Oxidative Stress In Pathophysiology Research Articles

Knockdown of LincRNACOX2 Alleviates Oxidative Stress in Pathophysiology of Acute Lung Injury

Acute lung injury (ALI) has a complicated etiology that involves oxidative stress and inflammation. The role of lncRNACox2 (lincCOX2) in ALI regulation remains unclear. In this study, the ALI model of mice and MLE-12 cell was induced by LPS. To investigate the expression of lncRNACox2 in these ALI models, we employed a nanomagnetic bead-based RNA extraction method for quantitative reverse transcription polymerase chain reaction (qRT-PCR) analysis. This enabled us to determine the levels of lncRNACox2 expression and evaluate knockdown efficiency. Moreover, we also examined lung tissue histopathology using H&E staining. Cell survival and apoptosis rates were evaluated through CCK-8 and flow cytometry, respectively. The concentration of inflammatory factors was measured using ELISA. Additionally, the concentration (8-OHdG and MDA) and enzymatic activity (CAT, GSH-Px, and SOD) of oxidative stress related factors were measured by biochemical method. The western blot was performed to present the key proteins expression level in Nrf2/ARE signaling pathway in cytoplasm and nucleoprotein. The ALI mouse model was successfully established. The histopathology change and inflammatory cells were observed by H&E staining in LPS treated groups. The expression of lincCOX2 was up-regulated in ALI tissue. LPS induced more cell death in ALI, and the knockdown of lincCOX2 improved the cell survival and suppressed the apoptosis in ALI cell. Furthermore, In addition, downregulation of lincCOX2 attenuated inflammation and oxidative stress in lung cells in ALI. The concentration of 8-OHdG and MDA were highest in the LPS group while reduced by the sh-lincCOX2, the activity of CAT, GSH-Px, and SOD was reduced in the LPS induced ALI and increased by the sh-lincCOX2. In ALI, the distribution of Nrf2 protein is transferred from cytoplasm to nucleus. Furthermore, the lincCOX2 regulated oxidative stress via Nrf2/ARE signaling pathway in ALI. Overall, downregulation of lincRNACOX2 alleviates oxidative stress in ALI via Nrf2/ARE Pathway. This study suggests that lincCOX2 may be a potential target for the treatment of ALI.

Effect of probiotics on total salivary antioxidant level and physical properties of saliva: An ex-vivo study

Background: Role of oxidative stress in pathophysiology of various diseases has already been established. Antioxidants act as free radical scavenger and prevent damage to cell, at the same time affects the metabolism of several pathogenic microbes. With increasing incidence of antibiotic resistance, alternative therapeutic treatment options are coming into picture. WHO claims probiotics to be the next most important immune defence system following antibiotic resistance. Even though there are several studies emphasising on the positive outcome of probiotics on diseases, their exact mechanism of action still remains debatable. The present study tried to unveil the antioxidant property of probiotics in saliva along with its effect on salivary pH and buffering capacity. Methods: Unstimulated saliva from 10 individuals were analysed for total antioxidant level, pH and buffering capacity using spectrophotometer, pH paper and buffering strips respectively, before and after probiotic intake for 2 weeks. Results: Probiotic intake led to increase in total salivary antioxidant level with no significant changes in pH and buffering capacity. Results obtained were statistically analysed using “paired t-test”. Conclusions: Probiotics are effective in increasing antioxidant level thereby minimizing cellular damage and hence can be used for prevention of several diseases. Also increase in antioxidant level can be easily assessed in saliva, thus, saliva can be used as a routine diagnostic tool.

A study of the role of calcium and oxidative stress in pathophysiology of osteoporosis in postmenopausal women-a review

The aim of this review was to identify the role of calcium and oxidative stress as factors associated with osteoporosis in postmenopausal women. There are many diseases related to post-menstruation in women, the most important of which is osteoporosis. Calcium levels remains stable until menopause, when the bone resorption rate increases in association with the decrease in ovarian estrogen production that effect the intestinal calcium absorption. On the other hand, studies support that oxidative stress is directly involved in the genesis and development of osteoporosis. However, Oxidative stress blocks the activation of osteoblasts and activates the differentiation of osteoclasts which led to increased resorption rate without adequate and proper bone formation. In conclusion, Physiological changes in postmenopausal women lead to fluctuations in calcium metabolism and oxidative stress, which may lead to the occurrence or development of osteoporosis.

