Importance Of Oxidative Stress Research Articles

The importance of oxidative stress in the pathogenesis and treatment of bipolar affective disorder: a review of the literature

Introduction: Bipolar affective disorder (BD), also known as manic-depressive illness, is a chronic and recurrent psychiatric disorder characterised by significant mood disturbances. It is one of the leading causes of disability worldwide and is associated with a high risk of suicide. Recent studies highlight the role of oxidative stress (OS) in the pathogenesis of BD. The body's pro/antioxidant imbalance adversely affects cellular and molecular processes. Aim: The aim of this review is to synthesise the current state of knowledge on the role of OS in the aetiology and course of BD, including key biomarkers and potential therapeutic interventions. Methods: A review of the scientific literature was conducted, including articles published between 2000 and 2024. Searches were conducted in PubMed, Scopus and Web of Science databases, using the following keywords: 'bipolar disorder', 'oxidative stress', 'antioxidants', 'biomarkers', 'mitochondrial dysfunction', 'redox homeostasis', 'treatment'. Results: Results indicate that patients with BD have elevated levels of OS markers, including increased lipid peroxidation, altered antioxidant enzyme activity and impaired redox homeostasis. Treatment with lithium and other mood stabilisers may modulate levels of OS markers, which is one potential mechanism of drug action. However, inconclusive data suggest the need for further research to clarify the relationship between OS and BD. Conclusions: OS plays an important role in the pathophysiology of BD, offering potential directions for therapeutic interventions. Understanding the complex interactions between OS and BD may lead to the development of more targeted therapies aimed at reducing oxidative damage and improving patient health. Keywords: oxidative stress, bipolar affective disorder, redox, lipid peroxidation, protein damage, antioxidants, lithium

A review of the therapeutic effects of polyphenols on non-alcoholic fatty liver disease: Focus on oxidative stress

A substantial body of research suggests that polyphenols may have health benefits, particularly in metabolic disorders associated with obesity, such as non-alcoholic fatty liver (NAFLD), type 2 diabetes, and cardiovascular disease. Given the importance of oxidative stress in the pathogenesis of metabolic disorders, significant emphasis has recently been placed on the characteristics of polyphenols in obesity-related problems. This narrative review summarizes the current knowledge on the inhibitory effects of polyphenols, including curcumin, resveratrol, baicalin, nobiletin, and quercetin, on oxidative stress, with a focus on the role of the Nrf2 pathway. This review compiles the data from articles showing that the aforementioned polyphenols improve health in metabolic diseases by regulating Nrf2 and its target proteins involved in reducing oxidative stress. However, due to the limitations of in vitro and in vivo investigations, as well as the lack of long-term human clinical trial studies, further high-quality research is required to definitively demonstrate the clinical usefulness of polyphenols for the prevention and management of NAFLD.

Potential role of oxidative stress in pathogenesis of benign prostatic hyperplasia in male dogs.

The pathogenesis of benign prostatic hyperplasia (BPH) in dogs is still not fully understood. Some studies suggest that oxidative stress may have a potential role in the pathogenesis of BPH in dogs. Age-related hormonal changes may activate a chronic inflammatory response in the prostate. This causes the generation of reactive oxygen species (ROS) and results in oxidative stress. Excessive production of ROS results in DNA damage and hyperplastic transformation of prostatic cells. The use of antioxidants for improvement of treatment outcomes for canine PBH has been discussed. Further research is needed on the importance of oxidative stress in the development of BPH in dogs and the usefulness of antioxidants in the supportive treatment of this condition.

Expression of Human L-Dopa Decarboxylase (DDC) under Conditions of Oxidative Stress.

Oxidative stress is known to influence mRNA levels, translation, and proteolysis. The importance of oxidative stress has been demonstrated in several human diseases, including neurodegenerative disorders. L-Dopa decarboxylase (DDC) is the enzyme that converts L-Dopa to dopamine (DA). In spite of a large number of studies, little is known about the biological significance of the enzyme under physiological and pathological conditions. Here, we investigated the relationship between DDC expression and oxidative stress in human neural and non-neural cells. Oxidative stress was induced by treatment with H2O2. Our data indicated that mRNA and protein expression of DDC was enhanced or remained stable under conditions of ROS induction, despite degradation of total RNA and increased cytotoxicity and apoptosis. Moreover, DDC silencing caused an increase in the H2O2-induced cytotoxicity. The current study suggests that DDC is involved in the mechanisms of oxidative stress.

