scholarly journals Exploitation of siderophore producing bacteria Acinetobacter soli (MTCC-5918) for lipids and reactive oxygen species in Chlorella variabilis (ATCC- PTA 12198) through co-cultivation

2020 ◽  
Author(s):  
Soundarya Rajapitamahuni ◽  
Pooja Bachani ◽  
Vamsi Bharadwaj ◽  
Sandhya Mishra
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Lipid Accumulation ◽  
Reactive Oxygen ◽  
Ash Content ◽  
Ros Generation ◽  
Oxygen Species ◽  
Chlorella Variabilis ◽  
Iron Deficient ◽  
Acinetobacter Soli

Abstract Background Increased iron uptake via siderophores triggers a series of physiological processes and generation of reactive oxygen species (ROS) which causes damage to proteins, lipids, carbohydrates, resulting into micro algal cell lysis. Moreover, there are reports mentioning oxidative stress is a mediator for increased lipid accumulation in microalgae. The main aim of this study is co-cultivation of the bacteria Acinetobacter soli (MTCC- 5918) and the microalgae Chlorella variabilis (ATCC-PTA 12198) under iron limiting conditions and the threshold value of iron that trigger oxidizing stress to microalgae. Further, the ROS generation in the microalgae C. variabilis was determined in terms of OH, SO2 and H2O2 concentration in the cells while co-cultivation. Results The co-cultured biomass contains (45.92 ± 0.74%) lipid content which was about 21% higher than that of the axenically grown microalgae. Carbohydrate content also increased to 40% than that of the control culture. Oxidative stress is a mediator for increased lipid accumulation in microalgae. As growth inhibition triggered due to the generation of high ROS toxicity during iron deficiency an increase in concentration of OH and H2O2 content was observed. In iron sufficient medium ash content of co-cultivated microalgae showed 32% and in iron deficient medium showed 14.23% which shows 44% decrease of ash content. Our novel approach significantly outperforms the involvement of different reactive oxygen species (ROS) in induction and in regulation of chelator release from cells at adequate Fe supply, which is also affecting the growth,lipids, carbohydrates, proteins, pigments, etc. Conclusions The findings of the present study highlights that oxidative stress is a mediator for increased lipid accumulation in microalgae that simultaneously becomes an alternative strategy for the improvement of biofuel potential in C. variabilis. The study portraysthe significance of co-cultivation of A. soli and C. variabilis induced oxidative stress (ROS generation) in microalgae caused due to higher uptake of iron via siderophore

scholarly journals Impacts of Oxidative Stress and Antioxidants on Semen Functions

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Amrit Kaur Bansal ◽  
G. S. Bilaspuri
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Sperm Quality ◽  
Reactive Oxygen ◽  
The Body ◽  
Atp Depletion ◽  
Contributory Factor ◽  
Ros Generation ◽  
Oxygen Species ◽  
High Concentrations

Oxidative stress (OS) has been considered a major contributory factor to the infertility. Oxidative stress is the result of imbalance between the reactive oxygen species (ROS) and antioxidants in the body which can lead to sperm damage, deformity, and eventually male infertility. Although high concentrations of the ROS cause sperm pathology (ATP depletion) leading to insufficient axonemal phosphorylation, lipid peroxidation, and loss of motility and viability but, many evidences demonstrate that low and controlled concentrations of these ROS play an important role in sperm physiological processes such as capacitation, acrosome reaction, and signaling processes to ensure fertilization. The supplementation of a cryopreservation extender with antioxidant has been shown to provide a cryoprotective effect on mammalian sperm quality. This paper reviews the impacts of oxidative stress and reactive oxygen species on spermatozoa functions, causes of ROS generation, and antioxidative strategies to reduce OS. In addition, we also highlight the emerging concept of utilizing OS as a tool of contraception.

scholarly journals Lipid droplets alleviate cadmium induced cytotoxicity in Saccharomyces cerevisiae