Investigation of Thiol/Disulfide Balance and Oxidative DNA Damage in Patients Experiencing Avalanche Disaster and with a Diagnosis of Post-Traumatic Stress Disorder.

There are few studies on oxidative stress in patients with post-traumatic stress disorder (PTSD). The thiol/disulfide homeostasis is a new marker of oxidative stress. This study aimed to examine the oxidative DNA damage and thiol/disulfide homeostasis after 6 months in patients who developed PTSD after an avalanche disaster and to compare them with healthy controls. A total of 31 patients who developed PTSD after 2 consecutive avalanche disasters that occurred in Van on February 4 and 5, 2020, resulting in 42 deaths, and 33 healthy volunteers were included in the study. The patients were followed up by a psychiatrist within the framework of psychosocial intervention during their admission to Yüzüncü Yil University Medical Faculty Emergency Service. The patients monitored for a long time were diagnosed according to DSM-5 diagnostic criteria. The clinical follow-up was evaluated with the post-traumatic stress disorder self-assessment (PTSD-KD) and the impact of events scale. To determine oxidative DNA damage, 8-hydroxy-2-deoxyguanosine (8-OHdG) and deoxyguanosine (dG) levels were determined by isolating leukocyte DNA. Oxidative DNA damage was given as a ratio of 8-OHdG/106dG. Total thiol/native thiol levels were also determined. Disulfide levels were calculated by subtracting native thiol results from the total thiol results and dividing them by 2. It was determined that total thiol and native thiol levels in patients with PTSD were statistically significantly lower than in the healthy control group (P = .001), and the disulfide levels were higher in the PTSD group compared with that in the healthy control group (P = .001). In addition, 8-OHdG, an indicator of DNA damage, was found to be significantly lower in the control group than in the patient group (P = .001). In our study, thiol/disulfide homeostasis was observed to shift toward disulfide in patients with PTSD when compared with healthy controls. The level of 8-OHdG, the indicator of DNA damage, was observed to increase in patients with PTSD. This result indicates that thiol/disulfide homeostasis can be significant in the pathophysiology of oxidative stress in these patients.

Oxidative Stress, Antioxidant Capabilities, and Bioavailability: Ellagic Acid or Urolithins?

Oxidative stress (OS), triggered by overproduction of reactive oxygen and nitrogen species, is the main mechanism responsible for several human diseases. The available one-target drugs often face such illnesses, by softening symptoms without eradicating the cause. Differently, natural polyphenols from fruits and vegetables possess multi-target abilities for counteracting OS, thus representing promising therapeutic alternatives and adjuvants. Although in several in vitro experiments, ellagitannins (ETs), ellagic acid (EA), and its metabolites urolithins (UROs) have shown similar great potential for the treatment of OS-mediated human diseases, only UROs have demonstrated in vivo the ability to reach tissues to a greater extent, thus appearing as the main molecules responsible for beneficial activities. Unfortunately, UROs production depends on individual metabotypes, and the consequent extreme variability limits their potentiality as novel therapeutics, as well as dietary assumption of EA, EA-enriched functional foods, and food supplements. This review focuses on the pathophysiology of OS; on EA and UROs chemical features and on the mechanisms of their antioxidant activity. A discussion on the clinical applicability of the debated UROs in place of EA and on the effectiveness of EA-enriched products is also included.

