all. For 24 hours, cells in the H2O2 group were exposed to 0.5 mM H2O2. The indatraline group received indatraline treatments for 24 hours at various doses (0.5, 1, 2.5, 5 and 10 μM). For one hour, indatraline was administered to the indatraline + H2O2 group at various concentrations (0.5, 1, 2.5, 5 and 10 μM) before the group was subjected to 0.5 mM H2O2 for 24 hours. Following the occurrence of oxidative damage, total antioxidant status (TAS) and total oxidant status (TOS) levels were determined. Cell viability was also evaluated using the XTT assay. As a result, after hydrogen peroxide-induced oxidative damage, indatraline at doses of 10, 5, and 2.5 μM showed a protective effect by significantly enhanced cell survival in C6 cells(p &amp;lt; 0.001). Additionally, indatraline boosted the lowered TAS level while decreasing the elevated TOS levels following hydrogen peroxide-induced oxidative damage (p&amp;lt;0.001).

Potential effect dietary supplementation of calcium tetraborate in quails exposed to cadmium: Its impact on productive performance, oxidative stress, cecal microflora, and histopathological changes

Cadmium (Cd) is a ubiquitous environmental pollutant, and Cd exposure harms human health, agriculture, and animal husbandry. The present study aimed to investigate the potential protective effect of dietary supplementation of calcium tetraborate (CTB) on productive performance, oxidative stress, cecal microflora, and histopathological changes in quail exposed to Cd. A total of one hundred twenty, 6-week-old Japanese quail (four females and two males/replicate) were divided into four groups (30 quails/group): the control group (feeding basic diet), CTB group (basic diet containing 300 mg/kg CaB4O7, 22.14% elemental B/kg diet), the Cd group (basic diet containing 100 mg/kg cadmium chloride (CdCl2) (total Cd content of 92.1 mg/kg)) and the CTB + Cd group (basic diet containing 300 mg/kg CTB and 100 mg/kg CdCl2). The results showed that Cd exposure caused decreased performance, increased the proportion of broken and soft-shelled eggs, induced oxidative stress, affected cecal microflora, epicardial hemorrhages in the heart, focal necrosis in the liver, degeneration in the kidneys, and degenerated and necrotic seminiferous tubules in the testicles. CTB prevented Cd-induced oxidative stress in liver tissue by increasing total antioxidant status and reducing total oxidant status. In addition, CTB improved egg production and feed conversion ratio (FCR). CTB protected the cecal microflora by inhibiting Enterobacteriaceae and promoting Lactobacillus. CTB also reduced Cd-induced histopathological damage in the heart, liver, kidneys, and testicles. In conclusion, these findings suggest that CTB could be used in Cd-challenged quail, and this compound provides new insights into the toxicity of environmental Cd.

THE AMELIORATING EFFECTS OF BILBERRY ON METHOTREXATE-INDUCED INTESTINAL INJURY

Objective: Methotrexate (MTX) is a folic acid analogue chemotherapeutic used in the treatment of some malignant tumors and autoimmune diseases. In addition to its antitumoral properties, it can also exhibit toxic effects on the kidney and intestines. Bilberry (BB) fruit is a potent natural antioxidant rich in anthocyanidins. The purpose of this study was to investigate the potential ameliorating effects of BB against MTX-induced intestinal damage using biochemical and histological methods.&#x0D; Material and Methods: Twenty-one adult female Sprague Dawley rats were divided into three equal groups. No procedure was performed on the control group (ControlG), while the MTX group (MTXG) and MTX+BB extract group (MTX+BBG) received a single intraperitoneal dose of 30 mg/kg MTX on the first day of the experiment. MTX+BBG also received 200 mg/kg BB extract by oral gavage once daily for five days starting on the first day of the experiment. Half the intestinal tissues removed from the duodenal region at the experiment were used for biochemical evaluation, and the other half for histological examination.&#x0D; Results: Malondialdehyde (MDA), total oxidant status (TOS), oxidative stress index (OSI), and 8-oxo-2′-deoxyguanosine (8- OHdG) values were all higher in MTXG intestinal tissues than in ControlG. MDA, TOS, OSI, and 8-OHdG values were lower in MTX+BBG than in MTXG. In addition, caspase-3 levels in MTXG were higher than those in both ControlG and MTX+BBG, while total antioxidant status (TAS) values were lower. In terms of histology, villous hemorrhage, inflammatory cell infiltration, fusion, and degeneration in the villus epithelium were present in MTXG intestinal tissue, and the total damage score was also high. Improvement in all these parameters was present in MTX+BBG.&#x0D; Conclusion: Orally administered BB extract can improve MTX-induced intestinal damage through its antioxidant and anti-inflammatory effects.

Pediatric nephrotic syndrome: The interplay of oxidative stress and inflammation.

The pathophysiological mechanisms crucial in the development of nephrotic syndrome (NS) in the pediatric population are still not fully understood. This study aimed to investigate the relationship between hypertension, oxidative stress, and inflammation in pediatric patients during the acute phase of the disease. The study included 33 children, aged 2 to 9 years, with nephrotic syndrome. Blood samples were collected during the acute phase and remission. Parameters of oxidative status were determined, including total oxidative status (TOS), advanced oxidation protein products (AOPP), prooxidant-antioxidant balance (PAB), sulfhydryl groups (-SH), paraoxonase 1 (PON1), and total antioxidant status (TAS) in serum, measured spectrophotometrically. Inflam - matory parameters such as pentraxin 3 (PTX3), leptin, program med cell death ligand 1 (PD-L1), and E-cadherin were determined using enzyme-linked immunosorbent assay (ELISA). Patients with nephrotic syndrome and hypertension had significantly higher levels of advanced oxidation protein products and total antioxidant status (p=0.029 and p=0.003, respectively). During the acute phase of the disease, lower activity of sulfhydryl groups and paraoxonase 1 was observed compared to remission (p<0.001, for both). Pentraxin 3 levels were higher, while leptin levels were lower during the acute phase (p<0.001, for both). Pentraxin 3 correlated with advanced oxidation protein products and total antioxidant status during the acute phase but not in remission (rs=0.42, p=0.027 and rs=0.43, p=0.025, respectively). A negative correlation between Advanced oxidation protein products and leptin was observed during the acute phase, which disappeared in remission (rs=-0.42, p=0.028). Results of this study show that hypertension influences oxidative stress markers, and decreased antioxidant capacity may contribute to nephrotic syndrome development. Pentraxin 3 appears as a potential disease activity marker, indicating a dynamic connection between inflammation and oxidative stress. Leptin may also play a role in oxidative stress in nephrotic syndrome.