2017 ◽  
Vol 6 (1) ◽  
pp. 30-41 ◽  
Author(s):  
Selvaraj Rajakumar ◽  
Vasanthi Nachiappan
Keyword(s):  
Oxidative Stress ◽  
Saccharomyces Cerevisiae ◽  
Reactive Oxygen Species ◽  
Lipid Accumulation ◽  
Lipid Droplets ◽  
Reactive Oxygen ◽  
Oxygen Species

Cadmium (Cd) induces oxidative stress that generates reactive oxygen species (ROS) and increased lipid accumulation.

scholarly journals The impact of reactive oxygen species in the development of cardiometabolic disorders: a review

2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Roland Akhigbe ◽  
Ayodeji Ajayi
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Reactive Oxygen ◽  
Acid Oxidation ◽  
Ros Generation ◽  
Metabolic Memory ◽  
Oxygen Species ◽  
Cardiometabolic Disorders ◽  
The Impact

AbstractOxidative stress, an alteration in the balance between reactive oxygen species (ROS) generation and antioxidant buffering capacity, has been implicated in the pathogenesis of cardiometabolic disorders (CMD). At physiological levels, ROS functions as signalling mediators, regulates various physiological functions such as the growth, proliferation, and migration endothelial cells (EC) and smooth muscle cells (SMC); formation and development of new blood vessels; EC and SMC regulated death; vascular tone; host defence; and genomic stability. However, at excessive levels, it causes a deviation in the redox state, mediates the development of CMD. Multiple mechanisms account for the rise in the production of free radicals in the heart. These include mitochondrial dysfunction and uncoupling, increased fatty acid oxidation, exaggerated activity of nicotinamide adenine dinucleotide phosphate oxidase (NOX), reduced antioxidant capacity, and cardiac metabolic memory. The purpose of this study is to discuss the link between oxidative stress and the aetiopathogenesis of CMD and highlight associated mechanisms. Oxidative stress plays a vital role in the development of obesity and dyslipidaemia, insulin resistance and diabetes, hypertension via various mechanisms associated with ROS-led inflammatory response and endothelial dysfunction.

scholarly journals Regulation of Reactive Oxygen Species and Antioxidant Defense in Plants under Salinity

2021 ◽  
Vol 22 (17) ◽  
pp. 9326
Author(s):  
Mirza Hasanuzzaman ◽  
Md. Rakib Hossain Raihan ◽  
Abdul Awal Chowdhury Masud ◽  
Khussboo Rahman ◽  
Farzana Nowroz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Salt Stress ◽  
Oxidative Damage ◽  
Antioxidant Defense ◽  
Reactive Oxygen ◽  
Antioxidant Defense System ◽  
Ros Generation ◽  
Oxygen Species ◽  
Defense System

The generation of oxygen radicals and their derivatives, known as reactive oxygen species, (ROS) is a part of the signaling process in higher plants at lower concentrations, but at higher concentrations, those ROS cause oxidative stress. Salinity-induced osmotic stress and ionic stress trigger the overproduction of ROS and, ultimately, result in oxidative damage to cell organelles and membrane components, and at severe levels, they cause cell and plant death. The antioxidant defense system protects the plant from salt-induced oxidative damage by detoxifying the ROS and also by maintaining the balance of ROS generation under salt stress. Different plant hormones and genes are also associated with the signaling and antioxidant defense system to protect plants when they are exposed to salt stress. Salt-induced ROS overgeneration is one of the major reasons for hampering the morpho-physiological and biochemical activities of plants which can be largely restored through enhancing the antioxidant defense system that detoxifies ROS. In this review, we discuss the salt-induced generation of ROS, oxidative stress and antioxidant defense of plants under salinity.

scholarly journals TRPC1 Deficiency Exacerbates Cerebral Ischemia/Reperfusion-Induced Neurological Injury by Potentiating Nox4-Derived Reactive Oxygen Species Generation

2018 ◽  
Vol 51 (4) ◽  
pp. 1723-1738 ◽  
Author(s):  
Ning Xu ◽  
Hao Meng ◽  
Tianyi Liu ◽  
Yingli Feng ◽  
Yuan Qi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Severity Score ◽  
Ischemia Reperfusion ◽  
Reactive Oxygen ◽  
Neurological Injury ◽  
Ros Generation ◽  
Oxygen Species ◽  
Neurological Severity Score

