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Acute kidney injury (AKI) is a severe medical condition that can lead to illness and death. A disintegrin and metalloprotease (ADAM) protein family is a potential treatment target for AKI due to its involvement in inflammation, growth, and differentiation. While ADAM10 and ADAM17 have been identified as significant contributors to inflammation, it is unclear whether they play a critical role in AKI. In this study, we induced AKI in male and female mice using lipopolysaccharide, a bacterial endotoxin that causes inflammation and oxidative stress. The role of kaempferol, which is found in many natural products and known to have antioxidant and anti-inflammatory activity in many pre-clinical studies, was investigated through ADAM10/17 enzymes in AKI. We also investigated the efficacy of a selective synthetic inhibitor named GW280264X for ADAM10/17 inhibition in AKI. Blood urea nitrogen and creatinine levels were measured in serum, while tumor necrosis factor-α, vascular adhesion molecule, interleukin (IL)-1β, glucose regulatory protein-78, IL-10, nuclear factor κ-B, thiobarbituric acid reactive substances, total thiol, ADAM10, and ADAM17 levels were measured in kidney tissue. We also evaluated kidney tissue histologically using hematoxylin and eosin, periodic acid-schiff, and caspase-3 staining. This research demonstrates that GW280264X and kaempferol reduces inflammation and oxidative stress, as evidenced by biochemical and histopathological results in AKI through ADAM10/17 inhibition. These findings suggest that inhibiting ADAM10/17 may be a promising therapeutic approach for treating acute kidney injury., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Aluminum is a potent neurotoxin, responsible for memory impairment and cognitive dysfunction. The neurotoxic effect of aluminum on cognitive impairment is well documented, however, exposure to aluminum in a time-dependent manner and post-exposure self-recovery still needs to be elaborated. This research aimed to (1) study the time-dependent effect of aluminum exposure by administering a total dose of 5850 mg/kg of Al over two different time periods: 30 and 45 days (130 and 195 mg/kg of AlCl 3 respectively), and (2) study 20 days post-exposure self-recovery effect in both aluminum-exposed groups by giving distilled water. Cognitive abilities were investigated through Morris water maze test and hole board test and compared in both exposure and recovery groups. Oxidative stress markers and neurotransmitter levels were measured for both exposure and recovery groups. To understand the mechanism of aluminum exposure and recovery, immunohistochemical analysis of synaptophysin (Syp) and glial fibrillary acidic protein (GFAP) was performed. Results showed cognitive dysfunction, oxidative stress-induced damage, reduced neurotransmitter levels, decreased immunoreactivity of Syp, and increased GFAP. However, these parameters showed a larger improvement in the recovery group where rats were given aluminum for 30 days period in comparison to recovery group followed by 45 days of aluminum exposure. These results suggest that restoration of cognitive ability is affected by the duration of aluminum exposure. The study findings provide us with insight into the adverse effects of aluminum exposure and can be utilized to guide future preventive and therapeutic strategies against aluminum neurotoxicity., (© 2024. The Author(s), under exclusive licence to Springer Nature B.V.)

Anxiety-like conditions can interfere with daily activities as the adaptive mechanism fails to cope with stress. These conditions are often linked with increased oxidative stress, and abrupt neurotransmission and electroencephalography (EEG) wave pattern. Geraniol, a monoterpenoid, has antioxidant and anti-inflammatory activities, as well as brain-calming effects. Therefore, in this study, geraniol was tested for the potential anxiolytic effects in a rat model of anxiety. The rats were exposed to an electric foot shock (1 mA for 1 s) to develop anxiety-like symptoms. Treatment was carried out using geraniol (10 and 30 mg/kg) and the standard diazepam drug. The behavior of the rats was analyzed using the open field test, light-dark test, and social interaction test. Afterward, the rats were decapitated to collect samples for neurochemical and biochemical analyses. The cortical-EEG wave pattern was also obtained. The study revealed that the electric foot shock induced anxiety-like symptoms, increased oxidative stress, and altered hippocampal neurotransmitter levels. The power of low-beta and high-beta was amplified with the increased coupling of delta-beta waves in anxiety group. However, the treatment with geraniol and diazepam normalized cortical-EEG wave pattern and hippocampal serotonin and catecholamines profile which was also reflected by reduced anxious behavior and normalized antioxidant levels. The study reports an anxiolytic potential of geraniol, which can be further explored in future., Competing Interests: Declaration of Competing Interest The authors have no conflicts of interest to disclose., (Copyright © 2024 The Authors. Published by Elsevier Masson SAS.. All rights reserved.)

Inappropriate disposal of plastic wastes and their durability in nature cause uncontrolled accumulation of plastic in land/marine ecosystems, also causing destructive effects by bioaccumulating along the food chain. Microplastics may cause chronic inflammation in relation to their permanent structures, especially through oxidative stress and cytotoxic cellular damage, which could increase the risk of cancer development. The accumulation of microplastics in the liver is a major concern, and therefore, the identification of the mechanisms of their hepatotoxic effects is of great importance. Polymethyl methacrylate (PMMA) is a widely used thermoplastic. It has been determined that PMMA disrupts lipid metabolism in the liver in various aquatic organisms and causes reproductive and developmental toxicity. PMMA-induced hepatotoxic effects in humans have not yet been clarified. In our study, the toxic effects of PMMA (in the range of 3-10 μm) on the human liver were investigated using the HepG2/THP-1 macrophage co-culture model, which is a sensitive immune-mediated liver injury model. Cellular uptake of micro-sized PMMA in the cells was done by transmission electron microscopy. Determination of its effects on cell viability and inflammatory response, oxidative stress, along with gene and protein expression levels that play a role in the mechanism pathways underlying the effects were investigated. The results concluded that inflammation, oxidative stress, and disruptions in lipid metabolism should be the focus of attention as important underlying causes of PMMA-induced hepatotoxicity. Our study, which points out the potential adverse effects of microplastics on human health, supports the literature information on the subject., (© 2024. The Author(s).)