The role of oxidative stress on subclinical atherosclerosis in premature ovarian insufficiency and relationship with carotid intima-media thickness

Objective: We aimed to investigate the relationship between oxidative stress (OS) and subclinical atherosclerosis in patients with premature ovarian insufficiency (POI), by analyzing the dynamic thiol/disulfide homeostasis (TDH) parameters as an OS marker and carotid intima-media thickness (CIMT).Materials and methods: A total of 69 women, 34 with POI and 35 healthy controls were included in this prospective cross-sectional study. TDH parameters (plasma native thiol, total thiol, disulfide, disulfide/native thiol, native thiol/total thiol, and disulfide/total thiol ratios) and CIMT were measured and compared between the two groups.Results: In primary ovarian insufficiency group, native thiol (p=.009) and total thiol (p=.010) levels were significantly decreased, and CIMT values were significantly increased (p= <.001). CIMT values were negatively correlated with native thiol (r=–0.553, p=.001) and total thiol levels (r=–0.565, p=.001); and positively correlated with age (r = 0.457, p=.007), BMI (r = 0.408, p=.017), and total cholesterol (r = 0.605, p<.001) in POI group.Conclusions: Decreased native thiol and total thiol levels demonstrate the defective anti-oxidant mechanism in POI. Negative correlation between native thiol, total thiol levels, and CIMT means the presence of abnormal anti-oxidant mechanisms may play a role in the development of subclinical atherosclerosis in patients with POI. This is a novel report on the mechanism of subclinical atherosclerosis in women with POI, which needs to be supported with further studies evaluating the pathophysiology of OS.

Perioperative Oxidative Stress: The Unseen Enemy.

Reactive oxygen species (ROS) are essential for cellular signaling and physiological function. An imbalance between ROS production and antioxidant protection results in a state of oxidative stress (OS), which is associated with perturbations in reduction/oxidation (redox) regulation, cellular dysfunction, organ failure, and disease. The pathophysiology of OS is closely interlinked with inflammation, mitochondrial dysfunction, and, in the case of surgery, ischemia/reperfusion injury (IRI). Perioperative OS is a complex response that involves patient, surgical, and anesthetic factors. The magnitude of tissue injury inflicted by the surgery affects the degree of OS, and both duration and nature of the anesthetic procedure applied can modify this. Moreover, the interindividual susceptibility to the impact of OS is likely to be highly variable and potentially linked to underlying comorbidities. The pathological link between OS and postoperative complications remains unclear, in part due to the complexities of measuring ROS- and OS-mediated damage. Exogenous antioxidant use and exercise have been shown to modulate OS and may have potential as countermeasures to improve postoperative recovery. A better understanding of the underlying mechanisms of OS, redox signaling, and regulation can provide an opportunity for patient-specific phenotyping and development of targeted interventions to reduce the disruption that surgery can cause to our physiology. Anesthesiologists are in a unique position to deliver countermeasures to OS and improve physiological resilience. To shy away from a process so fundamental to the welfare of these patients would be foolhardy and negligent, thus calling for an improved understanding of this complex facet of human biology.

Role of Oxidative Stress and Antioxidant Therapies in Endometriosis

Endometriosis (EMS) is a common gynecological disorder characterized by the presence of endometrial tissue outside the uterine cavity. It is commonly associated with pelvic pain and infertility. The exact pathogenesis remains unclear and many hypotheses have been suggested. In recent years, accumulating evidence indicates that oxidative stress (OS) plays a role in the development of EMS. The treatment of EMS remains a challenge. Antioxidant therapies for effective management of reactive oxygen species and inflammation have generated considerable research interest. Antioxidant agents such as Vitamins C and E, resveratrol, curcumin, melatonin, epigallocatechin-3-gallate, and others have been studied for the treatment of EMS. This review presents the role of OS in pathophysiology of EMS and the antioxidant therapies in its management.

Burn-induced Oxidative Stress and Serum Glutathione Depletion; a Cross Sectional Study.

