scholarly journals The effects of Femarelle and Vitamin D Analog on Lipoxygenase Products and Reactive Oxygen Species (ROS) formation in the Female and Male Human-Derived Cultured Osteoblastic Cells

2017 ◽  
pp. 00-00
Author(s):  
D. Somjen ◽  
S. Katzburg ◽  
F. Kohen ◽  
O. Sharon ◽  
E. Knoll ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Vitamin D ◽  
Reactive Oxygen ◽  
Osteoblastic Cells ◽  
Oxygen Species ◽  
Vitamin D Analog ◽  
Lipoxygenase Products ◽  
Ros Formation

scholarly journals Intradialytic granulocyte reactive oxygen species production: a prospective, crossover trial.

1993 ◽  
Vol 4 (2) ◽  
pp. 178-186 ◽  
Author(s):  
J Himmelfarb ◽  
K A Ault ◽  
D Holbrook ◽  
D A Leeber ◽  
R M Hakim
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Fold Increase ◽  
Ros Production ◽  
Oxygen Species ◽  
Susceptibility To Infection ◽  
Flow Cytometric ◽  
Ros Formation ◽  
Dialysis Membranes ◽  
Species Production

By the use of flow cytometric techniques, this prospective, randomized crossover study was designed to analyze intradialytic granulocyte reactive oxygen species (ROS) formation in whole blood with complement-activating and noncomplement-activating hollow fiber membranes. Dialysis with a complement-activating membrane resulted in a 6.5-fold increase in granulocyte hydrogen peroxide production 15 min after dialysis initiation and remained significantly elevated (P < 0.01) through the first 30 min with this membrane in comparison to both predialysis values and simultaneous values with a noncomplement-activating membrane. Further studies demonstrated that blood obtained at 15 min with a complement-activating membrane generated significantly less granulocyte ROS production in response to Staphylococcus aureus incubation than blood obtained either predialysis or at the same time in dialysis with a noncomplement-activating membrane. Both complement-activating and noncomplement-activating dialysis membranes caused slightly decreased granulocyte responsiveness to phorbol myristate acetate. It was concluded that hemodialysis with complement-activating membranes results in increased granulocyte ROS production and decreased responsiveness to S. aureus challenge during the dialysis procedure. These results document the potential role of ROS in hemodialysis-associated pathology and susceptibility to infection.

scholarly journals The Role of Mitochondrial Reactive Oxygen Species in Cardiovascular Injury and Protective Strategies

2016 ◽  
Vol 2016 ◽  
pp. 1-19 ◽  
Author(s):  
Danina M. Muntean ◽  
Adrian Sturza ◽  
Maria D. Dănilă ◽  
Claudia Borza ◽  
Oana M. Duicu ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Myocardial Injury ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Early Reperfusion ◽  
Coronary Syndromes ◽  
Ros Formation ◽  
St Elevation ◽  
Protective Strategies ◽  
Routine Therapy

Ischaemia/reperfusion (I/R) injury of the heart represents a major health burden mainly associated with acute coronary syndromes. While timely coronary reperfusion has become the established routine therapy in patients with ST-elevation myocardial infarction, the restoration of blood flow into the previously ischaemic area is always accompanied by myocardial injury. The central mechanism involved in this phenomenon is represented by the excessive generation of reactive oxygen species (ROS). Besides their harmful role when highly generated during early reperfusion, minimal ROS formation during ischaemia and/or at reperfusion is critical for the redox signaling of cardioprotection. In the past decades, mitochondria have emerged as the major source of ROS as well as a critical target for cardioprotective strategies at reperfusion. Mitochondria dysfunction associated with I/R myocardial injury is further described and ultimately analyzed with respect to its role as source of both deleterious and beneficial ROS. Furthermore, the contribution of ROS in the highly investigated field of conditioning strategies is analyzed. In the end, the vascular sources of mitochondria-derived ROS are briefly reviewed.

Mechanisms of pulmonary vasoconstriction induced by chemotactic peptide FMLP in isolated rabbit lungs

1992 ◽  
Vol 72 (4) ◽  
pp. 1549-1556 ◽  
Author(s):  
H. Tanaka ◽  
J. D. Bradley ◽  
L. J. Baudendistel ◽  
T. E. Dahms
Keyword(s):  
Reactive Oxygen Species ◽  
Polymorphonuclear Leukocytes ◽  
Reactive Oxygen ◽  
Cyclooxygenase Inhibitors ◽  
Oxygen Species ◽  
Chemotactic Peptide ◽  
Middle Segment ◽  
Pulmonary Vasoconstriction ◽  
Lipoxygenase Products ◽  
Reactive Oxygen Species Scavenger

