Effects of superoxide radicals on transport (Na+K) adenosine triphosphatase and protection by superoxide dismutase

Hexum, Terry D.; Fried, Rainer

doi:10.1007/bf00963833

Cited by 69 publications

(23 citation statements)

References 20 publications

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“…Watson and Ginsberg, 1989) and for the long-term changes in Na,K-ATPase kinetic properties seen in the reperfusion (Stojanovic et al, 1988). Both free radicals and arachidonic acid have been shown to cause a protracted inhibition of the Na,K-ATPase in tissues and cells (Hexum and Fried, 1979;Stahl, 1986;Stanimirovic et al, 1995b) and reduction of glutamate uptake into the astrocytes (Barbour et al, 1989;Voltera et al, 1994) independent of their effects on Na,KATPase. The present study demonstrates that the predominant functional effect of sublethal ischemia-like insults in neonatal rat astrocyte cultures is the simultaneous stimulation of both the glutamate uptake and sodium pump activity.…”

Section: Discussionmentioning

confidence: 96%

Stimulation of glutamate uptake and Na, K-ATPase activity in rat astrocytes exposed to ischemia-like insults

Stanimirovic

Ball

Durkin

1997

Glia

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Section: Discussionmentioning

confidence: 96%

Stimulation of glutamate uptake and Na, K-ATPase activity in rat astrocytes exposed to ischemia-like insults

Stanimirovic

Ball

Durkin

1997

Glia

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“…Peroxy radicals abstract hydrogen from adjacent fatty acid chains, thereby propagating the lipid peroxidation process. Free radicals also attack the Na + , K + -ATPase [19], which already malfunctioned due to decreased ATP levels under anoxia, leading to ionic imbalance. Thus, the disappearance of the ERG immediately after retinal ischemia is thought to be partly due to oxygen free radicals.…”

Section: Discussionmentioning

confidence: 99%

Involvement of Oxygen Free Radicals in Experimental Retinal Ischemia and the Selective Vulnerability of Retinal Damage

Kuriyama

Waki

Nakagawa³

et al. 2001

Ophthalmic Res

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Protective effects of CV-3611, a free radical scavenger, on retinal ischemic injury in the rat and on glutamate-induced cytotoxicity in a cell line were evaluated. Transient retinal ischemia was induced by raising intraocular pressure of rats to 110 mm Hg for 45 min, and the electroretinogram (ERG) was measured to evaluate retinal function. No ERG could be recorded immediately after reperfusion, and thereafter the ERG gradually recovered. Recovery of the a-wave latency and the amplitudes of the a and b waves in the CV-3611-treated (10 mg/kg, p.o.) group were significantly better than those in the control group up to 24 h after reperfusion. In both the control and CV-3611 group, the b wave showed better recovery than the a wave up to 6 h after reperfusion, while the relationship was reversed after 24-hour reperfusion. Glutamate (10 mM)-induced cytotoxicity in the N18-RE-105 cell, a neural retina-neuroblastoma hybridoma, was quantified by measuring lactate dehydrogenase. Three and 10 µM of CV-3611 significantly attenuated the glutamate-induced cytotoxicity in N18-RE-105 cells. Thus, the radical scavenger (CV-3611) promoted the recovery of retinal function after ischemia-reperfusion injury and ameliorated glutamate-induced cytotoxicity. These results suggest that oxygen free radicals play an important role in the early phase of retinal ischemic injury. Moreover, differential recovery processes of the a and b waves after ischemia suggest that the selective vulnerability of the retina to ischemia could change functionally during the period of reperfusion.

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“…This may reflect the normalization (reduction) of free radical generation, and maximal tissue recovery. Also, it is known that oxyradicals decrease (Na++K+)-ATPase activity (Sun, 1972;Hexum and Fried, 1979;Kovachich and Mishra, 1981). However, at 7 d in the primary ischemic area, (Na + +K+)-ATPase losses do not recover, indicative of irreversible membrane damage (Mahadik et al, 1992) and cell death (Siesjo, 1981).…”

Section: Antioxidant Enzymes In Ischemic Injurymentioning

confidence: 99%

Temporal changes in superoxide dismutase, glutathione peroxidase, and catalase levels in primary and peri-ischemic tissue

Mahadik

Makar

Murthy

et al. 1993

Molecular and Chemical Neuropathology

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Time-dependent changes in levels of the antioxidant enzymes, superoxide dismutase (SOD), glutathione peroxidase (GSHPOD), and catalase (CAT) after cortical focal ischemia in rat indicate that: (1) primary and peri-ischemic tissues differ in both rate and the magnitude of oxyradical-induced ischemic injury, and (2) ischemic tissue remains vulnerable to oxyradical damage as long as 72 h after ischemia since the antioxidant enzyme levels remain at or below basal levels. After 72 h, the increased levels of these enzymes are sufficient to protect tissue against oxyradical damage. GM1 ganglioside (10 mg/kg, im) further increased the already elevated levels of the enzymes after ischemia, thereby indicating the GM1 treatment increases the capacity of ischemic tissue to protect against oxyradical injury.

show abstract

Effects of superoxide radicals on transport (Na+K) adenosine triphosphatase and protection by superoxide dismutase

Cited by 69 publications

References 20 publications

Stimulation of glutamate uptake and Na, K-ATPase activity in rat astrocytes exposed to ischemia-like insults

Stimulation of glutamate uptake and Na, K-ATPase activity in rat astrocytes exposed to ischemia-like insults

Involvement of Oxygen Free Radicals in Experimental Retinal Ischemia and the Selective Vulnerability of Retinal Damage

Temporal changes in superoxide dismutase, glutathione peroxidase, and catalase levels in primary and peri-ischemic tissue

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