Several studies have shown the role of oxidative stress in pathophysiology of burn injuries. This study aimed to evaluate the changes of oxidant-antioxidant levels during the week following burn injuries and its correlation with grade of burn. In this prospective cross-sectional study, changes of total glutathione, reduced glutathione (GSH), oxidized GSH (GSSG), GSH/GSSG ratio, as well as Pro-oxidant-antioxidant balance (PAB) were investigated on the 1st, 2nd and 7th days of admission in patients with > 15 % burns. 40 patients with the mean age of 21.1 ± 14.5 were studied (47.5% male). More than 50% of patients were in the 18 - 55 years age range and over 70% had 20% - 60% grade of burn. Total serum glutathione level and GSH had significant decreasing trends (P < 0.001) and GSSG and GSH/GSSG ratio had increasing trends (p < 0.001). No significant correlation was observed between serum GSH level and the total body surface area (TBSA) of burn injury (r = 0.047; p = 0.779). The evaluation of PAB and its correlation with TBSA showed a significant and direct association between them on the 1st (coefficient = 0.516; p = 0.001), 2nd (coefficient = 0.62; p <0.001), and 3rd (coefficient = 0.471; p = 0.002) day of follow up. According to this study, the redox perturbation occurred in burn injury which was measured and proved by decreased GSH/GSSG ratio as well as the shift of PAB in favour of oxidants. Besides, since PAB positively correlated with the severity of dermal damage, it might suggest the application of antioxidants as a part of therapeutic protocol for which the dosage should be proportionate to the surface area of the damaged skin.

Oxidative stress in organophosphate poisoning: role of standard antidotal therapy.

Despite the main mechanism of organophosphate (OP) toxicity through inhibition of acetylcholinesterase (AChE) being well known over the years, some chronic adverse health effects indicate the involvement of additional pathways. Oxidative stress is among the most intensively studied. Overstimulation of cholinergic and glutamatergic nervous system is followed by intensified generation of reactive species and oxidative damage in many tissues. In this review, the role of oxidative stress in pathophysiology of OP poisoning and the influence of commonly used medical interventions on its levels are discussed. Current standardized therapy of OP intoxications comprises live-saving administration of the anticholinergic drug atropine accompanied by oxime AChE reactivator and diazepam. The capability of these antidotes to ameliorate OP-induced oxidative stress varies between both therapeutic groups and individual medications within the drug class. Regarding oxidative stress, atropine does not seem to have a significant effect on oxidative stress parameters in OP poisoning. In a case of AChE reactivators, pro-oxidative and antioxidative properties could be found. It is assumed that the ability of oximes to trigger oxidative stress is rather associated with their chemical structure than reactivation efficacy. The data indicating the potency of diazepam in preventing OP-induced oxidative stress are not available. Based on current knowledge on the mechanism of OP-mediated oxidative stress, alternative approaches (including antioxidants or multifunctional drugs) in therapy of OP poisoning are under consideration.

Role of Oxidative Stress in Pathophysiology of Nonalcoholic Fatty Liver Disease.

Liver steatosis without alcohol consumption, namely, nonalcoholic fatty liver disease (NAFLD), is a common hepatic condition that encompasses a wide spectrum of presentations, ranging from simple accumulation of triglycerides in the hepatocytes without any liver damage to inflammation, necrosis, ballooning, and fibrosis (namely, nonalcoholic steatohepatitis) up to severe liver disease and eventually cirrhosis and/or hepatocellular carcinoma. The pathophysiology of fatty liver and its progression is influenced by multiple factors (environmental and genetics), in a “multiple parallel-hit model,” in which oxidative stress plays a very likely primary role as the starting point of the hepatic and extrahepatic damage. The aim of this review is to give a comprehensive insight on the present researches and findings on the role of oxidative stress mechanisms in the pathogenesis and pathophysiology of NAFLD. With this aim, we evaluated the available data in basic science and clinical studies in this field, reviewing the most recent works published on this topic.

Role of nitric oxide and oxidative stress in pathophysiology of liver injury in streptozotocin-induced type 1 diabetic rats