Background/Aims: Transient receptor potential cation channel 1 (TRPC1)-mediated the calcium (Ca2+) influx plays an important role in several brain disorders. However, the function of TRPC1 in ischemia/reperfusion (I/R)-induced neurological injury is unclear. Methods: Wild-type or TRPC1 knockout mice underwent middle cerebral artery occlusion for 90 min followed by 24 h of reperfusion. In an in vitro study, neuronal cells were treated with oxygen–glucose deprivation and reoxygenation (OGD/R) to mimic I/R. The intracellular Ca2+ concentration [Ca2+]i was measured by Fura 2-AM under a microscope. Cerebral infarct volume was measured by triphenyltetrazolium chloride staining. Neurological function was examined by neurological severity score, Morris water maze test, rotarod test and string test. Oxidative parameters were detected by malondialdehyde, glutathione peroxidase, and superoxide dismutase commercially available kits. The protein expression levels of TRPC1, Nox4, p22phox, p47phox, and p67phox were analyzed by western blotting. Results: Brain tissues from cerebral I/R mice showed decreased TRPC1 expression. Similarly, TRPC1 expression was reduced in HT22 cells upon exposure to OGD/R treatment, followed by decreased Ca2+ influx. However, TRPC1 overexpression reversed the OGD/R-induced decrease in [Ca2+]i. TRPC1 knockout significantly exacerbated I/R-induced brain infarction, edema, neurological severity score, memory impairment, neurological deficits, and oxidative stress. In contrast, TRPC1 upregulation inhibited the increase in reactive oxygen species (ROS) generation induced by OGD/R. Analysis of key subunits of the Nox family and mitochondrial ROS revealed that the effects of TRPC1 downregulation on oxidative stress were associated with activation of Nox4-containing NADPH oxidase. TRPC1 interacted with Nox4 and facilitated Nox4 protein degradation under OGD/R conditions. In addition, TRPC1 inhibition potentiated the OGD/R-induced translocation of p47phox and p67phox as well as the interaction between Nox4 and p47phox or p67phox, whereas TRPC1 overexpression had the opposite effects. Conclusion: TRPC1 deficiency potentiates ROS generation via Nox4-containing NADPH oxidase, which exacerbates cerebral I/R injury. TRPC1 may be a promising molecular target for the treatment of stroke.

scholarly journals Significance of Mitochondrial Reactive Oxygen Species in the Generation of Oxidative Stress in Spermatozoa

2008 ◽  
Vol 93 (8) ◽  
pp. 3199-3207 ◽  
Author(s):  
Adam J. Koppers ◽  
Geoffry N. De Iuliis ◽  
Jane M. Finnie ◽  
Eileen A. McLaughlin ◽  
R. John Aitken
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Complex I ◽  
Mitochondrial Membrane ◽  
Reactive Oxygen ◽  
Human Spermatozoa ◽  
Ros Generation ◽  
Oxygen Species ◽  
Mitochondrial Ros ◽  
Sperm Movement

Abstract Context: Male infertility has been linked with the excessive generation of reactive oxygen species (ROS) by defective spermatozoa. However, the subcellular origins of this activity are unclear. Objective: The objective of this study was to determine the importance of sperm mitochondria in creating the oxidative stress associated with defective sperm function. Method: Intracellular measurement of mitochondrial ROS generation and lipid peroxidation was performed using the fluorescent probes MitoSOX red and BODIPY C11 in conjunction with flow cytometry. Effects on sperm movement were measured by computer-assisted sperm analysis. Results: Disruption of mitochondrial electron transport flow in human spermatozoa resulted in generation of ROS from complex I (rotenone sensitive) or III (myxothiazol, antimycin A sensitive) via mechanisms that were independent of mitochondrial membrane potential. Activation of ROS generation at complex III led to the rapid release of hydrogen peroxide into the extracellular space, but no detectable peroxidative damage. Conversely, the induction of ROS on the matrix side of the inner mitochondrial membrane at complex I resulted in peroxidative damage to the midpiece and a loss of sperm movement that could be prevented by the concomitant presence of α-tocopherol. Defective human spermatozoa spontaneously generated mitochondrial ROS in a manner that was negatively correlated with motility. Simultaneous measurement of general cellular ROS generation with dihydroethidium indicated that 68% of the variability in such measurements could be explained by differences in mitochondrial ROS production. Conclusion: We conclude that the sperm mitochondria make a significant contribution to the oxidative stress experienced by defective human spermatozoa.