Kaempferol and Isorhamnetin alleviate Lipopolysaccharide-Induced Anxiety and Depression-Like Behavioral in Balb/C Mice

The etiology of anxiety and depression is linked to inflammation and oxidative stress. Isorhamnetin and Kaempferol are strong antioxidants with antiinflammatory and neuroprotective properties. This study, it was aimed to investigate the effect of Kaempferol and Isorhamnetin in Lipopolysaccharide (LPS)-induced anxiety and depression model in mice. Thirty Balb/C mice were divided into six groups of five mice each weighing 25-35 gr. Kaempferol (50 mg/kg and 100 mg/kg) and Isorhamnetin (30 mg/kg and 60 mg/kg) were given orally to the treatment group, and the vehicle was given to the control and LPS groups for fourteen days, followed by intraperitoneal (0.83 mg/kg) LPS injection (control group excluding) on the fifteenth day. Kaempferol and Isorhamnetin ameliorated LPS-induced anxiety evaluated by open field test, light/dark test, and elevated plus maze test, and LPS-induced depression evaluated by forced swimming test and tail suspension test. Kaempferol and Isorhamnetin alleviated LPS-induced increased oxidative stress in the prefrontal cortex and hippocampus by decreasing MDA and total oxidant status (TOS) levels and increased total antioxidant status (TAS) levels. In addition, it was observed that Kaempferol and Isorhamnetin regulated the increase in prefrontal and hippocampal inflammation caused by LPS by decreasing TNF-α, IL-1β, and IL-6 levels. Most importantly, LPS reduced prefrontal and hippocampal brain-derived neurotrophic factor (BDNF) levels, but the treatment groups reversed it. These results show the possible therapeutic potential of Kaempferol and Isorhamnetin, along with the importance of oxidative stress, inflammation, and BDNF in the etiopathogenesis of anxiety and depression.

Redox Signaling in Chronic Kidney Disease-Associated Cachexia.

Redox signaling alterations contribute to chronic kidney disease (CKD)-associated cachexia. This review aims to summarize studies about redox pathophysiology in CKD-associated cachexia and muscle wasting and to discuss potential therapeutic approaches based on antioxidant and anti-inflammatory molecules to restore redox homeostasis. Enzymatic and non-enzymatic systems of antioxidant molecules have been studied in experimental models of kidney diseases and patients with CKD. Oxidative stress is increased by several factors present in CKD, including uremic toxins, inflammation, and metabolic and hormone alterations, leading to muscle wasting. Rehabilitative nutritional and physical exercises have shown beneficial effects for CKD-associated cachexia. Anti-inflammatory molecules have also been tested in experimental models of CKD. The importance of oxidative stress has been shown by experimental studies in which antioxidant therapies ameliorated CKD and its associated complications in the 5/6 nephrectomy model. Treatment of CKD-associated cachexia is a challenge and further studies are necessary to investigate potential therapies involving antioxidant therapy.

The effect of antioxidants on increased oocyte competence in IVM: a review

In vitro maturation (IVM) is considered a potential assisted reproductive technology that is a safer and simpler alternative to conventional in vitro fertilization. It is primarily used in patients with impaired oocyte maturation and for the treatment of infertile women who are at risk of fertility loss. In addition, IVM is currently used mainly in polycystic ovarian syndrome patients with a high ovarian response and is still considered an experimental option in fertility preservation. Producing highly competent oocytes during IVM is considered a key step in the success of in vitro production (IVP) of embryos. Some factors, such as culture medium conditions and other supplements, have a significant impact on oocyte IVM performance. One of the known disruptors of oocyte developmental competence in IVP is oxidative stress (OS), which is caused by an imbalance between the production and neutralization of reactive oxygen species (ROS). In vitro conditions induce supraphysiological ROS levels due to exposure to an oxidative environment and the isolation of the oocyte from the follicle protective antioxidant milieu. Given the importance of OS in oocyte competence, the establishment of standardized antioxidant IVM systems is critical for improving the overall success of IVP. This review focuses on the main antioxidants tested to protect oocytes against OS in IVM.