Background: The increasing incidence and mortality rate of HCC is a major concern, especially for developing countries of the world. Hence, extensive research is being carried out in order to explore new approaches for developing successful therapeutic strategies for HCC. The controversial role of oxidative stress in the prognosis and treatment of various diseases such as cancer has become an area of great interest and intrigue for many scientists throughout the world., Objective: We aim to investigate the role of induced oxidative stress on the suppression of HCC Huh-7 cancerous cells as a therapeutic approach., Methods: Induction of oxidative stress via H 2 O 2 treatment produced cell cytotoxicity in a dose dependent manner and also led to the overexpression of GSTP-1 and PRX-2. The expression of GSTP- 1 and PRX-2 was compared in HCC Huh-7 treated, untreated cells and normal hepatocytes using immunocytochemistry. Furthermore, the effects of oxidative stress on cell cycle arrest were also studied through flow cytometry., Results: Our study demonstrated the inhibition of cancer cell proliferation as a result of H 2 O 2 induction by arresting the cell cycle at the G2 phase., Conclusion: The induction of oxidative stress could be a potential therapeutic approach for treating HCC in the future. GSTP-1 and PRX-2 can serve as substantial therapeutic targets for the treatment of HCC., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)

Objective: To assess the preventive role of metformin on rat ovarian ischemia reperfusion injury., Materials and Methods: Forty rats were divided equally into five groups; Group 1: sham, Group 2: surgical control with 3-hr torsion and detorsion, Group 3: 50 mg/kg p.o. metformin 30 min before 3-hr torsion, Group 4; metformin just after detorsion, Group 5; metformin 30 min before torsion and just after detorsion. Bilateral ovaries and blood sample were obtained seven days after detorsion for biochemical and histopathological evaluation., Results: Ovarian tissue total anti-oxidant status (TAS) levels were significantly increased in group 4 when compared to group 1, 2 and 3 (all p < 0.01). In addition, there was a significant decrease in tissue oxidative stress index (OSI) level in group 4 with respect to group 2 (p < 0.01). Moreover, serum levels of OSI were significantly higher in group 2 with respect to group 1 and 5 (both p < 0.05). Similarly, there was significant increase in serum levels of peroxynitrite in group 2 as compared to serum levels in group 3 and 5 (p < 0.01 and 0.05, respectively). Furthermore, there were significant decrease in histopathological scores metformin and sham groups when compared to rats in the control group (Group 2)., Conclusion: Metformin reduces ischemia reperfusion injury in rat torsion detorsion model by improving histopathological and biochemical findings including TAS, OSI and peroxynitrite., Competing Interests: Declaration of competing interest Authors report no conflict of interest., (Copyright © 2021. Published by Elsevier B.V.)

Olanzapine is a second-generation antipsychotic (AP) drug commonly prescribed for the treatment of schizophrenia. Recently, olanzapine has been found to cause brain tissue volume loss in rodent and primate studies; however, the underlying mechanism remains unknown. Abnormal autophagy and oxidative stress have been implicated to have a role in AP-induced neurodegeneration, while N-acetylcysteine (NAC) is a potent antioxidant, shown to be beneficial in the treatment of schizophrenia. Here, we investigate the role of olanzapine and NAC on cell viability, oxidative stress, mitochondrial mass and mitophagy in hypothalamic cells. Firstly, cell viability was assessed in mHypoA-59 and mHypoA NPY/GFP cells using an MTS assay and flow cytometric analyses. Olanzapine treated mHypoA-59 cells were then assessed for mitophagy markers and oxidative stress; including quantification of lysosomes, autophagosomes, LC3B-II, p62, superoxide anion (O 2 - , mitochondrial mass and LC3B-II. We found that olanzapine significantly impacted cell viability in mHypoA-59 hypothalamic cells in a dose and time-dependent manner. Olanzapine inhibited mitophagy, instigated oxidative stress and prompted mitochondrial abnormalities. NAC was able to mitigate olanzapine-induced effects. These findings suggest that high doses of olanzapine may cause neurotoxicity of hypothalamic neurons via increased production of reactive oxygen species (ROS), mitochondrial damage and mitophagy inhibition. This could in part explain data suggesting that APs may reduce brain volume.2 - , mitochondrial mass and LC3B-II. We found that olanzapine significantly impacted cell viability in mHypoA-59 hypothalamic cells in a dose and time-dependent manner. Olanzapine inhibited mitophagy, instigated oxidative stress and prompted mitochondrial abnormalities. NAC was able to mitigate olanzapine-induced effects. These findings suggest that high doses of olanzapine may cause neurotoxicity of hypothalamic neurons via increased production of reactive oxygen species (ROS), mitochondrial damage and mitophagy inhibition. This could in part explain data suggesting that APs may reduce brain volume.

Noise has always been an important environmental factor that induces health problems in the general population. Due to ever increasing noise pollution, humans are facing multiple auditory and non-auditory problems including neuropsychiatric disorders. In modern day life it is impossible to avoid noise due to the rapid industrialization of society. Continuous exposure to noise stress creates a disturbance in brain function which may lead to memory disorder. Therefore, it is necessary to find preventive measures to reduce the deleterious effects of noise exposure. Supplementation of taurine, a semi essential amino acid, is reported to alleviate psychiatric disorders. In this study noise-exposed (100 db; 3 h daily for 15 days) rats were supplemented with taurine at a dose of 100 mg/kg for 15 days. Spatial and recognition memory was assessed using the Morris water maze and novel object recognition task, respectively. Results of this study showed a reversal of noise-induced memory impairment in rats. The derangements of catecholaminergic and serotonergic levels in the hippocampus and altered brain antioxidant enzyme activity due to noise exposure were also restored by taurine administration. This study highlights the importance of taurine supplementation to mitigate noise-induced impaired memory via normalizing the neurochemical functions and reducing oxidative stress in rat brain.

Exposure to cadmium has been extensively increased due to its usage in modern daily life. Inside the human body it induces deteriorating effects in every vital organ including brain. Oxidative stress has been widely implicated in neurotoxicity induced by cadmium exposure. Consumption of dietary source of exogenous antioxidants is one of the recommended ways to extenuate heavy metal-induced oxidative stress. The potential of nuts against heavy-metal induced neurotoxicity has not been investigated earlier. This study was, therefore, conducted to find out the antioxidant ability of almond and walnut in the prevention of cadmium-induced oxidative stress. Rats were treated with nuts (400 mg/kg) daily for 28 days whereas, cadmium (50 mg/kg) was given once in a week. Brain function was monitored in terms of memory performance using Morris water maze and elevated plus maze. Moreover, oxidative stress status was also evaluated. Results showed that weekly exposure of cadmium significantly reduced %memory retention, increased lipid per oxidation and inhibited antioxidant enzymes activity. When nuts supplemented rats were monitored for these parameters, it was observed that almond and walnut have a great potential to reduce cadmium-induced neurotoxicity as evident by decreased oxidative stress and improved memory function in cadmium intoxicated rats.