Tip 1 diyabet (T1D), insulinin salgi veya gorevlerinde anormalliklerle karakterize kronik metabolik bir hastaliktir. Daha onceleri diyabetik hayvanlarda, hiperglisemi ile tetiklenen oksidatif stres (OS) ve nitrik oksit (NO) seviyelerindeki patolojik yukselmelerin bobrek ve beyinde siddetli komplikasyonlara neden oldugunu gosterdik. Bu calisma NO’in sitotoksik etkisinin ve OS’in T1D ile iliskili hepatopatolojilerde herhangi bir iliskinin olup olmadigini tanimlamak icin tasarlanmistir. Bu amacla 8-hidroksi-2'deoxyguanosine (8-OHdG), endotelyal nitrik oksit sentaz (eNOS), uyarilabilir nitrik oksit sentaz (iNOS), Cu/Zn superoksit dismutaz (SOD1) ve glutatyon reduktaz (GR) immunoreaktiviteleri karaciger dokusunda arastirildi. Calismada, 8-OHdG (P<0.001), eNOS (P<0.001), eNOS (P<0.001), SOD1 (P<0.001) ve GR (P<0.001) immunoreaktivitelerinin T1D’li hayvanlara ait karaciger dokularinda, saglikli kontrol gruplara gore ciddi anlamda bir artisin oldugu tespit edildi. Bu calismada en onemli bulgu, 8-OHdG sunumlarinin genelde sitoplazmada oldugudur. Bu sonuclar STZ ile induklenen karaciger dejenerasyonlarinda OS’in ana kaynaginin patolojik duzeylerde uretilen NO oldugunu da gosterdi. Ayrica, oksidatif DNA hasari ve oksidatif stresin diyabete bagli karaciger dejenerasyonlarinda cok onemli bir rol aldigi ve hucresel mekanizmalarin ortaya konmasinda anahtar gorevi ustlenecegi gosterildi. Bu bulgular birlikte ele alindiginda, T1D’le iliskili karaciger patolojileri NO aracili karaciger yangilari ve dejenerasyonlarin onemli bir faktor oldugu gorulmektedir. Ayrica, bu calisma OS’in karaciger patofizyolojisinde gorev aldigini ve OS belirleyicilerinin hastaligin takibinde onemli gorevler alabilecegini gosterdi

Abstract 031: Placental Ischemia Causes Mitochondrial Dysfunction in Reduced Uterine Perfusion Pressure Rats

Introduction: Placental ischemia is believed to be the initial event in the development of preeclampsia (PE). PE is characterized by new onset hypertension and is associated with reduced fetal weight and placental oxidative stress. Mitochondrial dysfunction is the major cause of reactive oxygen species (ROS) generation. We hypothesize that the placental ischemia causes mitochondrial dysfunction in the reduced uterine perfusion pressure (RUPP) rat model of PE. Thus, the purpose of this study is to examine the effect of placental ischemia on mitochondrial function. Methods: Female Sprague Dawley rats were dived into two groups; normal pregnant (NP) and RUPP rats. On gestational day (GD) 14, RUPP surgery was performed, GD18 carotid catheters were inserted, and GD19 conscious blood pressure (MAP) was measured. GD 19 placentas were collected and mitochondria were isolated for respiration measurements. Respiration measurements included: basal state (isolated mitochondria with no substrates), state 2 (glutamate and malate as complex I substrates), state 3 (ADP stimulated), leak state (oligomycin induced ATP synthase inhibition), and maximal state (FCCP stimulated uncoupled). Cytochrome C oxidase (complex IV) activity was also measured in isolated mitochondria. Results: MAP was elevated in RUPP (n=16) compared to NP rats (n=14) (119±2 vs. 100±2 mmHg, p&lt;0.05). State 3 (149±8 vs 220±12 pmol/sec/mg, p&lt;0.05) and maximal (123±8 vs 159±5 pmol/sec/mg, p&lt;0.05) respiration rates were significantly reduced in RUPP (n=5) vs NP (n=7) rats. However, basal, state 2, and state 4 respiratory rates were not different between RUPP vs NP. Respiratory control ratio (state 3/ state 4) was significantly reduced in RUPP (n=5) vs NP (n=7) (7±1 vs 10±1, p&lt;0.05). Complex IV activity was reduced in RUPP (n=5) vs. NP (n=6) rats (508±14 vs 644±17 nmol e-/min/mg, P&lt;0.05). Conclusion: Reduced mitochondrial respiration and cytochrome c oxidase activity, indicators of mitochondrial dysfunction, occur in response to placental ischemia during pregnancy. Thus, suggesting that mitochondrial dysfunction may contribute to the pathophysiology of oxidative stress and hypertension during PE.