Diminazene aceturate or losartan ameliorates the functional, radiological and histopathological alterations in knee osteoarthritis rodent model: repurposing of the ACE2/Ang1-7/MasR cascade

PurposeCurrent therapies for osteoarthritis (OA) are limited to analgesics and anti-inflammatory drugs. Considering the importance of oxidative stress and inflammatory mediators in OA etiology, we tested the hypothesis that targeting the renin–angiotensin–aldosterone system (RAAS) can improve OA anomalies. Diminazene (DIZE), an activator of angiotensin-converting enzyme 2 and the angiotensin 2 type-1 receptor blocker losartan (LOS) were used for this purpose.MethodsOA was induced by a single intra-articular injection of monosodium iodoacetate. The effects of exposure to DIZE or LOS for 21 days on OA anomalies in rats’ knees were investigated. Evaluation of motor function, nociception, and inflammatory response was done using rotarod, knee bend and knee swelling tests. Markers of knee joint inflammation, and cellular oxidation in addition to the RAAS biomarkers, were assessed in knee tissues, along with radiological and histopathological investigations.ResultsElevations in inflammatory and oxidative markers in knee tissues of OA rats were mostly improved by the two therapeutic drugs. Such effect was also reflected in the rotarod, knee bend and knee swelling tests. Treatment with DIZE has shown a more prominent effect than LOS in controlling OA-associated inflammation and cellular oxidation. Markers of RAAS have also shown better responsiveness to DIZE over LOS.ConclusionsDIZE has shown a prominent increase in the angiotensin 1–7 amount, highlighting the involvement of the signaling pathway in the immunomodulatory effect. The radiological and histopathology examination came to confirm the outcome of biochemical markers, nominating diminazene aceturate as a possible therapeutic option for OA.Graphical

Glutathione: A Samsonian life-sustaining small molecule that protects against oxidative stress, ageing and damaging inflammation.

Many local and systemic diseases especially diseases that are leading causes of death globally like chronic obstructive pulmonary disease, atherosclerosis with ischemic heart disease and stroke, cancer and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) causing coronavirus disease 19 (COVID-19), involve both, (1) oxidative stress with excessive production of reactive oxygen species (ROS) that lower glutathione (GSH) levels, and (2) inflammation. The GSH tripeptide (γ- L-glutamyl-L-cysteinyl-glycine), the most abundant water-soluble non-protein thiol in the cell (1-10 mM) is fundamental for life by (a) sustaining the adequate redox cell signaling needed to maintain physiologic levels of oxidative stress fundamental to control life processes, and (b) limiting excessive oxidative stress that causes cell and tissue damage. GSH activity is facilitated by activation of the Kelch-like ECH-associated protein 1 (Keap1)-Nuclear factor erythroid 2-related factor 2 (Nrf2)-antioxidant response element (ARE) redox regulator pathway, releasing Nrf2 that regulates expression of genes controlling antioxidant, inflammatory and immune system responses. GSH exists in the thiol-reduced (>98% of total GSH) and disulfide-oxidized (GSSG) forms, and the concentrations of GSH and GSSG and their molar ratio are indicators of the functionality of the cell. GSH depletion may play a central role in inflammatory diseases and COVID-19 pathophysiology, host immune response and disease severity and mortality. Therapies enhancing GSH could become a cornerstone to reduce severity and fatal outcomes of inflammatory diseases and COVID-19 and increasing GSH levels may prevent and subdue these diseases. The life value of GSH makes for a paramount research field in biology and medicine and may be key against systemic inflammation and SARS-CoV-2 infection and COVID-19 disease. In this review, we emphasize on (1) GSH depletion as a fundamental risk factor for diseases like chronic obstructive pulmonary disease and atherosclerosis (ischemic heart disease and stroke), (2) importance of oxidative stress and antioxidants in SARS-CoV-2 infection and COVID-19 disease, (3) significance of GSH to counteract persistent damaging inflammation, inflammaging and early (premature) inflammaging associated with cell and tissue damage caused by excessive oxidative stress and lack of adequate antioxidant defenses in younger individuals, and (4) new therapies that include antioxidant defenses restoration.