scholarly journals Reactive Oxygen Species-Induced Oxidative Stress in the Development of Insulin Resistance and Hyperandrogenism in Polycystic Ovary Syndrome

2006 ◽  
Vol 91 (1) ◽  
pp. 336-340 ◽  
Author(s):  
Frank González ◽  
Neal S. Rote ◽  
Judi Minium ◽  
John P. Kirwan
Keyword(s):  
Oxidative Stress ◽  
Insulin Resistance ◽  
Reactive Oxygen Species ◽  
Polycystic Ovary Syndrome ◽  
Polycystic Ovary ◽  
Reactive Oxygen ◽  
Ros Generation ◽  
Oxygen Species ◽  
Ovary Syndrome ◽  
Percent Change

Abstract Context: Insulin resistance and chronic low level inflammation are often present in women with polycystic ovary syndrome (PCOS). Objective: The purpose of this study was to determine the effects of hyperglycemia on reactive oxygen species (ROS) generation from mononuclear cells (MNCs) in PCOS. Design: This was a prospective controlled study. Setting: The study was conducted at an academic medical center. Patients: The study population consisted of 16 women with PCOS (eight lean, eight obese) and 15 age- and body composition-matched controls (eight lean, seven obese). Main Outcome Measures: Insulin sensitivity was derived from a 2-h, 75-g oral glucose tolerance test (ISOGTT). ROS generation and p47phox protein expression were quantitated from MNCs obtained from blood drawn fasting and 2 h after glucose ingestion. Results: ISOGTT was lower in PCOS, compared with controls (3.1 ± 0.3 vs. 6.3 ± 0.9, P < 0.003). The percent change in ROS generation from MNCs was higher in lean and obese PCOS, compared with lean controls (138.8 ± 21.3 and 154.2 ± 49.1 vs. 0.6 ± 12.7, P < 0.003). The percent change in ROS generation from MNCs correlated positively with glucose area under the curve (r = 0.38, P < 0.05), and plasma levels of testosterone (r = 0.59, P < 0.002) and androstenedione (r = 0.50, P < 0.009). The percent change in p47phox from MNCs was also higher in lean and obese PCOS, compared with lean controls (36.2 ± 18.2 and 39.1 ± 8.0 vs. −13.7 ± 8.7, P < 0.02), and correlated negatively with ISOGTT (r = −0.39, P < 0.05). Conclusion: ROS generation from MNCs in response to hyperglycemia is increased in PCOS independent of obesity. The resultant oxidative stress may contribute to a proinflammatory state that induces insulin resistance and hyperandrogenism in women with this disorder.

scholarly journals Oxidative Stress and Its Association with COVID-19: A Narrative Review

2020 ◽  
pp. 97-105 ◽  
Author(s):  
Hardi Rafat Baqi ◽  
Halgord Ali M. Farag ◽  
Abdel Hamid H. El Bilbeisi ◽  
Rafee Habib Askandar ◽  
Amany M. El Afifi
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Cell Entry ◽  
Chronic Obstructive ◽  
Ros Generation ◽  
Oxygen Species ◽  
Obstructive Pulmonary Disease ◽  
Angiotensin Converting Enzyme 2 ◽  
Obesity And Diabetes

