Role of reactive oxygen species in hippocampal long-term potentiation: Contributory or inhibitory?

2002 ◽  
Vol 70 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Lauren T. Knapp ◽  
Eric Klann
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
Long Term Potentiation ◽  
Oxygen Species ◽  
Term Potentiation

Nitrate tolerance does not increase production of peroxynitrite in the heart

2002 ◽  
Vol 283 (1) ◽  
pp. H69-H76 ◽  
Author(s):  
Tamás Csont ◽  
Csaba Csonka ◽  
Annamária Ónody ◽  
Anikó Görbe ◽  
László Dux ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Vascular Dysfunction ◽  
Reactive Oxygen ◽  
Nitrate Tolerance ◽  
Oxygen Species ◽  
Mechanical Function ◽  
Nitrate Treatment

Clinical studies have suggested that long-term nitrate treatment does not improve and may even worsen cardiovascular mortality, and the possible role of nitrate tolerance has been suspected. Nitrate tolerance has been recently shown to increase vascular superoxide and peroxynitrite production leading to vascular dysfunction. Nevertheless, nitrates exert direct cardiac effects independent from their vascular actions. Therefore, we investigated whether in vivo nitroglycerin treatment leading to vascular nitrate tolerance increases cardiac formation of nitric oxide (NO), reactive oxygen species, and peroxynitrite, thereby leading to cardiac dysfunction. Nitrate tolerance increased bioavailability of NO in the heart without increasing formation of reactive oxygen species. Despite elevated myocardial NO, neither cardiac markers of peroxynitrite formation nor cardiac mechanical function were affected by nitroglycerin treatment. However, serum free nitrotyrosine, a marker for systemic peroxynitrite formation, was significantly elevated in nitroglycerin-treated animals. This is the first demonstration that, although the systemic effects of nitroglycerin may be deleterious due to enhancement of extracardiac peroxynitrite formation, nitroglycerin does not result in oxidative damage in the heart.

scholarly journals Involvement of Reactive Oxygen Species in Long-Term Potentiation in the Spinal Cord Dorsal Horn

2010 ◽  
Vol 103 (1) ◽  
pp. 382-391 ◽  
Author(s):  
Kwan Yeop Lee ◽  
Kyungsoon Chung ◽  
Jin Mo Chung
Keyword(s):  
Reactive Oxygen Species ◽  
Spinal Cord ◽  
Dorsal Horn ◽  
Dorsal Root ◽  
Long Term Potentiation ◽  
Oxygen Species ◽  
Tert Butyl ◽  
Term Potentiation ◽  
C Fiber

Recent studies suggest that reactive oxygen species (ROS) are functional messenger molecules in central sensitization, an underlying mechanism of persistent pain. Because spinal cord long-term potentiation (LTP) is the electrophysiological basis of central sensitization, this study investigates the effects of the increased or decreased spinal ROS levels on spinal cord LTP. Spinal cord LTP is induced by either brief, high-frequency stimulation (HFS) of a dorsal root at C-fiber intensity or superfusion of a ROS donor, tert-butyl hydroperoxide (t-BOOH), onto rat spinal cord slice preparations. Field excitatory postsynaptic potentials (fEPSPs) evoked by dorsal root stimulations with either Aβ- or C-fiber intensity are recorded from the superficial dorsal horn. HFS significantly increases the slope of both Aβ- and C-fiber evoked fEPSPs, thus suggesting LTP development. The induction, not the maintenance, of HFS-induced LTP is blocked by a N-methyl-d-aspartate (NMDA) receptor antagonist, d-2-amino-5-phosphonopentanoic acid (d-AP5). Both the induction and maintenance of LTP of Aβ-fiber-evoked fEPSPs are inhibited by a ROS scavenger, either N-tert-butyl-α-phenylnitrone or 4-hydroxy-2,2,6,6-tetramethylpiperidine- N-oxyl. A ROS donor, t-BOOH-induced LTP is inhibited by N-tert-butyl-α-phenylnitrone but not by d-AP5. Furthermore, HFS-induced LTP and t-BOOH-induced LTP occlude each other. The data suggest that elevated ROS is a downstream event of NMDA receptor activation and an essential step for potentiation of synaptic excitability in the spinal dorsal horn.

The role of reactive oxygen species and antioxidants during precooling stages of axis cryopreservation in recalcitrantTrichilia dregeana

Botany ◽  
2016 ◽  
Vol 94 (5) ◽  
pp. 391-403 ◽  
Author(s):  
Cassandra Naidoo ◽  
Patricia Berjak ◽  
Norman W. Pammenter ◽  
Boby Varghese
Keyword(s):  
Reactive Oxygen Species ◽  
Cathodic Protection ◽  
Reactive Oxygen ◽  
Static Field ◽  
Oxygen Species ◽  
Embryonic Axes ◽  
Feasible Method ◽  
Shoot Production

Cryopreservation is currently the only feasible method for long-term conservation of non-orthodox germplasm. Previous attempts to cryopreserve embryonic axes of Trichilia dregeana Sond. indicated that the inability to produce shoots, suggestedly associated with a wound-induced burst of reactive oxygen species (ROS) accompanied by declining antioxidant potential, consistently accompanied procedures necessary for cryopreservation. This study involved the provision of cathodic protection, both in the aqueous phase (electrolysis of a solution containing dilute electrolytes) and dry state (rapid drying of axes on a grid on which a static field is generated via the cathode of a power-pack) with the addition of other antioxidants, i.e., ascorbic acid and DMSO, to counteract uncontrolled ROS activity. The production of superoxide ([Formula: see text]), hydrogen peroxide (H2O2), and hydroxyl radical ([Formula: see text]) in conjunction with the corresponding total aqueous antioxidant activity and viability was quantitatively assessed after each stage of the cryoprocedure, with or without cathodic protection and (or) antioxidants. No shoot production occurred in the treatments without cathodic protection and (or) antioxidants. In contrast, 80% of axes produced seedlings after excision, 40% after cryoprotection, and 40% after flash (rapid) drying, when the treatments included a form of cathodic protection.

The Role of Reactive Oxygen Species in Tumor Treatment and its Impact on Bone Marrow Hematopoiesis

2020 ◽  
Vol 21 (5) ◽  
pp. 477-498
Author(s):  
Yongfeng Chen ◽  
Xingjing Luo ◽  
Zhenyou Zou ◽  
Yong Liang
Keyword(s):  
Reactive Oxygen Species ◽  
Bone Marrow ◽  
Oxidative Damage ◽  
Tumor Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tumor Treatment ◽  
Normal Cells ◽  
Treatment And Prevention

Reactive oxygen species (ROS), an important molecule inducing oxidative stress in organisms, play a key role in tumorigenesis, tumor progression and recurrence. Recent findings on ROS have shown that ROS can be used to treat cancer as they accelerate the death of tumor cells. At present, pro-oxidant drugs that are intended to increase ROS levels of the tumor cells have been widely used in the clinic. However, ROS are a double-edged sword in the treatment of tumors. High levels of ROS induce not only the death of tumor cells but also oxidative damage to normal cells, especially bone marrow hemopoietic cells, which leads to bone marrow suppression and (or) other side effects, weak efficacy of tumor treatment and even threatening patients’ life. How to enhance the killing effect of ROS on tumor cells while avoiding oxidative damage to the normal cells has become an urgent issue. This study is a review of the latest progress in the role of ROS-mediated programmed death in tumor treatment and prevention and treatment of oxidative damage in bone marrow induced by ROS.

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