Importance of oxidative stress in the evaluation of acute pulmonary embolism severity

BackgroundPulmonary embolism (PE) is a common and potentially life-threatening disorder. Our study was aimed to investigate whether oxidative stress markers can be used as clinical markers in the evaluation of acute PE (APE) severity.Methods47 patients with objectively documented diagnosis of APE were recorded. Of these patients, 14 had low-risk PE, 16 had moderate-risk PE, and 17 had high-risk PE. 21 healthy subjects were also enrolled in this study. Ischemia-modified albumin (IMA), prooxidants-antioxidants balance (PAB), advanced protein oxidation products (AOPPs), and ferric reducing antioxidant power (FRAP) were measured as oxidative stress parameters to evaluate the role of oxidative stress.ResultsIn the low-risk and moderate-risk APE groups, AOPPs and PAB levels were significantly higher and FRAP levels were significantly lower than those in the control group. AOPPs and IMA levels in the patients with high-risk PE were significantly higher than those in both the low-risk and moderate-risk APE patients. There was a significant correlation between levels of AOPPs and the levels of both IMA (r: 0.462, p < 0.001) and PAB (r:0.378, p < 0.005). Serum FRAP levels were negatively correlated with PAB (r:− 0.683, p < 0.001) and AOPPs levels (r:− 0,384, p < 0.001). There was also a significant positive correlation between the serum IMA and PAB levels.ConclusionsWe clearly demonstrated that reactive oxygen species formation is significantly enhanced in APE. IMA and AOPPs may be used as clinical markers in the evaluation of APE severity in clinical practice. However, further studies with larger patient populations and longer follow-up periods are required to confirm the mechanisms underlying these findings.

PROTEOMIC PROFILE OF CYSTEINE OXIDATION IN VASCULAR SMOOTH MUSCLE CELLS IN HUMAN HYPERTENSION

Objective: Phenotypic switching of vascular smooth muscle cells (VSMCs) is a fundamental process in vascular dysfunction and remodeling associated with hypertension. Mechanisms underlying this process involve reactive oxygen species (ROS) and redox-dependent signaling pathways. However, the proteomic signature and effects of ROS on VSMC proteome in human hypertension are unknown. Using high fidelity proteomic analysis, we characterized the proteome of VSMC in human hypertension. Design and method: VSMC from resistance arteries from normotensive (NT) and hypertensive (HT) subjects were studied. Protein expression and cell migration were assessed by immunoblotting and wound healing assay respectively. VSMC proteins were labelled with isobaric tandem mass tags and identified by liquid chromatography tandem mass spectrometry. The oxidative proteome was assessed using stable isotope-labelled iodoacetamide to target cysteine thiols. Results: VSMCs from HT subjects exhibit reduced expression of alpha-SMA (0.05+0.01 vs NT:0.20 + 0.03, p &lt; 0.05), increased expression of the proliferation marker, PCNA (0.162 + 0.3 vs NT:051 + 0.004, p &lt; 0.05) and increased migration (54.68 + 2.86 vs NT:23.37 + 8.36, p &lt; 0.05). The proteomic analysis identified 207 proteins upregulated in HT subjects (fold change&gt; 1.5, p &lt; 0.05). Gene ontology enrichment of upregulated proteins in HT showed that most proteins belong to extracellular space and plasma membrane compartments and were involved in biological processes such as extracellular matrix organization, immune response, proteolysis and cell proliferation. Extracellular matrix (ECM) proteins COL1A1, COL9A1, COL10A1, FBN1, FBLN1 were increased in cells from HT (fold change&gt; 1.5, p &lt; 0.05), suggesting a switch to a fibroblast-like phenotype in hypertension. Expression of proteins related to the interferon and IL-1beta pathways (IFIT1, IFIT2, IFIT3, MX1, MX2, ABCA1, ABCA2, IL1RAP, CD36, ICAM1) were also increased in cells from HT subjects (fold change&gt; 1.5, p &lt; 0.05). Considering the importance of oxidative stress in hypertension, we assessed the VSMC oxidative proteome. Results identified 130 significant cysteine-containing peptides, 88 showed increased oxidation in HT (fold change&gt; 1.5, p &lt; 0.05). Among the highly oxidized proteins in HT were ECM proteins, COL11A1, COL16A1, FBLN1 and FBLN2 (fold change&gt; 1.5, p &lt; 0.05). Conclusions: Our study provides new insights into the proteomic changes related to vascular phenotype in hypertension and highlights differentially oxidised candidate targets that may drive phenotypic switching associated with vascular injury and remodeling in hypertension.

