Production of reactive oxygen species after reperfusion in vitro and in vivo: protective effect of nitric oxide

Mason, R B; Pluta, Ryszard; Walbridge, Stuart; Wink, David A.; Oldfield, Edward H.; Boock, Robert J.

doi:10.3171/jns.2000.93.1.0099

Cited by 82 publications

(44 citation statements)

References 55 publications

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“…3). This finding may not be entirely unexpected as the improvement of endothelial dysfunction due to the scavenging of endogenous O 2 Ϫ has been suggested to be linked with enhanced NO bioavailability (18,35). In other words, the vasodilator effect of scavenging O 2 Ϫ is primarily due to the action of NO in the vasculature.…”

Section: Discussionmentioning

confidence: 61%

“…Previous studies also provided evidence that NO reacts with oxygen free radicals and thus antagonizes the prooxidant properties of heme proteins in the biological tissues (8). An NO donor has also been shown to provide a cytoprotective effect in the ischemic tissue by reacting with excess oxygen free radicals in ischemia-reperfusion injuries (18). Thus it is conceivable that the interaction between NO and O 2 Ϫ has a role in maintaining a desired state of balance between oxidative and antioxidative processes in the kidney, any imbalance of which would lead to derangements in renal function.…”

Section: Perspectivesmentioning

confidence: 97%

“…1 and 2) indicates that the basal tissue concentration of O 2 Ϫ may be kept to a minimal level in the intact condition due to efficient antioxidant effect of endogenous NO (3,8,18), and thus there would be no O 2 Ϫ -scavenging effects of tempol. In other studies in rats (27,28), it was also demonstrated that tempol administration had no significant effect on systemic blood pressure in Wistar-Kyoto rats but caused hypotension in spontaneously hypertensive rats.…”

Section: Discussionmentioning

confidence: 99%

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Inhibition of nitric oxide synthase enhances superoxide activity in canine kidney

Majid

Nishiyama

Jackson

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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. In one group of dogs (n ϭ 10), tempol infusion alone for 30 min before NLA infusion did not cause any significant changes in renal blood flow (RBF; 5.2 Ϯ 0.4 to 5.0 Ϯ 0.4 ml ⅐ min Ϫ1 ⅐ g Ϫ1 ), glomerular filtration rate (GFR; 0.79 Ϯ 0.04 to 0.77 Ϯ 0.04 ml ⅐ min Ϫ1 ⅐ g Ϫ1 ), urine flow (V; 13.6 Ϯ 2.1 to 13.9 Ϯ 2.5 l ⅐ minInterestingly, when tempol was infused in another group of dogs (n ϭ 12) pretreated with NLA, it caused increases in V (4.4 Ϯ 0.4 to 9.7 Ϯ 1.4 l⅐min Ϫ1 ⅐g Ϫ1) and in UNaV (0.7 Ϯ 0.1 to 1.3 Ϯ 0.2 mol⅐min Ϫ1 ⅐g Ϫ1 ) without affecting RBF or GFR. Although NO inhibition caused usual qualitative responses in both groups of dogs, the antidiuretic (47 Ϯ 5 vs. 26 Ϯ 4%) and antinatriuretic (67 Ϯ 4 vs. 45 Ϯ 11%) responses to NLA were seen much less in dogs pretreated with tempol. NLA infusion alone increased urinary excretion of 8-isoprostane (13.9 Ϯ 2.7 to 22.8 Ϯ 3.6 pg ⅐ min Ϫ1 ⅐ g Ϫ1

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Section: Discussionmentioning

confidence: 61%

Section: Perspectivesmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Inhibition of nitric oxide synthase enhances superoxide activity in canine kidney

Majid

Nishiyama

Jackson

et al. 2004

American Journal of Physiology-Regulatory, Integrative and Comp

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“…During ischemic stroke with reduced perfusion, hypoglycemia and hypoxia result in energy depletion (62), ion imbalance, and release of cellular mediators (38,53) that may lead to cell injury or death (38). Recent attention has been given to investigating cellular mechanisms affected by ischemia (1,44). Whereas hypoxia-aglycemia has been shown to induce increased BMEC permeability via calcium-dependent pathways (1), the effects on TJ complexes are not well defined.…”

mentioning

confidence: 99%

Cerebral microvascular changes in permeability and tight junctions induced by hypoxia-reoxygenation