Background/aim: To evaluate the protective effect of melatonin on ovarian ischemia reperfusion injury in a rat model., Materials and Methods: Forty-eight rats were separated equally into 6 groups. Group 1: sham; Group 2: surgical control with 3-h bilateral ovarian torsion and detorsion; Group 3: intraperitoneal 5% ethanol (1 mL) just after detorsion (as melatonin was dissolved in ethanol); Group 4: 10 mg/kg intraperitoneal melatonin 30 min before 3-h torsion; Group 5:10 mg/kg intraperitoneal melatonin just after detorsion; Group 6:10 mg/kg intraperitoneal melatonin 30 min before torsion and just after detorsion. Both ovaries and blood samples were obtained 7 days after detorsion for histopathological and biochemical analysis., Results: In Group 1, serum levels of total oxidant status (TOS) (μmol H2O2 equivalent/g wet tissue)were significantly lower than in Group2 (P = 0.0023), while tissue TOS levels were lower than in Group 3 (P = 0.0030). Similarly, serum and tissue levels of peroxynitrite in Group 6were significantly lower than those ofGroup 2 (P = 0.0023 and P = 0.040, respectively). Moreover, serum oxidative stress index (OSI) (arbitrary unit) levels were significantly increased in Group 2 when compared to groups 1 and 6 (P = 0.0023 and P= 0.0016, respectively) and in Group 3 with respect to groups 1, 4, 5, and 6 (P = 0.0023, P = 0.0026, P = 0.0008, and P = 0.0011, respectively). Furthermore, there was a significant decrease in histopathological scores including follicular degeneration, vascular congestion, hemorrhage, and inflammation in the melatonin and sham groups in comparison with control groups. Additionally, primordial follicle count was significantly higher in Group 6 than in Group 2 (P = 0.0002)., Conclusion: Melatonin attenuates ischemia reperfusion damage in a rat torsion/detorsion model by improving histopathological and biochemical findings including OSI and peroxynitrite., Competing Interests: The authors report no conflict of interest with any funding agency or commercial sectors., (This work is licensed under a Creative Commons Attribution 4.0 International License.)

Spirulina platensis (blue-green algae) is a nutritional supplement. It constitutes of high content of protein, antioxidants, various phytopigments and possesses neuroprotective activities. Schizophrenia (SZ) is recognized as a neuropsychiatric disorder in humans with a reduced lifespan followed with impairments in social as well as vocational functioning. Major psychotic symptoms of SZ cluster into three categories: positive, negative and cognitive dysfunctions. Dizocilpine recognized as one of the best drugs to mimic full spectrum of SZ can develop an animal model of the disorder. Various antipsychotics are considered as approved treatment therapy for the psychotic symptoms of SZ but they also exert adverse effects. Thus, there is an excessive need for novel treatment(s) with negligible adverse effects. Present study was designed to evaluate the neuroprotective effects of spirulina in ameliorating the psychosis- like symptoms in dizocilpine-induced rat model of SZ. Spirulina was tested at the dose of 180 mg/kg. Results showed that administration of spirulina improved behavioral deficits and combated the oxidative damage evident by a significant reduction in lipid peroxidation and increase in antioxidant level. Thus, from present findings it may be suggested that spirulina can be used as a therapy for preventive or therapeutic measures.

Objective: To determinate the effects of bilirubin and phototherapy on oxidative stress in newborns., Study Design: A case-control study., Place and Duration of Study: Third level Newborn Intensive Care Unit, Ankara Etlik Zubeyde Hanim Women's Health Teaching and Research Hospital, Turkey, from May to August 2017., Methodology: Blood samples of 62 term newborns were grouped as control, before and after phototherapy. Total and native thiol, disulfide and ischemia modified albumin values in expressed blood samples were measured. Disulfide-native thiol ratio, disulfide-total thiol ratio and native thiol-total thiol ratio values were computed., Results: Bilirubin levels were positively correlated with native and total thiol levels and negatively correlated with ischemia modified albumin levels (r=0.409 p= 0.001, r= 0.328 p<0.009, r=-0.503 p<0.001). Native and total thiol levels of the control group were lower (p<0.001) and ischemia modified albumin levels were higher than those before and after phototherapy (p<0.001). In jaundiced newborns, native and total thiol values reduced after phototherapy, while IMA levels increased (p=0.001, p<0.001, p<0.001)., Conclusion: Bilirubin showed antioxidant effect without increasing oxidative stress. Oxidative stress increased after phototherapy. This result was associated with decrease in bilirubin rather than oxidative effect of phototherapy.

Unpredictable chronic mild stress (UCMS) model is the most established method to study neurobiological mechanisms of depression. This work was intended to explore the efficacy of curcumin to revert the UCMS-induced oxidative burden and associated depression as well as potential of curcumin as an acetyl cholinesterase (AchE) inhibitor. Animals were initially grouped into control and curcumin (200mg/kg, p.o) and further subdivided into unstressed and stressed groups. Depression and anxiety were evaluated by forced swim test (FST) and light/dark transition (LDT) while memory function was assessed by passive avoidance test (PAT). Effect of curcumin on oxidative stress following UCMS was determined by measuring peroxidation of lipid (LPO) and antioxidant enzyme activities. AchE activity was also determined. Findings showed that curcumin supplementation significantly attenuated the UCMS-induced depression and anxiety like symptoms, decreased the load of UCMS propagated oxidative stress by improving antioxidant enzymes activities. Curcumin also improved the memory function and exhibited inhibitory effect on AchE activity. In conclusion it can be suggested that supplementation of curcumin in daily life can help in combating the stress-induced depression and ever increasing load of oxidative stress. Study also highlights the anti-acetylcholinesterase potential of curcumin which may be responsible for improved memory function following UCMS.