Oxidative stress promotes fibrosis in systemic sclerosis through stabilization of a kinase-phosphatase complex.

Systemic sclerosis (SSc) is a fibrotic autoimmune disease characterized by pathogenic activation of fibroblasts enhanced by local oxidative stress. The tyrosine phosphatase PTP4A1 was identified as a critical promoter of TGF-β signaling in SSc. Oxidative stress is known to functionally inactivate tyrosine phosphatases. Here, we assessed whether oxidation of PTP4A1 modulates its profibrotic action and found that PTP4A1 forms a complex with the kinase SRC in scleroderma fibroblasts, but surprisingly, oxidative stress enhanced rather than reduced PTP4A1’s association with SRC and its profibrotic action. Through structural assessment of the oxo-PTP4A1-SRC complex, we unraveled an unexpected mechanism whereby oxidation of a tyrosine phosphatase promotes its function through modification of its protein complex. Considering the importance of oxidative stress in the pathogenesis of SSc and fibrosis, our findings suggest routes for leveraging PTP4A1 oxidation as a potential strategy for developing antifibrotic agents.

An Oxidative Stress Marker in Pediatric Migraine Patients: Dynamic Thiol-Disulfide Homeostasis

Objective: Migraine is a common disease in childhood. Oxidative stress has been implicated in the pathogenesis of migraine. Dynamic thiol/disulfide homeostasis is proven to be a marker of oxidative stress. We aimed to investigate the correlation between migraine and dynamic thiol/disulfide homeostasis. Material and Methods: A total of 141 children (71 migrain and 70 controls) were included. The serum total thiol, native thiol, and disulfide levels were measured and the ratios of disulfide/native thiol, disulfide/total thiol and native thiol/total thiol were compared between migraine patients and healthy children during attack-free period. Results: Native thiol levels and native thiol/total thiol ratio were significantly lower in the migraine group than the control group (p=0.022, p=0.005, respectively); whereas disulfide levels, disulfide/native thiol and disulfide/total thiol ratios were significantly higher in the migraine group than the control group (p=0.039, p=0.022, p=0.005 respectively). Conclusion: Our results demonstrate that there is an ongoing oxidative process in pediatric migraineurs even during attack-free period. This result may shed light on further studies analyzing dynamic changes in the oxidant-antioxidant balance during the attack and the aura phase to support the presence and importance of oxidative stress in pediatric migraine.

Correlation Between Telomere Length and Biomarkers of Oxidative Stress in Human Aging.

The telomere length (TL) has increasingly been used as a biomarker of human aging because it has been shown to predict the chances of survival and longevity. Oxidative stress is presumed to be a major cause of telomere shortening, but the importance of oxidative stress as a determinant of telomere shortening remains less clear and has recently been questioned. We analyzed 105 healthy subjects of both sexes between the ages of 20-77 years. The TL and biomarkers of oxidative stress were estimated as per standard protocols. A significant (p < 0.001) age-dependent decline in TL was observed. TL was positively correlated with the ferric reducing ability of plasma value (r = 0.8811) and reduced glutathione (r = 0.8209), whereas negatively correlated with malondialdehyde (r = -0.7191). Our findings supported the idea of a possible correlation between the TL and biomarkers of oxidative stress in aging. The study has remarkable scope in medical science as the findings on correlation of TL with biomarkers of oxidative stress in aging are novel and they will help in further research against oxidative stress.