The naturalness of severe acute respiratory syndrome coronavirus 2 infections (SARS-Cov-2) appears to impact the respiratory system and lungs, however, the etiology of many cases exhibited several various features of the disease. The Coronavirus disease 2019 (COVID-19) symptoms are not limited to the virus’s first definitions. This review gathered the contemporary information throughout PubMed, Scopus, and Science Direct databases regarding possible effects of the virus in generating reactive oxygen species and causing oxidative stress. However, this ensures a hypothesis for now, yet from the literature and incidence of COVID-19 symptoms along with comorbidities we can observe the potentials of the virus in the generation of oxidative stress. Especially the virus’s route to cell entry via angiotensin-converting enzyme 2 (ACE2) receptor is well known that leads to pathogenesis in angiotensin II (AT II) which are critical in NADH/NADPH oxidase inducing ROS generation. Moreover, the virus’s activity to replicate seems to be reduced in high antioxidant glutathione level concentrations. The outcome of the review proposes a hypothesis that COVID-19 is associated with reactive oxygen species and its comorbidities mostly joined with oxidative stress including hypertension, cardiovascular, thrombosis, obesity, and diabetes besides of chronic obstructive pulmonary disease and asthma.

Are reactive oxygen species important mediators of vascular dysfunction?

2019 ◽  
Vol 15 ◽  
Author(s):  
Gabriel T. do Vale ◽  
Carlos R. Tirapelli
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cardiovascular Diseases ◽  
Vascular Dysfunction ◽  
Critical Role ◽  
Reactive Oxygen ◽  
Oxygen Metabolism ◽  
Ros Generation ◽  
Oxygen Species ◽  
Promising Alternative

Reactive oxygen species (ROS) are reactive derivatives of oxygen metabolism. The ROS generation can be mediated by distinctive enzymatic systems including NADPH oxidases. The components of this enzyme are expressed in endothelial and vascular smooth muscle cells, adventitial fibroblasts, and infiltrating monocytes/macrophages. Oxidative stress is a molecular dysregulation in ROS generation/elimination, which plays a key role in the development of vascular dysfunction in distinctive conditions including hypertension. It is characterized by vascular inflammation, a loss of NO bioavailability and endothelial dysfunction. Considering that oxidative stress is a key mediator of vascular dysfunction, antioxidant therapy with classic antioxidants seemed to be a promising alternative for the treatment of vascular diseases. In this sense, some commonly used drugs for the treatment of cardiovascular diseases such as angiotensin converting enzyme (ACE) inhibitors or angiotensin receptor AT1 antagonists showed antioxidant effects that might have contributed, at least in part, to the beneficial effects of these drugs on the treatment of cardiovascular diseases. The effectiveness of these drugs shows that ROS are in fact important mediators of vascular dysfunction and that angiotensin II plays a critical role in such response.

scholarly journals The Differential Reactive Oxygen Species Production of Tear Neutrophils in Response to Various Stimuli In Vitro

2021 ◽  
Vol 22 (23) ◽  
pp. 12899
Author(s):  
Yutong Jin ◽  
Brian Dixon ◽  
Lyndon Jones ◽  
Maud Gorbet
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Magnetic Bead ◽  
Polymorphonuclear Neutrophils ◽  
Ros Generation ◽  
Ros Production ◽  
Oxygen Species ◽  
High Level

A large number of polymorphonuclear neutrophils (PMNs) invade the ocular surface during prolonged eye closure (sleep); these leukocytes are commonly referred as tear PMNs. PMNs contribute to homeostasis and possess an arsenal of inflammatory mediators to protect against pathogens and foreign materials. This study examined the ability of tear PMNs to generate reactive oxygen species (ROS), an essential killing mechanism for PMNs which can lead to oxidative stress and imbalance. Cells were collected after sleep from healthy participants using a gentle eye wash. ROS production in stimulated (phorbol-12-myristate-13-acetate (PMA), lipopolysaccharides (LPS) or N-Formylmethionyl-leucyl-phenylalanine (fMLP)) and unstimulated tear PMNs was measured using luminol-enhanced chemiluminescence for 60 min. A high level of constitutive/spontaneous ROS production was observed in tear PMNs in the absence of any stimulus. While tear PMNs were able to produce ROS in response to PMA, they failed to appropriately respond to LPS and fMLP, although fMLP-stimulated tear PMNs generated ROS extracellularly in the first three minutes. Higher ROS generation was observed in isolated tear PMNs which may be due to priming from the magnetic bead cell separation system. The differential responses of tear PMNs in ROS generation provide further evidence of their potential inflammatory roles in ocular complications involving oxidative stress.

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