Scopolamine, an anti-muscarinic agent, has been shown to induce amnesia and oxidative stress similar to that observed in the older age. The present study was designed to determine the relationship between the oxidative status and memory improvement in scopolamine injected rats pre-administered with almonds. Rats (n = 8) in the almond group were administered orally with 400 mg/kg almond suspension for 28 days daily before the intraperitoneal injection of scopolamine (0.5 mg/kg). Passive avoidance task (PAT) was used to assess memory function at the end of treatment. The present study revealed that scopolamine injection significantly impaired the memory function in rats pre-treated with saline which was accompanied by increased oxidative stress as evident by increased brain malondialdehyde (MDA) levels and reduced activities of antioxidant enzymes as compared to healthy controls. Pre-treatment with almond significantly ameliorated scopolamine-induced oxidative stress and memory dysfunction. These findings suggest that dietary supplementation with almonds may have a beneficial effect in reducing the risk of oxidative stress-induced memory loss and delaying or preventing the onset of age-related memory impairment.

Aims: Free radical mediated neurotoxicity is a leading cause of neurodegenerative disorders. Neurodegeneration due to oxidative stress can produce cognitive dysfunctions. Flavonoids and curcuminoids are naturally occurring polyphenolic compounds that display a variety of therapeutic importance against oxidative stress., Main Methods: This study was designed to assess potential role of polyphenolic compounds in neurocognitive functions and prevention against oxidative stress. For this purpose, young rats were orally treated with naringenin (NAR), curcumin (CUR) and quercetin (QUE) at a dose of 50mg/kg, 200mg/kg and 50mg/kg respectively for 16days. At 4th day of drug administration cognitive functions were monitored by Morris water maze (MWM) test. In MWM cognitive functions in terms of learning acquisition (1h after training), retention (24h after training), memory extinction (4days after training), and reconsolidation (8 and 12days after training) were monitored. Biochemical and neurochemical analysis were done in whole brain., Key Findings: Treatment of NAR, CUR and QUE significantly enhanced learning acquisition, memory retention and reconsolidation and prevented memory extinction. Treatment of NAR and QUE prevented the alteration of brain antioxidant defence system by enhancing antioxidant enzyme activities and increasing antioxidant compound concentration. Oxidative stress in terms of lipid peroxidation was significantly prevented in treated rats. Serotonergic and cholinergic improvement was also found in treated rats., Significance: The present study therefore provides biological evidence supporting the usefulness of these polyphenolic compounds in daily life for improvement of cognitive abilities and hence may have a potential role in the management of dementia and related disorders., (Copyright © 2017 Elsevier Inc. All rights reserved.)

The brain is highly susceptible to the damaging effects of oxidative reactive species. The free radicals which are produced as a consequence of aerobic respiration can cause cumulative oxygen damage which may lead to age-related neurodegeneration. Scopolamine, the anti-muscarinic agent, induces amnesia and oxidative stress similar to that observed in the older age. Studies suggest that antioxidants derived from plant products may provide protection against oxidative stress. Therefore, the present study was designed to investigate the attenuation of scopolamine-induced memory impairment and oxidative stress by walnut supplementation in rats. Rats in test group were administrated with walnut suspension (400 mg/kg/day) for four weeks. Both control and walnut-treated rats were then divided into saline and scopolamine-treated groups. Rats in the scopolamine group were injected with scopolamine (0.5 mg/kg dissolved in saline) five minutes before the start of each memory test. Memory was assessed by elevated plus maze (EPM), Morris water maze (MWM), and novel object recognition task (NOR) followed by estimation of regional acetylcholine levels and acetylcholinesterase activity. In the next phase, brain oxidative status was determined by assaying lipid peroxidation, and measuring superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) activities. Results showed that scopolamine-treatment impaired memory function, caused cholinergic dysfunction, and induced oxidative stress in rats compared to that saline-treated controls. These impairments were significantly restored by pre-administration of walnut. This study demonstrates that antioxidant properties of walnut may provide augmented effects on cholinergic function by reducing oxidative stress and thus improving memory performance.

Aim: To investigate the effects of severity of preeclampsia on thiol-disulfide homeostasis (TDH)., Material and Methods: A total of 108 participants were divided into three groups: Group 1 was composed of pregnant women with no obstetric complications, Group 2 included pregnant women with mild preeclampsia, and Group 3 consisted of pregnant women with severe preeclampsia. TDH parameters were determined, and comparisons of clinical and routine laboratory test findings were made in all groups., Results: The serum native thiol level was 347.9 ± 27.4 in the control group, 237.2 ± 44.2 in the mild preeclampsia group, and 227.9 ± 53.1 in the severe preeclampsia group (p < 0.001). The serum total thiol level was 376.1 ± 31.9 in the control group, 261.8 ± 49.4 in the mild preeclampsia group, and 248.3 ± 57.4 in the severe preeclampsia group (p < 0.001). The disulfide level was 14.1 ± 5.6 in the control group, 12.3 ± 5.1 in the mild preeclampsia group, and 10.2 ± 4.8 in the severe preeclampsia group (p = 0.001). A significant correlation between impairment in degree of TDH and severity of preeclampsia was observed., Conclusion: TDH was impaired in women with preeclampsia, and this impairment increased with disease severity. Therefore, impaired TDH may have a role in the etiopathogenesis of the disease.

Purpose: The purpose of the current prospective study was to evaluate the effects of low sodium dialysate on oxidative stress parameters, blood pressure (BP) and endothelial dysfunction in maintenance hemodialysis (HD) patients., Methods: After baseline measurements were taken, the dialysate sodium concentration was reduced from 140 to 137 mEq/L. Oxidative stress parameters and flow-mediated dilatation (FMD %) were measured before and after 6 months of HD with low sodium dialysate. Interdialytic weight gain (IDWG) and pre- and post-dialysis BP were monitored during the study., Results: A total of 52 patients were enrolled and 41 patients completed the study. There was a significant reduction in systolic blood pressure at the end of the study [130.00 (90.00-190.00) vs. 120.00 (90.00-150.00), p < 0.001]. Similarly, there were significant improvements in IDWG [2670.00 (1670.00-4300.00) vs. 1986.00 (1099.00-3998.00), p < 0.001] and FMD % [7.26 (4.55-8.56) vs. 9.56 (6.55-12.05), p < 0.001]. Serum MDA levels (p < 0.001) were significantly decreased; serum SOD (p < 0.001) and GPx (p < 0.001) activities were significantly increased after low sodium HD compared to standard sodium HD., Conclusion: Our data seem to suggest a potential role of 137 mEq/L sodium dialysate for improving hemodynamic status, endothelial function and reducing oxidative stress than 140 mEq/L sodium dialysate in maintenance HD patients.