Abstract 56: Proteome Profile Of Vascular Smooth Muscle Cells During Phenotypic Switching In Human Hypertension

Vascular smooth muscle cells (VSMCs) are key players in vascular dysfunction associated with hypertension, where phenotypic switch is a fundamental process. While various transcription factors have been implicated in this process, the proteomic signature associated with phenotypic switching in human hypertension is unknown. Using high fidelity proteomic analysis, we characterized the proteome profile of VSMC in human hypertension. VSMC derived from resistance arteries from normotensive (NT) and hypertensive (HT) subjects were studied. Protein expression and cell migration were assessed by immunoblotting and wound healing assay. VSMC proteins were labelled with isobaric tandem mass tags and identified by liquid chromatography tandem mass spectrometry. The oxidative proteome was assessed using stable isotope-labelled iodoacetamide to target free reduced cysteine thiols. VSMCs from HT subjects exhibit reduced expression of α-SMA (0.05±0.01 vs NT:0.20±0.03, p&lt;0.05), increased expression of the proliferation marker, PCNA (0.162±0.3 vs NT:0.51±0.004, p&lt;0.05), and increased migration (54.68±2.86 vs NT:23.37±8.36, p&lt;0.05). The proteomic analysis identified 207 proteins upregulated in HT subjects (fold change&gt;1.5, p&lt;0.05). There were no changes in protein expression of pathways related to the contractile phenotype (MYH11, CNN1, TAGLN, TPM, CALD1). However, extracellular matrix (ECM) proteins such as COL1A1, COL9A1, COL10A1, FBN1, FBLN1 were increased in cells from HT (fold change&gt;1.5, p&lt;0.05), suggesting a switch to a fibroblast-like phenotype in hypertension. Expression of proteins related to the interferon and IL-1β pathways (IFIT1, IFIT2, IFIT3, MX1, MX2, ABCA1, ABCA2, IL1RAP, CD36, ICAM1) were also increased in cells from HT subjects (fold change&gt;1.5, p&lt;0.05). Considering the importance of oxidative stress in hypertension, we assessed the VSMC oxidative proteome. Results demonstrate that ECM proteins, such as COL11A1 and COL16A1, were highly oxidized in cells from HT (fold change&gt;1.5, p&lt;0.05). Our study provides new insights into the proteomic changes that define the vascular phenotype in hypertension and highlights candidate targets that may drive phenotypic switching associated with vascular injury in hypertension.

Methylmercury-Mediated Oxidative Stress and Activation of the Cellular Protective System.

Methylmercury (MeHg) is a well-known neurotoxicant that causes severe intoxication in humans. In Japan, it is referred to as Minamata disease, which involves two characteristic clinical forms: fetal type and adult type depending on the exposed age. In addition to MeHg burden level, individual susceptibility to MeHg plays a role in the manifestation of MeHg toxicity. Research progress has pointed out the importance of oxidative stress in the pathogenesis of MeHg toxicity. MeHg has a high affinity for selenohydryl groups, sulfhydryl groups, and selenides. It has been clarified that such affinity characteristics cause the impairment of antioxidant enzymes and proteins, resulting in the disruption of antioxidant systems. Furthermore, MeHg-induced intracellular selenium deficiency due to the greater affinity of MeHg for selenohydryl groups and selenides leads to failure in the recoding of a UGA codon for selenocysteine and results in the degradation of antioxidant selenoenzyme mRNA by nonsense-mediated mRNA decay. The defect of antioxidant selenoenzyme replenishment exacerbates MeHg-mediated oxidative stress. On the other hand, it has also been revealed that MeHg can directly activate the antioxidant Keap1/Nrf2 signaling pathway. This review summarizes the incidence of MeHg-mediated oxidative stress from the viewpoint of the individual intracellular redox system interactions and the MeHg-mediated aforementioned intracellular events. In addition, the mechanisms of cellular stress pathways and neuronal cell death triggered by MeHg-mediated oxidative stress and direct interactions of MeHg with reactive residues of proteins are mentioned.

Oxidative Stress in Cardiovascular Diseases.

Reactive oxygen species (ROS) are subcellular messengers in signal transductions pathways with both beneficial and deleterious roles. ROS are generated as a by-product of mitochondrial respiration or metabolism or by specific enzymes such as superoxide dismutases, glutathione peroxidase, catalase, peroxiredoxins, and myeloperoxidases. Under physiological conditions, the low levels of ROS production are equivalent to their detoxification, playing a major role in cellular signaling and function. In pathological situations, particularly atherosclerosis or hypertension, the release of ROS exceeds endogenous antioxidant capacity, leading to cell death. At cardiovascular levels, oxidative stress is highly implicated in myocardial infarction, ischemia/reperfusion, or heart failure. Here, we will first detail the physiological role of low ROS production in the heart and the vessels. Indeed, ROS are able to regulate multiple cardiovascular functions, such as cell proliferation, migration, and death. Second, we will investigate the implication of oxidative stress in cardiovascular diseases. Then, we will focus on ROS produced by NAPDH oxidase or during endothelial or mitochondrial dysfunction. Given the importance of oxidative stress at the cardiovascular level, antioxidant therapies could be a real benefit. In the last part of this review, we will detail the new therapeutic strategies potentially involved in cardiovascular protection and currently under study.