The chemotactic peptide N-formyl-methionyl-leucyl-phenylalanine (FMLP) has been shown to constrict both bronchial and coronary vascular smooth muscle through the action of cyclooxygenase or lipoxygenase products. We observed that intravenous FMLP increased pulmonary vascular resistance (PVR) in isolated buffer-perfused rabbit lungs. FMLP increased the PVR (primarily in the middle segment of the pulmonary vascular bed) at concentrations greater than or equal to 10(-7) M. Maximum vasoconstriction occurred at 5 min and then slowly declined to a level that remained above baseline at 30 min. Tachyphylaxis was observed in response to FMLP. When polymorphonuclear leukocytes (PMNs) were added to the perfusate, FMLP caused a greater increase in PVR. PMN depletion with dimethylmyleran significantly reduced the PVR response to FMLP. Pretreatment with two dissimilar cyclooxygenase inhibitors, meclofenamate and ibuprofen, and the leukotriene synthesis blocker MK 886 had no effect on the FMLP-induced vasoconstriction. However, the reactive oxygen species scavenger catalase significantly reduced the vasoconstriction. These results suggest that FMLP induces vasoconstriction that is dependent on PMNs and mediated by reactive oxygen species with no involvement of cyclooxygenase or lipoxygenase products.

Interaction of electrophilic lipid oxidation products with mitochondria in endothelial cells and formation of reactive oxygen species

2006 ◽  
Vol 290 (5) ◽  
pp. H1777-H1787 ◽  
Author(s):  
Aimee Landar ◽  
Jaroslaw W. Zmijewski ◽  
Dale A. Dickinson ◽  
Claire Le Goffe ◽  
Michelle S. Johnson ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Reactive Oxygen ◽  
Direct Interaction ◽  
Oxidation Products ◽  
Antioxidant Defenses ◽  
Heme Oxygenase 1 ◽  
Oxygen Species ◽  
Lipid Oxidation Products ◽  
Ros Formation

Electrophilic lipids, such as 4-hydroxynonenal (HNE), and the cyclopentenones 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) and 15-J2-isoprostane induce both reactive oxygen species (ROS) formation and cellular antioxidant defenses, such as heme oxygenase-1 (HO-1) and glutathione (GSH). When we compared the ability of these distinct electrophiles to stimulate GSH and HO-1 production, the cyclopentenone electrophiles were somewhat more potent than HNE. Over the concentration range required to observe equivalent induction of GSH, dichlorofluorescein fluorescence was used to determine both the location and amounts of electrophilic lipid-dependent ROS formation in endothelial cells. The origin of the ROS on exposure to these compounds was largely mitochondrial. To investigate the possibility that the increased ROS formation was due to mitochondrial localization of the lipids, we prepared a novel fluorescently labeled form of the electrophilic lipid 15d-PGJ2. The lipid demonstrated strong colocalization with the mitochondria, an effect which was not observed by using a fluorescently labeled nonelectrophilic lipid. The role of mitochondria was confirmed by using cells deficient in functional mitochondria. On the basis of these data, we propose that ROS formation in endothelial cells is due to the direct interaction of these lipids with the organelle.

scholarly journals Vitamin D, reactive oxygen species and calcium signalling in ageing and disease

2016 ◽  
Vol 371 (1700) ◽  
pp. 20150434 ◽  
Author(s):  
Michael J. Berridge
Keyword(s):  
Reactive Oxygen Species ◽  
Vitamin D ◽  
Neuronal Cell Death ◽  
Memory Loss ◽  
Neuronal Cell ◽  
Reactive Oxygen ◽  
Cardiac Cells ◽  
Amyloid Formation ◽  
Oxygen Species ◽  
Age Related

Vitamin D is a hormone that maintains healthy cells. It functions by regulating the low resting levels of cell signalling components such as Ca 2+ and reactive oxygen species (ROS). Its role in maintaining phenotypic stability of these signalling pathways depends on the ability of vitamin D to control the expression of those components that act to reduce the levels of both Ca 2+ and ROS. This regulatory role of vitamin D is supported by both Klotho and Nrf2. A decline in the vitamin D/Klotho/Nrf2 regulatory network may enhance the ageing process, and this is well illustrated by the age-related decline in cognition in rats that can be reversed by administering vitamin D. A deficiency in vitamin D has also been linked to two of the major diseases in man: heart disease and Alzheimer's disease (AD). In cardiac cells, this deficiency alters the Ca 2+ transients to activate the gene transcriptional events leading to cardiac hypertrophy and the failing heart. In the case of AD, it is argued that vitamin D deficiency results in the Ca 2+ landscape that initiates amyloid formation, which then elevates the resting level of Ca 2+ to drive the memory loss that progresses to neuronal cell death and dementia. This article is part of the themed issue ‘Evolution brings Ca 2+ and ATP together to control life and death’.

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