Purpose: Insulin resistance (IR) and increased oxidative stress (OS) are the characteristics of polycystic ovary syndrome (PCOS). In this study, we aimed to evaluate the effects of oral glucose tolerance (OGTT) and mixed meal tests (MMT) on plasma total oxidant (TOS) and total antioxidant status (TAS) in patients with PCOS and the relationship between these parameters and IR, calculated via homeostasis of model assessment-IR (HOMA-IR) and Matsuda's insulin sensitivity index (ISI) derived from OGTT and MMT., Methods: Twenty-two patients with PCOS, and age- and body mass index (BMI)-matched 20 women as controls were enrolled into the study. Five-hour OGTT and MMT were performed on different days, and before and after these tests, plasma TOS and TAS levels were investigated. IR was calculated with HOMA-IR and Matsuda's ISI., Results: HOMA-IR levels were higher in patients with PCOS, compared to controls, while Matsuda's ISI derived from OGTT and MMT was higher in controls. Plasma TOS levels before OGTT and MMT were higher in patients with PCOS than controls, while TAS levels were similar. After OGTT, plasma TOS levels became decreased at 5th hour, when compared to baseline values in PCOS group. Likewise, the same decrement was found in controls, but the decrement was not significant. After OGTT and MMT at 5th hour, no changes were observed in TAS levels, compared to baseline., Conclusion: Matsuda's ISIs derived from OGTT and MMT can be used instead of each other, and interestingly, we found a decrease in TOS levels after OGTT in patients with PCOS.

Objectives: Asthma is a chronic inflammatory lung disease characterized by bronchial hyperresponsiveness and airflow obstruction. Genetic and oxidative stress factors, in addition to pulmonary and systemic inflammatory processes, play a pivotal role in the pathogenesis of asthma. The products of the multidrug resistance-1 gene protect lung tissue from oxidative stress. Here, we aimed to evaluate the association between the multidrug resistance-1 gene C>T polymorphism and asthma with regard to oxidative stress-related parameters of asthmatic patients., Methods: Forty-five patients with asthma and 27 healthy age-matched controls were included in this study. Blood samples were collected in tubes with ethylenediaminetetraacetic acid. DNA was extracted from the blood samples. The multidrug resistance-1 gene polymorphism was detected by polymerase chain reaction and a subsequent enzyme digestion technique. The serum levels of total oxidant status and total antioxidant status were determined by the colorimetric measurement method., Results: The heterozygous polymorphic genotype was the most frequent in both groups. A significant difference in the multidrug resistance-1 genotype frequencies between groups indicated an association of asthma with the TT genotype. A significant difference between groups was found for wild type homozygous participants and carriers of polymorphic allele participants. The frequency of the T allele was significantly higher in asthmatic patients. The increase in the oxidative stress index parameter was significant in the asthma group compared with the control group., Conclusions: The multidrug resistance-1 gene C/T polymorphism may be an underlying genetic risk factor for the development of asthma via oxidant-antioxidant imbalance, leading to increased oxidative stress.

Background: Increased levels of reactive oxygen species during and after surgery may affect inflammatory response, post-operative adhesion molecule formation, and hemodynamic stability. The glutathione redox cycle is an important regulator in oxidative stress and its reduced forms scavenge free radicals. N-acetyl cysteine, a precursor of reduced glutathione, is considered as a potentially therapeutic wide spectrum agent in clinical practice. We therefore examined whether N-acetyl cysteine improves some biochemical parameters in cancer patients undergoing major abdominal surgery., Methods: Thirty-three patients diagnosed with pancreas, stomach, rectum, colon malignancies, and undergoing major abdominal surgery at Ankara Numune Training and Research Hospital were randomly divided into two groups; control (CON) and N-acetyl cysteine (NAC). The NAC group had 1,200 mg N-acetyl cysteine starting two days before the operation day, in addition to isonitrogenous and isocaloric total parenteral nutrition of 1.2 g/kg protein, 25 kcal/kg, and 60:40 carbohydrate/fat ratio. Blood and urine samples were drawn two days before the operation, on operation day, and on the first, third, and fifth days post-operation., Results: Plasma malondialdehyde was significantly lower in the NAC group (P < 0.001). N-acetyl cysteine treatment did not affect plasma levels of vitamin A, C or E. The NAC group exhibited a higher ratio of reduced glutathione to oxidised glutathione (P = 0.019). Urinary nitrate level was also significantly lower in the NAC group (P = 0.016)., Conclusion: The study demonstrated the clinical importance of N-acetyl cysteine supplementation on antioxidant parameters in abdominal surgery patients. In these patients N-acetyl cysteine and vitamin administration can be considered as an effective method for improvement of oxidative status.

The aim of this study was to evaluate the protective effects of Pycnogenol® (Pyc), a complex plant extract from the bark of French maritime pine, on oxidative stress parameters (superoxide dismutase (SOD), and glutathione peroxidase (GPx) activities and total glutathione (GSH) and malondialdehyde (MDA) levels), an inflammatory cytokine (tumor necrosis factor alpha (TNF-α) level) and also DNA damage in Wistar albino rats. Rats were treated with 100 mg/kg intraperitonally Pyc following the induction of sepsis by cecal ligation and puncture. The decreases in MDA levels and increases in GSH levels, and SOD and GPx activities were observed in the livers and kidneys of Pyc-treated septic rats. Plasma TNF-α level was found to be decreased in the Pyc-treated septic rats. In the lymphocytes, kidney, and liver tissue cells of the sepsis-induced rats, Pyc treatment significantly decreased the DNA damage and oxidative base damage using standard alkaline assay and formamidopyrimidine DNA glycosylase-modified comet assay, respectively. In conclusion, Pyc treatment might have a role in the prevention of sepsis-induced oxidative damage not only by decreasing DNA damage but also increasing the antioxidant status and DNA repair capacity in rats., (Copyright © 2014 John Wiley & Sons, Ltd.)