Oxidative Stress: A Possible Trigger for Pelvic Organ Prolapse.

Pelvic organ prolapse is a frequent health problem in women, encountered worldwide, its physiopathology being still incompletely understood. The integrity of the pelvic-supportive structures is a key element that prevents the prolapse of the pelvic organs. Numerous researchers have underlined the role of connective tissue molecular changes in the pathogenesis of pelvic organ prolapse and have raised the attention upon oxidative stress as an important element involved in its appearance. The advancements made over the years in terms of molecular biology have allowed researchers to investigate how the constituent elements of the pelvic-supportive structures react in conditions of oxidative stress. The purpose of this paper is to underline the importance of oxidative stress in the pathogenesis of pelvic organ prolapse, as well as to highlight the main oxidative stress molecular changes that appear at the level of the pelvic-supportive structures. Sustained mechanical stress is proven to be a key factor in the appearance of pelvic organ prolapse, correlating with increased levels of free radicals production and mitochondrial-induced fibroblasts apoptosis, the rate of cellular apoptosis depending on the intensity of the mechanical stress, and the period of time the mechanical stress is applied. Oxidative stress hinders normal cellular signaling pathways, as well as different important cellular components like proteins, lipids, and cellular DNA, therefore significantly interfering with the process of collagen and elastin synthesis.

Impact of oxidative stress on treatment outcomes in adult patients with sepsis: A prospective study.

Purpose:Oxidative stress has been shown to reflect on the development of sepsis and disease severity. In the present study, we evaluated the effects of increased levels of oxidative stress and decreased antioxidant coactivity in patients with sepsis, and the importance of oxidative stress on treatment outcomes.Methods:Biomarkers of oxidative stress (thiobarbituric acid-reactive substances [TBARS]) and antioxidant capacity (glutathione peroxidase [GPx] and glutathione content [thiol]) were prospectively evaluated along with biochemical and clinical data in 100 patients with sepsis on days 1, 4, and 7 after admission.Results:The TBARS level of the non-survivor group was significantly higher than that of the survivor group on day 1 and day 4 and negatively correlated with thiol upon admission. However, thiol was positively correlated with lactate concentration. The TBARS and lactate levels upon admission were independent predictors of fatality.Conclusions:We conclude that a TBARS cut-off value of 18.30 μM can be used to predict fatality, and an increase in the TBARS concentration by 1 μM will increase the fatality rate by 0.94%. In the panel of biomarkers, the TBARS assay can be considered as a prognostic biomarker for the treatment of patients with sepsis.

Sperm Antioxidant Biomarkers and Their Correlation with Clinical Condition and Lifestyle with Regard to Male Reproductive Potential.

Measurement of sperm oxidative-antioxidant indicators is widely used in the assessment and detection of biochemical causes of male infertility. The main purpose of this study was to identify biomarkers that assist in diagnostics and monitoring of male reproductive potential. We performed the assessment of oxidative-antioxidant malondialdehyde (MDA), glutathione (GSH), and total redox antioxidant potential (TRAP) indicators in seminal plasma, seminogram, clinical condition, and lifestyle of people with reproductive problems. The combined assessment of GSH and TRAP as potential biomarkers of male infertility in semen plasma was characterized by the highest total sensitivity and specificity. Furthermore, we provide evidence that male reproductive potential is significantly correlated with basic sperm parameters, sperm cell membrane integrity, their morphology, lifestyle, eating habits, occupation, and mental health. Our results provide evidence on the importance of oxidative stress and defense against free radicals in diagnosing and monitoring men with infertility that are consistent with previously conducted research. We provide an alternative approach on the possibility of interpreting the combination of the biomarkers that can bring benefits to a multi-threaded approach to the diagnosis and treatment of male infertility.