Genesis Of Reactive Oxygen Species Research Articles

Biomaterials Designed to Modulate Reactive Oxygen Species for Enhanced Bone Regeneration in Diabetic Conditions.

Diabetes mellitus, characterized by enduring hyperglycemia, precipitates oxidative stress, engendering a spectrum of complications, notably increased bone vulnerability. The genesis of reactive oxygen species (ROS), a byproduct of oxygen metabolism, instigates oxidative detriment and impairs bone metabolism in diabetic conditions. This review delves into the mechanisms of ROS generation and its impact on bone homeostasis within the context of diabetes. Furthermore, the review summarizes the cutting-edge progress in the development of ROS-neutralizing biomaterials tailored for the amelioration of diabetic osteopathy. These biomaterials are engineered to modulate ROS dynamics, thereby mitigating inflammatory responses and facilitating bone repair. Additionally, the challenges and therapeutic prospects of ROS-targeted biomaterials in clinical application of diabetic bone disease treatment is addressed.

Mitigation of Salinity Stress and Lead Toxicity in Maize by Exogenous Application of the Sorghum Water Extract.

The increased concentration of lead (Pb) in soils is a serious threat to human beings and plants all over the world. Salinity stress is also a major issue across the globe, which limits crop productivity. The use of allelochemicals has become an effective strategy to mitigate the toxic effects of abiotic stresses. Sorghum is an important crop grown across the globe, and it also possesses an appreciably allelopathic potential. Therefore, this study was planned to determine the impacts of the sorghum water extract (SWE) on improving maize growth under Pb and salinity stress. The experiment included different treatments; control, SWE (3%), and different levels of Pb and salinity stress; T1: control, T2: 50 mM NaCl, T3: 100 mM NaCl, T4: 250 μM Pb, and T5: 500 μM Pb. Lead and salinity stress reduced the maize growth by the genesis of reactive oxygen species (ROS), as evidenced by higher production of malondialdehyde (MDA: 39.1 and 32.28%) and hydrogen peroxide (H2O2: 20.62 and 17.81%). Spraying plants with SWE improved the maize growth by increasing antioxidant activities (ascorbate peroxidase: APX, catalase: CAT, peroxidase: POD and superoxide dismutase: SOD), photosynthetic pigments, relative water contents (RWC), osmolyte accumulation (proline, total soluble proteins: TSP, free amino acids: FAA), potassium accumulation, and decreasing MDA, H2O2, sodium, chloride, and Pb accumulation. In conclusion, the application of SWE mitigates adverse impacts of Pb and salinity stresses by improving chlorophyll synthesis and osmolyte accumulation, activating the antioxidant defense system, and preventing the entry of toxic ions.

The critical role of mitochondrial lipid peroxidation in ferroptosis: insights from recent studies.

Ferroptosis is a regulated form of necrotic cell death reliant on iron-catalyzed lipid peroxidation. Although the precise involvement of mitochondria in ferroptosis remains incompletely elucidated, recent research indicates that mitochondrial oxidative events wield a pivotal influence in this mechanism. This article centers on the most recent discoveries, spotlighting the significance of mitochondrial lipid peroxidation in the occurrence of ferroptosis. Modern investigative tools, such as mitochondria-specific dyes responsive to lipid peroxidation and antioxidants targeting mitochondria, have been employed to delve into this phenomenon. The authors' recent empirical evidence demonstrates that mitochondrial lipid peroxidation, quantified using the innovative fluorescent ratiometric probe MitoCLox, takes place prior to the onset of ferroptotic cell death. The mitochondria-targeted antioxidant SkQ1 hinders mitochondrial lipid peroxidation and thwarts ferroptosis, all while leaving unaffected the buildup of reactive oxygen species within the cytoplasm, an antecedent to mitochondrial lipid peroxidation. Similarly, the redox agent methylene blue, impeding the genesis of reactive oxygen species in complex I of the electron transport chain, also imparts a comparable protective effect. These findings collectively imply that reactive oxygen species originating from complex I might hold particular significance in fomenting mitochondrial lipid peroxidation, a pivotal trigger of ferroptosis.

Alleviatory Effects of Silicon and 24-Epibrassinolide in Modulation of Growth, Osmolytes, Metabolites, Antioxidant Defense System, and Gene Expression in Lead-Exposed Fenugreek (Trigonella foenum-graecum L.) Plants