Pathophysiology of Oxidative Stress and Antioxidant Therapy in Acute Pancreatitis

Acute pancreatitis is an inflammatory disease of pancreas with varied clinical presentation ranging from mild self limiting disease to severe necrotising pancreatitis with high mortality. The exact pathogenesis of the disease is unclear despite extensive research. Recent studies have shown the role of oxidative stress in the pathogenesis of the disease. Many experimental studies have proven the role of oxygen free radicals in the initiation and progression of the disease. Antioxidant therapy has shown promising results in experimental animal models, whereas conflicting result has been seen in clinical studies in humans. This may suggest existence of different pathogenetic mechanism in humans. This review gives an overview of the role of oxidative stress in the pathophysiology of acute pancreatitis and outcomes of antioxidant therapy as a therapeutic agent in the treatment of acute pancreatitis.

Oxidative inhibition of erythrocyte sodium pump: A functionally relevant circulating marker of oxidative stress

O stress plays critical roles in the pathogenesis of diabetes and heart disease. The activity of Na pump has been shown to be depressed from the membrane of erythrocyte preparations of these patients coupled with alterations in membrane protein composition. We had previously discovered that the β1 subunit of the Na pump undergoes oxidative modification by oxidative stress in vitro (β1-GSS) and this mediates Na pump inhibition. This study aims to develop and validate erythrocyte β1-GSS as an oxidative stress biomarker in the premier emerging tool for prognosis of pathophysiological oxidative stress in patients with or at risk of cardiovascular disease (CVD) and diabetes. The marker is quickly and easily tested from blood using ELISA; and could be packaged and marketed as a simple kit. The eβ1-GSS biomarker is modified in heart attack, heart failure and diabetes, and exhibits potential to predict disease progression. With further investment, the eβ1-GSS biomarker could be developed initially as a versatile CVD prognosis tool for universal pre-hospital diagnostics, CVD-severity risk-stratification, and as a Companion Diagnostic (Dx) for CVD medications. Subsequently it could be adapted for diabetes.

Inflammation versus oxidative stress in pathophysiology of alzheimer's disease in rat model

Background: Alzheimer's disease (AD) is a highly debilitating neurodegenerative disorder characterized by cognitive dysfunction. Inflammation and oxidative stress are thought to play major roles in the pathophysiology. Which one has the principle role is unclear. Objectives: The role of brain growth factors, cytokines and oxidative biomarkers in cognitive dysfunction induced by Aluminium chloride (AlCl3) in rats with application of an anti-inflammatory (Cilostazol) and an antioxidant (N-acetyl cysteine, NAC) were investigated to clarify the predominant pathophysiological mechanism involved. Methods: Alzheimer's model group was given AlCl3 (100 mg/kg) orally for six weeks. Alzheimer's model + NAC, and Alzheimer's model + Cilostazol groups were given (NAC) and Cilostazol respectively one hour before AlCl3 for the same duration. Results: Anti-inflammatory or antioxidant interventions significantly improved memory retention, which was evaluated by Morris Water Maze, passive avoidance task, and eight-arm radial maze. This improvement was consistent with histological recovery and was mediated by reduction AlCl3 concentration in the brain hippocampus and frontal cortex, interference with the cholinergic dysfunction, as well as prevention of oxidative damage. In addition, anti-inflammatory agents can modulate superiorly the inflammatory response via reduction of the levels of inflammatory cytokines and adjustment of the levels of brain–derived neurotrophic factors and transforming growth factor B. Conclusions: These finding support the principal role of inflammation in pathophysiology of AD and suggests the potential therapeutic application of anti-inflammatory agents for this condition.

Macrophage mitochondrial damage from StAR transport of 7-hydroperoxycholesterol: Implications for oxidative stress-impaired reverse cholesterol transport

StAR family proteins in vascular macrophages participate in reverse cholesterol transport (RCT). We hypothesize that under pathophysiological oxidative stress, StARs will transport not only cholesterol to macrophage mitochondria, but also pro-oxidant cholesterol hydroperoxides (7-OOHs), thereby impairing early-stage RCT. Upon stimulation with dibutyryl-cAMP, RAW264.7 macrophages exhibited a strong time-dependent induction of mitochondrial StarD1 and plasma membrane ABCA1, which exports cholesterol. 7α-OOH uptake by stimulated RAW cell mitochondria (like cholesterol uptake) was strongly reduced by StarD1 knockdown, consistent with StarD1 involvement. Upon uptake by mitochondria, 7α-OOH (but not redox-inactive 7α-OH) triggered lipid peroxidation and membrane depolarization while reducing ABCA1 upregulation. These findings provide strong initial support for our hypothesis.