Background: It has been suggested that off-pump coronary artery bypass grafting (CABG) surgery reduces myocardial ischemia-reperfusion injury, postoperative systemic inflammatory response, and oxidative stress. The aim of this study was to measure serum malondialdehyde (MDA), high-sensitivity C-reactive protein (hs-CRP), M30, and M65 levels and to investigate the relationship between M30 levels and oxidative stress and inflammation in patients undergoing on-and off-pump CABG surgery., Methods: Fifty patients were randomly assigned to on-pump or off-pump CABG surgery (25 patients off-pump and 25 on-pump CABG surgery), and blood samples were collected prior to surgery, and 30 minutes, 60 minutes, 6 hours, and 24 hours after CABG surgery., Results: Compared to the on-pump group, serum MDA levels at 30 minutes, 60 minutes, 6 hours, and 24 hours after the CABG surgery were significantly lower in the off-pump group (P=.001, P=.001, P=.001, and P=.001, respectively). Serum M30 levels were found to be elevated in both groups, returning to baseline at 24 hours. When compared to baseline, the hs-CRP level reached its peak at 24 hours at 13.28±5.32 mg/dL in the on-pump group, and 15.44±4.02 mg/dL in the off-pump group., Conclusion: CABG surgery is associated with an increase in inflammatory markers and serum M30 levels, indicating epithelial/endothelial apoptosis in the early period.

Purpose: In this study, we tested the effects of L-carnitine (LC) on radiation-induced ileal mucosal damage., Materials and Methods: Thirty Wistar albino rats were divided into five groups. The control group received physiological saline intraperitoneally (i.p.). Radiation-1 and radiation-2 groups received whole-body X-irradiation of 8.3 Gy as a single dose. These groups were sacrificed at the 6th hour and 4th day after irradiation, respectively. The Radiation-1 + LC and the radiation-2 + LC groups received the same dose irradiation plus a daily dose of 200 mg/kg LC. LC was applied one day before and for four days after irradiation., Results: The levels of serum monocyte chemotactic protein-1 (MCP-1) and interferon gamma (IFN-γ) were significantly higher in the radiation groups when compared with the control. Treatment with LC decreased the serum MCP-1 and IFN-γ levels considerably. In the radiations groups, the Chiu score was significantly elevated compared with that of the control group. However, LC administered prior to the irradiation reduced the severity of mucosal damage. The number of apoptotic cells of the ileal crypt in the irradiated rats increased from the 6th hour after irradiation and then decreased at 4th day., Conclusions: Our data demonstrated that LC may be beneficial to radiation enteritis.

Objective: The aim of this study was to evaluate the association of tenascin-C (TnC) and total oxidant-antioxidant status to rheumatic or congenital heart valve diseases (HVD) in pediatric patients., Methods: Fifty pediatric patients (25 rheumatic HVD patients and 25 congenital HVD patients) and 20 healthy age-matched control subjects, aged 3-17 years, were enrolled in this observational and cross-sectional study. Serum total antioxidant capacity (TAC), total oxidant status (TOS), oxidative stress index (OSI) and TnC levels were compared among the groups. ANOVA and Kruskal-Wallis tests were used for statistical analysis., Results: Serum TnC level of the patients with rheumatic HVD [median 9.09 (0.94-46.30) ng/mL] was significantly higher than both congenital HVD and control groups [median 2.97 (0.66-11.80) ng/mL; p<0.01, 4.72±1.77 ng/mL; p<0.05, respectively]. However, there was no statistically significant difference between the congenital and control groups in terms of serum TnC level. The levels of serum TAC, TOS and OSI were found to be statistically similar in all groups. In addition, there were no correlations between the level of TnC, and TOS and OSI., Conclusion: Tenascin-C can be used as a biochemical marker in the differential diagnosis of rheumatic and congenital HVD. As the oxidant and antioxidant systems were found to be in equilibrium in rheumatic and congenital HVD, oxidative stress can be thought not to have a marked role in the etiopathogenesis of rheumatic HVD during childhood.

Chronic hyperglycemia causes increased level of reactive oxygen species which is thought to be involved in the pathogenesis of diabetes associated complications including cataract. In diabetic cataractous lens, over production of free radicals and decreased capacity of antioxidant defense system are the major contributors to oxidative damage by polyol pathway and advanced glycation end products. The current study focused on analysis of factors associated with osmotic imbalance and oxidative stress in aging and diabetic human cataractous lenses. We examined activities of polyol pathway enzymes, G6PD and glutathione system in lenses from subjects suffering from cataract due to aging and diabetes. We observed elevated activities of aldose reductase and sorbitol dehydrogenase while G6PD and glutathione system enzyme activities were found to be lower in cataractous subjects suffering from diabetes. The findings from the current study support the premise that osmotic imbalance, AGEs formation and oxidative stress contribute synergistically to the development of lens opacity in hyperglycemia., (Copyright © 2012 Elsevier Inc. All rights reserved.)

Background: Oxidative stress has a critical role in inflammatory responce against tobacco smoke (TS). Testing exhaled breath condensate (EBC) samples is one of the methods used for assessment of airway inflammation caused by TS. We aimed to investigate oxidative stress in the lungs associated with TS and to evaluate the effect of this stress with pulmonary function tests (PFTs)., Methods: We included 69 subjects as three groups into the study (Group I; 26 smokers, Group II; 21 passive smokers, Group III; 22 non-smokers without TS exposure). Levels of malondialdehyde (MDA), 8-hydroxydeoxyguanosine (8-OHdG), nitrite/nitrate [index of nitric oxide (NO) production], vitamin C, superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were measured in EBC samples collected using a condenser and PFTs were performed., Results: The levels of MDA, 8-OHdG, SOD and GSH-Px were higher in smokers. NO levels gradually increased from Group I to Group III. MDA levels were lower in Group III than Group II. The levels of vitamin C were similar in all groups. We determined negative correlation between 8-OHdG levels and forced expiratory volume in one second (FEV₁), and maximum mean expiratory flow (MMEF), and a positive correlation between SOD levels and FEV₁., Conclusions: TS exposure affected the balance between oxidative stress and antioxidant capacity of lungs. Preventing environmental TS exposure might decrease oxidative damage. Increased levels of 8-OHdG and SOD levels could be assessed as an early sign of airway damage.