Mark

Davis

2002

American Journal of Physiology-Heart and Circulatory Physiology

339

272

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Mark, Karen S., and Thomas P. Davis. Cerebral microvascular changes in permeability and tight junctions induced by hypoxia-reoxygenation. Am J Physiol Heart Circ Physiol 282: H1485-H1494, 2002; 10.1152/ajpheart.00645.2001.-Cerebral microvessel endothelial cells that form the bloodbrain barrier (BBB) have tight junctions (TJ) that are critical for maintaining brain homeostasis and low permeability. Both integral (claudin-1 and occludin) and membrane-associated zonula occluden-1 and -2 (ZO-1 and ZO-2) proteins combine to form these TJ complexes that are anchored to the cytoskeletal architecture (actin). Disruptions of the BBB have been attributed to hypoxic conditions that occur with ischemic stroke, pathologies of decreased perfusion, and high-altitude exposure. The effects of hypoxia and posthypoxic reoxygenation in cerebral microvasculature and corresponding cellular mechanisms involved in disrupting the BBB remain unclear. This study examined hypoxia and posthypoxic reoxygenation effects on paracellular permeability and changes in actin and TJ proteins using primary bovine brain microvessel endothelial cells (BBMEC). Hypoxia induced a 2.6-fold increase in [ 14 C]sucrose, a marker of paracellular permeability. This effect was significantly reduced (ϳ58%) with posthypoxic reoxygenation. After hypoxia and posthypoxic reoxygenation, actin expression was increased (1.4-and 2.3-fold, respectively). Whereas little change was observed in TJ protein expression immediately after hypoxia, a twofold increase in expression was seen with posthypoxic reoxygenation. Furthermore, immunofluorescence studies showed alterations in occludin, ZO-1, and ZO-2 protein localization during hypoxia and posthypoxic reoxygenation that correlate with the observed changes in BBMEC permeability. The results of this study show hypoxia-induced changes in paracellular permeability may be due to perturbation of TJ complexes and that posthypoxic reoxygenation reverses these effects. endothelial cells; cytoarchitecture; blood-brain barrier; immunofluorescence WHEREAS RESEARCH INVOLVING hypoxic stress has traditionally focused on identifying and treating risk factors associated with ischemic stroke (17,18,43), hypoxia as a result of high-altitude exposure has also been associated with impairment in neurological function (26,37). Early intervention after ischemic stroke has been shown to reduce tissue damage associated with increased cerebrovascular permeability (7, 39). Recently, research has expanded into examining cellular effects of cerebral ischemia-reperfusion. Ischemic stroke is a reduction or cessation of blood flow to the brain, which deprives the cerebral tissue of important nutrients and oxygen as well as removal of metabolic waste products. Whereas this decrease in oxygen supply to the brain (i.e., hypoxia) has been shown to increase cerebrovascular permeability (1,19), there are also reports (42, 66) of increased permeability in peripheral and cerebral endothelial cells during posthypoxic reperfusion (i.e., reoxygenation). Little is know...

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“…NO performs many important functions in the brain including working as a neurotransmitter, scavenging of reactive oxygen species, regulating cerebral blood flow and inflammations (15). NO could release cytotoxic factors like macrophage and active microglia.…”

Section: Introductionmentioning

confidence: 99%

The effects of electromagnetic fields to whole protein, myelin basic protein, neuron specific enolase profiles and nitric oxide levels in rat brains

NİSBET¹

2012

Ankara Üniversitesi Veteriner Fakültesi Dergisi

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Summary:The aim of the study was to investigate the effects of electromagnetic fields (EMF) to whole protein, neuron specific enolase (NSE), myelin basic protein (MBP) profiles and nitric oxide levels in rat brains. In addition, serum NSE was also determined. For this aim, 33 rats with 2-days-old age were divided into three groups. The rats in control group were kept in the normal conditions with no exposure of EMF. Group 2 and 3 were exposed to 900 and 1800MHz EMF respectively for 2 h/day for 90 days at the same time and everyday in the piecage restrainer. At the end of the exposure period, the brains of rats were excluded and splitted up to two parts (right and left), horizontally. The brain parts of same groups were mixed, homogenized and sonicated. The protein concentrations were equalized to 40 mg/ml with spectrophotometer. The protein profiles were determined for sizes and densities of bands with SDS-PAGE. NSE and MBP profiles were detected with western blot technique. Nitric oxide levels were determined by using ELISA test kit. The sizes of protein bands were detected as being same but the densities were found as variable into the groups for all parameters. The protein band, MBP and NSE densities of brains of rats were defined as increased in group 2, but decreased in group 3 when compared with control group. Also, there was no difference seen in right and left parts of brains in all groups. NSE in serum was determined to be higher in group 3 than the group 2 and control. Nitric oxide levels in the right and left brain parts were 224.09±20.32 µM/mL and 207.43±24.19 µM/mL in control group, 253.8±33.58 µM/mL and 336.9±24.47 µM/mL in group 2, 237.87±36.30 µM/mL and 281.53±36.75 µM/mL in group 3, respectively. The difference of nitric oxide levels among the groups was found as not significant (P>0.05). The results of this study may lighten the future and advance studies about the risks of the cellular and digital communication handsets against brain used by the general public.

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Production of reactive oxygen species after reperfusion in vitro and in vivo: protective effect of nitric oxide

Cited by 82 publications

References 55 publications

Inhibition of nitric oxide synthase enhances superoxide activity in canine kidney

Inhibition of nitric oxide synthase enhances superoxide activity in canine kidney

Cerebral microvascular changes in permeability and tight junctions induced by hypoxia-reoxygenation

The effects of electromagnetic fields to whole protein, myelin basic protein, neuron specific enolase profiles and nitric oxide levels in rat brains

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