Oxidative stress in Schizophrenia patients with and without diabetes mellitus

Introduction: In recent times schizophrenia has shown positive association with diabetes mellitus. Previous studies have suggested possible role of oxidative stress in pathophysiology of neuropsychiatric disorders. In the current work, we have measured oxidative damage to biomolecules in schizophrenia patients with and without diabetes mellitus to know the strength of association of schizophrenia with diabetes mellitus. Materials and methods: Serum samples from 39 patients having schizophrenia without diabetes mellitus (group I) and 21 patients having schizophrenia with diabetes mellitus (group II) and 50 healthy controls were collected to analyze lipid peroxidation marker malondialdehyde (MDA) and major antioxidant total thiol levels using colorimetric methods. Fasting blood glucose (FBG), serum urea, creatinine, aspartate transaminase (AST), alanine transaminase (ALT), total bilirubin and direct bilirubin were determined by automated analyzer Hitachi 912. Results: There was significant increase in FBG (P<0.001) and MDA (<0.001), and decrease in total thiols (p<0.001) in group I compared to healthy controls. There was significant increase in (FBG) (p<0.001) and MDA (p<0.001), decrease in total thiols (p<0.001) in group II compared to group I and healthy controls. However, there was no significant difference in serum urea, creatinine, AST, ALT, total bilirubin and direct bilirubin between patients and healthy controls. Serum MDA levels correlated negatively with total thiol levels (r = -0.275, p<0.01) and positively with FBG (r = 0.823, p<0.01) in group II patients. Conclusion: Our study has shown presence of oxidative stress in schizophrenia which is further enhanced in schizophrenia associated with diabetes mellitus.

Inflammation versus Oxidative Stress in Pathophysiology of Cognitive Dysfunction induced by Aluminum Chloride in Male Rats

Inflammation versus Oxidative Stress in Pathophysiology of Cognitive Dysfunction induced by Aluminum Chloride in Male Rats

Selenium and Cardiovascular Surgery: An Overview

Selenium is an essential nutritional element to mammalians necessary for the active function of different oxidant enzymes, as glutathione peroxidase (GPx), thioredoxin reductases (TrxR), and iodothyronine deiodinases (IDD). The anti-oxidative effect of selenium is pivotal for the human physiology. Oxidative stress is associated with various diseases, such as cardiovascular disease, diabetes mellitus or cancer, and is also associated with the majority of surgical procedures. Particularly, the use of cardiopulmonary bypass for open cardiac surgery with aortic clamping is always related to oxidative stress due to ischemia and reperfusion. Whereas myocardial protection with different temperatures and cardioplegic solutions has become more efficient, reperfusion is often followed by the activation of an injurious oxidative cascade. The pathogenesis of ischemia/reperfusion injury depends on many factors, among them, reactive nitrogen species (RNS) and reactive oxygen species (ROS) are considered as initiators of the injury. ROS formed during oxidative stress can initiate lipid peroxidation, oxidize proteins to inactive states and cause DNA strand breaks. ROS production is physiologically controlled by free radical scavengers such as GPx and TrxR, and superoxide dismutase systems. GPx and TrxR are seleno-cysteine dependent enzymes, and their activity is known to be related to selenium availability. Furthermore, selenium has been reported to regulate gene expression of these selenoproteins as a cofactor and there is some evidence that selenium supplementation can attenuate the oxidative stress and decrease the complications after cardiac surgery. However, other clinical studies failed to demonstrate an association between selenium deficiency and cardiovascular outcomes. The aim of our review is to summarize the experimental and clinical evidence of preoperative selenium supplementation and therapy after cardiac surgery, focusing on the pathophysiology of oxidative stress and the clinical usage of selenium.