Purpose: The relationship between increasing ratio of progesterone in estrogen/progesterone combination and oxidative stress (OS) was investigated., Methods: Thirty non-pregnant Wistar Albino female rats were divided into five groups and bilaterally ovariectomized (Ovx) except sham group. GROUPS: Sham + 0.3 cc seaseme oil, Ovx + 0.3 cc seaseme oil, Ovx + estradiol propionate (E2) (1 μg/kg), Ovx + E2 + medroxyprogesterone acetate (MPA) 1 mg/kg, Ovx + E2 + MPA 20 mg/kg. Hormones were applied for three consecutive days after 28 days of ovariectomy. Their uteri and blood samples were collected and nitric oxide (NO), malondialdehyde (MDA), total oxidative status (TOS) and total antioxidant capacity (TAC) levels were determined., Results: E2 + MPA1 treatment decreased NO, MDA and TOS levels and increased TAC levels in uterus. Plasma NO levels elevated in all groups and MDA production increased due to E2 treatment when compared to ovariectomy. E2 + MPA20 treatment increased TOS levels, while TAC levels decreased when compared to ovariectomy in plasma., Conclusions: Using E2 plus low dose progesterone may prevent pathologies resourced of OS.

Background: Even though there is ample evidence on the oxidative stress in asthma, there is limited information on the antioxidant defense systems., Objectives: To conduct a comprehensive evaluation of various components of both enzymatic and nonenzymatic antioxidants in a large group of children with asthma., Methods: A total of 164 children with mild asthma and 173 healthy children were included in the study. Levels of the enzymes glutathione peroxidase and superoxide dismutase were measured by using ELISA, whereas reduced glutathione, ascorbic acid, alpha-tocopherol, lycopene, beta-carotene, amino acids participating in glutathione synthesis, and amino acids susceptible to oxidation were measured by HPLC. All comparisons were adjusted for atopy, body mass index, smoke exposure, and pet ownership., Results: Levels of the enzymes glutathione peroxidase and superoxide dismutase and of the nonenzymatic components of the antioxidant system including reduced glutathione, ascorbic acid, alpha-tocopherol, lycopene, and beta-carotene were significantly lower in children with asthma compared with healthy controls (P < .001 for each). Of the amino acids contributing to glutathione synthesis, glycine and glutamine were significantly lower in children with asthma (P < .001). The majority of the amino acid susceptible to oxidative stress displayed lower levels in children with asthma (P < .05)., Conclusion: Childhood asthma is associated with significant decreases in various components of both enzymatic and nonenzymatic antioxidant defenses.

Oxidative stress may have a role in liver damage after acute renal injury due to various reasons such as ischemia reperfusion (IR). Diabetes mellitus (DM) is an important disease for kidneys and may cause nephropathy as a long term complication. The aim of this study was to investigate protective effect of melatonin, a potent antioxidant, against distant organ injury on liver induced by renal IR in rats with or without DM. The rats were divided into six groups: control (n=7), DM (n=5), IR (n=7), DM+IR (n=7), melatonin+IR (Mel+IR) (melatonin, 4 mg/ kg during 15 days) (n=7), and Mel+DM+IR groups (n=7). Diabetes developed 3 days after single i.p. dose of 45 mg/kg streptozotocin. After 15 day, the left renal artery was occluded for 30 min followed 24 h of reperfusion in IR performed groups. DM did not alter oxidative parameters alone in liver tissue. The levels of malondialdehyde, protein carbonyl and nitric oxide with activities of xanthine oxidase and myeloperoxidase were increased in liver tissues of diabetic and non-diabetic IR groups. Nitric oxide level in DM was higher than control. The activities of catalase and superoxide dismutase were increased in IR groups in comparison with control and DM. ALT and AST levels were higher in IR and DM+IR groups than control and DM. Melatonin treatment reversed all these oxidant and antioxidant parameters to control values as well as serum liver enzymes. We concluded that renal IR may affect distant organs such as liver and oxidative stress may play role on this injury, but DM has not an effect on kidney induced distant organ injury via oxidant stress. Also, it was concluded that melatonin treatment may prevent liver oxidant stress induced by distant injury of kidney IR.

This study was performed to evaluate the effect of melatonin on methanol-induced liver injury. We evaluated the levels of malondialdehyde (MDA), protein carbonylation (PC), myeloperoxidase (MPO) activities and to assess lipid peroxidation, protein oxidation, neutrophil accumulation and nitrite which is a stable end product of nitric oxide respectively. We also studied superoxide dismutase, catalase, and glutathione peroxidase activities of liver tissue to evaluate the changes in the antioxidant status. Histopathological alterations were also determined. The experiment was performed on Wistar rats, which received intragastric 3 g/kg methanol as a 50% solution in isotonic saline once. After 6 and 24 hr all the drug received and intoxicated rats were killed under anesthesia. Pretreatment with melatonin (10 mg/kg) decreased the MDA levels significantly, restored the PC levels to the control, prevented the increase of nitrite level and MPO activity significantly and reversed to the control levels, prevented the reduction in all of the antioxidant enzyme activities. Additionally in melatonin treated group piecemeal necrosis, lobular lytic necrosis, and portal inflammation returned to normal histologic appearances when compared with methanol administration. In conclusion, melatonin has protective effects against methanol-induced hepatic injury.

Objective: Acute coronary syndromes (ACS) encompass a continuum of cardiac ischaemic events, ranging from unstable angina pectoris (UA) to ST-segment elevation myocardial infarction (STEMI). Oxidative stress may play an important role in the pathogenesis of acute coronary diseases. In the present study, we examined the associations between lipid and protein susceptibility to oxidation and total sialic acid (SA) and antioxidant status and the severity of ACS as determined by having UA, non-STEMI or STEMI., Methods and Results: The study sample consisted of 102 patients with ACS and 45 controls. Malondialdehyde (MDA) as a marker of lipid peroxidation and protein carbonyls as a marker of protein oxidation were measured to show the susceptibility to oxidation. Antioxidant status was determined by measuring the carotenoids, vitamin C and vitamin E levels and paraoxonase and arylesterase activities. In addition to conventional lipid and lipoprotein analysis, MDA and vitamin E were quantitated by high-performance liquid chromatography. Total SA and other oxidant and antioxidant parameters were studied spectrophotometrically. As expected, patients had significantly higher total cholesterol, triacylglycerol, low-density lipoprotein cholesterol, lipoprotein (a), apolipoprotein (apo) B values and lower high-density lipoprotein cholesterol and apoAl values than controls. Our results demonstrated significant increases both in total SA levels and in indicators of oxidative stress in patients with ACS compared with the controls. However, antioxidant parameters were decreased in patients with ACS. When the patients were divided into groups with UA, non-STEMI and STEMI, respectively, total SA and oxidant parameters were significantly increased and antioxidant parameters were significantly decreased in going from UA to STEMI., Conclusions: Our study shows gradually increased lipid and protein oxidation and total SA and gradually decreased antioxidant status when the conditions advance from UA to STEMI. These results indicate that these markers may be useful both in understanding plaque destabilization and in determination of risk stratification of patients. Also, measurement of these markers may provide a noninvasive window to study atherosclerotic lesions.