Amplified concentrations of lead (Pb) in cultivable soils, being a major environmental concern, bring about malicious consequences for plant and human health. Trigonella foenum-graecum (fenugreek) is a multipurpose herb used as a spice, tonic, leafy vegetable, and therapeutic agent. Earlier works have revealed the inhibitory effects of Pb toxicity in Trigonella, affecting its growth and productivity. Therefore, the current experimental work was planned with the purpose of evaluating the effects of exogenously supplemented silicon (Si; 2 mM) and 24-epibrassinolide (24-EBL; 10−7 M) (in both individual and combined form) on growth attributes, osmolytes, metabolite measures, and antioxidant defense mechanisms of Trigonella foenum-graecum plants in response to three discrete concentrations of Pb stress (0.5, 0.7, and 0.9 mM). The results revealed that Pb stress affected morphological parameters of fenugreek plants via the genesis of reactive oxygen species (ROS), as indicated by higher measures of oxidative damage indicators like malondialdehyde (MDA) and hydrogen peroxide (H2O2). Spraying foliage with Si together with a pretreatment of 24-EBL alone as well as in a combined form yielded better outcomes in terms of growth parameters in the Pb-stressed plants. Pb toxicity decreased osmolytes, proteins, and metabolites. Components of the antioxidative defense system, i.e., enzymes [ascorbate peroxidase (APX), guaiacol peroxidase (POD), superoxide dismutase (SOD), and catalase (CAT), together with non-enzymes [ascorbic acid (AsA) and glutathione (GSH), were downregulated when subjected to Pb toxicity. Out of all, Pb III (0.9 mM) had a more adverse impact on various parameters in fenugreek compared to Pb I (0.5 mM) and Pb II (0.7 mM). However, external supplementation with Si and 24-EBL (individually and in combination) ameliorated the Pb-mediated oxidative stress in fenugreek plants by improving the content of different osmolytes and metabolites while upregulating the functioning of the antioxidative defense system. Downregulation in the expression of SOD and CAT genes was found in Pb-stressed plants, while their expression was upregulated by Si and 24-EBL both individually and in combination. The experimental study revealed that the combined application of Si and 24-EBL was significantly better at abating the Pb metal stress in fenugreek plants when compared with their individual applications.

Modulation of NADPH oxidase activity by known uraemic retention solutes.

Uraemia and cardiovascular disease appear to be associated with an increased oxidative burden. One of the key players in the genesis of reactive oxygen species (ROS) is nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. Based on initial experiments demonstrating a decreased inhibitory effect on NADPH oxidase activity in the presence of plasma from patients with CKD-5D after dialysis compared with before dialysis, we investigated the effect of 48 known and commercially available uraemic retention solutes on the enzymatic activity of NADPH oxidase. Mononuclear leucocytes isolated from buffy coats of healthy volunteers were isolated, lysed and incubated with NADH in the presence of plasma from healthy controls and patients with CKD-5D. Furthermore, the leucocytes were lysed and incubated in the presence of uraemic retention solute of interest and diphenyleneiodonium chloride (DPI), an inhibitor of NADPH oxidase. The effect on enzymatic activity of NADPH oxidase was quantified within an incubation time of 120min. Thirty-nine of the 48 uraemic retention solutes tested had a significant decreasing effect on NADPH oxidase activity. Oxalate has been characterized as the strongest inhibitor of NADPH oxidase (90% of DPI inhibition). Surprisingly, none of the uraemic retention solutes we investigated was found to increase NADPH oxidase activity. Furthermore, plasma from patients with CKD-5D before dialysis caused significantly higher inhibitory effect on NADPH oxidase activity compared with plasma from healthy subjects. However, this effect was significantly decreased in plasma from patients with CKD-5D after dialysis. The results of this study show that uraemic retention solutes modulated the activity of the NADPH oxidase. The results of this study might be the basis for the development of inhibitors applicable as drug in the situation of increased oxidative stress.

Human glomerular endothelium: interplay among glucose, free fatty acids, angiotensin II, and oxidative stress

Glomerular endothelial cells (GEC) are strategically situated within the capillary loop and adjacent to the glomerular mesangium. GEC serve as targets of metabolic, biochemical, and hemodynamic signals that regulate the glomerular microcirculation. Unequivocally, hyperglycemia, hypertension, and the local renin-angiotensin system partake in the initiation and progression of diabetic nephropathy (DN). Whether free fatty acids (FFA) and reactive oxygen species (ROS) that have been associated with the endothelial dysfunction of diabetic macrovascular disease also contribute to DN is not known. Since endothelial cells from different organs and from different species may display different phenotypes, we employed human GEC to investigate the effect of high glucose (22.5 mmol/l), FFA (800 micromol/l), and angiotensin II (ANG II; 10(-7) mol/l) on the genesis of ROS and their effects on endothelial nitric oxide synthase (eNOS), cyclooxygenase-2 (COX-2), and the synthesis of prostaglandins (PGs). We demonstrated that high glucose but not high FFA increased the expression of a dysfunctional eNOS as well as increased ROS from NADPH oxidase (100%) and likely from uncoupled eNOS. ANG II also induced ROS from NADPH oxidase. High glucose and ANG II upregulated (100%) COX-2 via ROS and significantly increased the synthesis of prostacyclin (PGI(2)) by 300%. In contrast, FFA did not upregulate COX-2 but increased PGI(2) (500%). These novel studies are the first in human GEC that characterize the differential role of FFA, hyperglycemia, and ANG II on the genesis of ROS, COX-2, and PGs and their interplay in the early stages of hyperglcyemia.

