Reactive Oxidant Species in Piriform Cortex Extracellular Fluid During Seizures Induced by Systemic Kainic Acid in Rats

1999 ◽  
Vol 13 (1-2) ◽  
pp. 63-68 ◽  
Author(s):  
Matthew E. Layton ◽  
Thomas L. Pazdernik
Keyword(s):  
Kainic Acid ◽  
Piriform Cortex ◽  
Extracellular Fluid ◽  
Reactive Oxidant Species ◽  
Reactive Oxidant

scholarly journals Role of oxidants in microbial pathophysiology.

1997 ◽  
Vol 10 (1) ◽  
pp. 1-18 ◽  
Author(s):  
R A Miller ◽  
B E Britigan
Keyword(s):  
Tissue Injury ◽  
Reactive Oxidant Species ◽  
Complex Interactions ◽  
Microbial Invasion ◽  
Adaptive Mechanisms ◽  
Complex Adaptive ◽  
Deleterious Consequence ◽  
Reactive Oxidant ◽  
Oxidant Production

Reactive oxidant species (superoxide, hydrogen peroxide, hydroxyl radical, hypohalous acid, and nitric oxide) are involved in many of the complex interactions between the invading microorganism and its host. Regardless of the source of these compounds or whether they are produced under normal conditions or those of oxidative stress, these oxidants exhibit a broad range of toxic effects to biomolecules that are essential for cell survival. Production of these oxidants by microorganisms enables them to have a survival advantage in their environment. Host oxidant production, especially by phagocytes, is a counteractive mechanism aimed at microbial killing. However, this mechanism may be contribute to a deleterious consequence of oxidant exposure, i.e., inflammatory tissue injury. Both the host and the microorganism have evolved complex adaptive mechanisms to deflect oxidant-mediated damage, including enzymatic and nonenzymatic oxidant-scavenging systems. This review discusses the formation of reactive oxidant species in vivo and how they mediate many of the processes involved in the complex interplay between microbial invasion and host defense.

scholarly journals Oxidative Stress as a Mediator of Cardiovascular Disease

2009 ◽  
Vol 2 (5) ◽  
pp. 259-269 ◽  
Author(s):  
Maqsood M. Elahi ◽  
Yu Xiang Kong ◽  
Bashir M. Matata
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Nitrosative Stress ◽  
Ischemia Reperfusion Injury ◽  
Cell Damage ◽  
Ischemia Reperfusion ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Redox Balance ◽  
Reactive Oxidant Species ◽  
Reactive Oxidant

During physiological processes molecules undergo chemical changes involving reducing and oxidizing reactions. A molecule with an unpaired electron can combine with a molecule capable of donating an electron. The donation of an electron is termed as oxidation whereas the gaining of an electron is called reduction. Reduction and oxidation can render the reduced molecule unstable and make it free to react with other molecules to cause damage to cellular and sub-cellular components such as membranes, proteins and DNA. In this paper, we have discussed the formation of reactive oxidant species originating from a variety of sources such as nitric oxide (NO) synthase (NOS), xanthine oxidases (XO), the cyclooxygenases, nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidase isoforms and metal-catalyzed reactions. In addition, we present a treatise on the physiological defences such as specialized enzymes and antioxidants that maintain reduction-oxidation (redox) balance. We have also given an account of how enzymes and antioxidants can be exhausted by the excessive production of reactive oxidant species (ROS) resulting in oxidative stress/nitrosative stress, a process that is an important mediator of cell damage. Important aspects of redox imbalance that triggers the activity of a number of signaling pathways including transcription factors activity, a process that is ubiquitous in cardiovascular disease related to ischemia/reperfusion injury have also been presented.

HIV/HAART-associated oxidative stress is detectable by metabonomics

2017 ◽  
Vol 13 (11) ◽  
pp. 2202-2217 ◽  
Author(s):  
Aurelia A. Williams ◽  
Lungile J. Sitole ◽  
Debra Meyer
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxidant Species ◽  
Markers Of Oxidative Stress ◽  
Reactive Oxidant

HIV and/or its treatment increases reactive oxidant species and concomitantly decreases antioxidants, collectively destabilizing DNA, protein and lipids, producing markers of oxidative stress, detectable by metabonomics.

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