Our aim was to investigate parameters of iron and copper status and oxidative stress and antioxidant function in women with healthy pregnancy, mild and severe preeclampsia with a view to exploring the possible contribution of these parameters to the aetiology. Thirty healthy, 30 mild preeclamptic and 30 severe preeclamptic pregnant women were included. Serum and placental lipid peroxides, and serum vitamin E and total carotene levels were measured by colorimetric assay. Cholesterol, copper, iron, total iron binding capacity (TIBC), ceruloplasmin and transferrin concentrations were measured by commercially available procedures. Data were analysed statistically using one-way analysis of variance and Pearson correlation test. Logistic regression procedures were used to calculate odds ratios. Lipid peroxides in serum and placental tissue, and iron, copper and ceruloplasmin levels in serum were significantly increased, and transferrin, TIBC, vitamin E/total cholesterol and total carotene/total cholesterol ratios in serum were significantly decreased especially in women with severe preeclampsia. Significant correlations were detected between serum iron and lipid peroxides in serum and placental tissue and between serum iron and vitamin E/total cholesterol in severe preeclamptic pregnancy. Furthermore, there were significant correlations between serum malondialdehyde and ceruloplasmin and vitamin E/total cholesterol in women with severe preeclampsia, and changes in serum and placental lipid peroxides and serum iron concentrations were significantly associated with preeclampsia. In conclusion, ischaemic placental tissue may be a primary source of potentially toxic iron in preeclampsia and the released iron species may contribute to the aetiology and would exacerbate lipid peroxidation and endothelial cell injury, which may be abated by antioxidant supplementation., (Copyright (c) 2005 John Wiley & Sons, Ltd.)

The purpose of this study was to investigate the oxidative status in experimental hypothyroidism and the antioxidant effect of taurine supplementation. Forty male Sprague Dawley rats were randomly divided into four groups (group 1, control; group 2, control + taurine; group 3, propylthiouracil (PTU); group 4, PTU + taurine). Hypothyroidism was induced by giving 0.05% PTU in drinking water for 8 weeks. Taurine was supplemented in drinking water at a concentration of 1% for 5 weeks. Plasma (p < 0.05), red blood cell (p < 0.01), liver (p < 0.001) and kidney tissue (p > 0.05) malondialdehyde levels were increased in the PTU group compared with those of the control rats and were decreased in the PTU + taurine group compared with the PTU alone group. No significant changes were observed in glutathione levels of kidney and liver in the PTU group, but taurine supplementation significantly increased the glutathione levels of these tissues. Paraoxonase and arylesterase activities were decreased in the PTU group while taurine supplementation caused no significant changes in paraoxonase and arylesterase activities. These findings suggest that taurine supplementation may play a protective role against the increased oxidative stress resulting from hypothyroidism., (Copyright 2005 John Wiley & Sons, Ltd.)

Recent evidence suggests that postischemic myocardial dysfunction ("stunning") may be mediated by oxygen free radicals. Various studies have reported the beneficial effects of antioxidants in ischemia-reperfusion injury. The aim of this study was to assess the effect of N-acetylcysteine (NAC) treatment on oxidative stress, infarct size, and left ventricular (LV) function, as adjunct therapy in myocardial infarction (MI). Patients with acute MI received either 15 g NAC infused over 24 h (n = 15) or no NAC (n = 15), combined with streptokinase. Peripheral venous blood was serially sampled to measure creatine kinase (CK)-MB levels. Plasma malondialdehyde (MDA) level was measured at admission and after 4 and 24 h. Echocardiography was performed within 3 days of MI and after 3 months. At admission, plasma MDA levels were not different between the groups. In the NAC-treated patients plasma MDA levels decreased, whereas in the nontreated NAC patients MDA levels increased at 4 and 24 h (P < 0.01 and P < 0.001, respectively). Left ventricular ejection fraction was higher (P < 0.05) and LV end-systolic and end-diastolic diameters were lower (P < 0.001 and P < 0.001) in patients receiving NAC on day 3. Left ventricular wall motion score index was significantly lower in patients treated with NAC on day 3 (P < 0.05). Left ventricular diastolic parameters were not different whether patients were treated with NAC or not. No difference in reduction of infarct size was detected between the groups according to CK-MB levels. It was thus demonstrated that administration of NAC in combination with streptokinase significantly diminished oxidative stress and improved LV function in patients with acute MI. These encouraging results would justify the performance of a larger controlled study.

Thyroid hormones are associated with the oxidative and antioxidative status of the organism. Since data on the oxidative status of hypothyroidism are limited and controversial, we investigated the oxidant and antioxidant status and serum paraoxonase/arylesterase activities in propylthiouracil-induced hypothyroidism and examined the effect of vitamin E supplementation on this experimental model. Forty male Sprague Dawley rats were randomly divided into four groups (group 1, control; group 2, control + vitamin E; group 3, propylthiouracil; group 4, propylthiouracil + vitamin E). Plasma, red blood cell, liver, heart and skeletal muscle malondialdehyde levels were increased in the propylthiouracil-treated group compared with the control rats and were decreased in propylthiouracil + vitamin E group compared with the propylthiouracil-treated group. Vitamin E supplementation also significantly increased liver and kidney reduced glutathione levels in propylthiouracil treated animals. Serum paraoxonase and arylesterase activities were decreased in propylthiouracil treated group and vitamin E supplementation caused significant increase in serum paraoxonase activity compared with the propylthiouracil-treated rats. These findings suggest that hypothyroidism is accompanied with increased oxidative stress and vitamin E supplementation exerts beneficial effects on this situation.