Have No Fear, MitoQ 10 Is Here

The physical manifestation of a trait is a constant interplay between one’s genetic makeup and environmental factors. This notion has been substantiated by nutrigenomic studies demonstrating the benefits of nutritional supplements along the continuum between health and disease.1 More importantly, these studies have revealed the plasticity by which the genetic substrate can interact with various environmental components to either exacerbate or mitigate the manifestation of a disease process in those genetically predisposed. Focusing on cardiovascular disease, a vast literature has demonstrated that this disease process is associated with impaired energy production, increased oxidative stress, and cell calcium overload. To these ends, both clinical and animal studies have demonstrated nutrient deficiencies, integral to these processes, to be associated with cardiovascular disease and that these deficiencies represent independent predictors of increased morbidity and mortality.2,3 One cellular component that has received considerable attention regarding function and nutrient supplementation is the mitochondria. Mitochondria are responsible for cellular bioenergetics via oxidative phosphorylation. However, the perpetual transfer of electrons from one molecule to another within the mitochondria renders this organelle a major site for the genesis of reactive oxygen species (ROS).4 Although the mitochondria have antioxidant defenses,4 the disequilibrium between ROS production and ROS neutralization paves the way for disease manifestation. ROS damage to mitochondrial proteins, lipids, and DNA poses …

VARICOCELECTOMY IMPROVES INTRAUTERINE INSEMINATION SUCCESS RATES IN MEN WITH VARICOCELE

We determined whether varicocele treatment before intrauterine insemination significantly affects intrauterine insemination success rates. A total of 58 infertile couples, of whom the women had normal evaluations and men had abnormal semen analyses and a history of varicocele, were included in this study. They were identified after reviewing the charts of all women undergoing intrauterine insemination for male factor infertility at our center. Of the men 24 participated in 63 intrauterine insemination cycles without varicocele treatment, while in the remaining 34 varicocele was treated before a total of 101 intrauterine insemination cycles. Variables associated with pregnancy or live birth were analyzed using repeat measures logistic regression with generalized estimating equation techniques. An initial stepwise generalized estimating equation was performed without including varicocele treatment status. Subsequently varicocele treatment status and the significant associated factors were included in analysis. The semen characteristics of untreated and treated varicocele groups were compared with repeat measures analysis of variance. On pre-wash semen analysis patients with untreated varicocele had significantly higher mean motility plus or minus standard error than patients whose varicoceles were treated (48.6% +/- 2.3% versus 38.1% +/- 1.8%, p = 0.02). However, no statistically significant difference was noted in the mean post-wash total motile sperm count in the treated and untreated groups (7.2 +/- 1.0 versus 14.8 +/- 2.6, p = 0.1). Despite these findings the pregnancy and live birth rates per cycle were significantly higher in patients in whom varicocele was treated than in those without varicocele treatment (11.8% versus 6.3%, p = 0.04 and 11.8% versus 1.6%, p = 0.007, respectively). Varicocele treatment may not improve semen characteristics in all men but it appears to improve pregnancy and live birth rates among couples undergoing intrauterine insemination for male factor infertility. A functional factor not measured on routine semen analysis may affect pregnancy rates in this setting. Men should be screened for varicocele before intrauterine insemination is initiated for male factor infertility.

Prooxidant role of histidine in hypoxic stressed mice and Fe3+-induced lipid peroxidation

An attempt was made to study the effect of histidine on reactive oxygen species in a rodent model of hypoxic stress and in Fe(3+)-ascorbic acid-induced lipid peroxidation in mouse brain homogenates. The latency for onset of hypoxic stress-induced convulsions was decreased in histidine-treated animals with a concomitant rise in brain lipid peroxidation levels. In vitro, histidine potentiated Fe(3+)-ascorbic acid-induced lipid peroxidation in mouse brain homogenates while other antioxidants like B-HT and U-74500A inhibited the same. Moreover, Fe(3+)-histidine-induced lipid peroxidation could not be inhibited by preincubation of the system with high concentrations of ascorbic acid. Thus, it is concluded that histidine acts as a strong prooxidant potentiating the genesis of reactive oxygen species during hypoxic stress as well as during Fe(3+)-ascorbic acid-induced lipid peroxidation.

Molecular biology of human male infertility: links with aging, mitochondrial genetics, and oxidative stress?

Molecular biology of human male infertility: links with aging, mitochondrial genetics, and oxidative stress?

Cellular basis of defective sperm function and its association with the genesis of reactive oxygen species by human spermatozoa.

Addition of the divalent cation ionophore, A23187, to washed populations of human spermatozoa resulted in a sudden burst of production of reactive oxygen species which peaked within 3-5 min. This activity was dependent upon the presence of calcium in the external medium and was unaffected by the mitochondrial inhibitors, oligomycin, antimycin and rotenone. Studies with scavengers of reactive oxygen species revealed that, while reagents directed against singlet oxygen and the hydroxyl radical were without effect, cytochrome C reduced the response to A23187 by about 50%, suggesting that the superoxide anion radical is a major product of the activated human spermatozoon. The clinical implications of these studies stem from the considerable variation observed between individuals in the levels of reactive oxygen species produced by the spermatozoa. This variability was shown to be inversely related to the ability of the spermatozoa to exhibit sperm-oocyte fusion on exposure to A23187; defective samples exhibited a basal level of reactive oxygen species production which was 40 times that observed with normal functional cells.