Interactions between Nitric Oxide and Arachidonic Acid in Lung Epithelial Cells: Possible Roles for Peroxynitrite and Superoxide

Offer, Sarit; Eliraz, A; Fink, Gershon; Stark, Aliza H.; Madar, Zecharia

doi:10.1159/000082375

Cited by 6 publications

(3 citation statements)

References 67 publications

(56 reference statements)

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“…This results in mitochondrial dysfunction, energy failure, and in activation of cytosolic enzymes that generate oxygen and nitrogen radicals, e.g., nitric oxide synthases (Figure 5C) (Karl et al, 2011). Free radicals stimulate the production of inflammatory lipids including arachidonic acid and prostaglandins (Figure 5C) (Landino et al, 1996; Offer et al, 2005). These lipids inhibit the sodium-potassium-ATPase which results in intracellular sodium overload, water influx, and cellular swelling (Figure 5C) (Lees, 1991; Staub et al, 1994).…”

Section: Glutamate Uptake and Metabolismmentioning

confidence: 99%

GABA and Glutamate Uptake and Metabolism in Retinal Glial (Müller) Cells

Bringmann¹,

Grosche²,

Pannicke³

et al. 2013

Front. Endocrinol.

137

123

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Müller cells, the principal glial cells of the retina, support the synaptic activity by the uptake and metabolization of extracellular neurotransmitters. Müller cells express uptake and exchange systems for various neurotransmitters including glutamate and γ-aminobutyric acid (GABA). Müller cells remove the bulk of extracellular glutamate in the inner retina and contribute to the glutamate clearance around photoreceptor terminals. By the uptake of glutamate, Müller cells are involved in the shaping and termination of the synaptic activity, particularly in the inner retina. Reactive Müller cells are neuroprotective, e.g., by the clearance of excess extracellular glutamate, but may also contribute to neuronal degeneration by a malfunctioning or even reversal of glial glutamate transporters, or by a downregulation of the key enzyme, glutamine synthetase. This review summarizes the present knowledge about the role of Müller cells in the clearance and metabolization of extracellular glutamate and GABA. Some major pathways of GABA and glutamate metabolism in Müller cells are described; these pathways are involved in the glutamate-glutamine cycle of the retina, in the defense against oxidative stress via the production of glutathione, and in the production of substrates for the neuronal energy metabolism.

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Section: Glutamate Uptake and Metabolismmentioning

confidence: 99%

GABA and Glutamate Uptake and Metabolism in Retinal Glial (Müller) Cells

Bringmann¹,

Grosche²,

Pannicke³

et al. 2013

Front. Endocrinol.

137

123

View full text Add to dashboard Cite

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“…The precise mechanisms of how oxidative-nitrosative stress and inflammatory lipids lead to cellular swelling remain to be determined in future experiments. The presence of cross talks between nitric oxide synthase, phospholipase A 2 , and cyclooxygenase, with intermediary roles for peroxynitrite and superoxide, was shown in various cell systems including retinal glial cells (Du et al, 2004;Offer et al, 2005).…”

Section: Discussionmentioning

confidence: 99%

Synergistic action of hypoosmolarity and glutamine in inducing acute swelling of retinal glial (Müller) cells

Karl

Wurm

Pannicke

et al. 2010

Glia

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High blood ammonia, elevated glutamine, and hyponatremia are pathogenic factors contributing to astrocytic swelling and brain edema in liver failure. We investigated the effects of hypoosmolarity, ammonia, and glutamine on the induction of glial cell swelling in freshly isolated slices of the rat retina. Glutamine, but not ammonia or hypoosmolarity per se, evoked a rapid (within one minute) swelling of retinal glial (Müller) cell bodies under hypoosmotic conditions. Under isoosmotic conditions, glutamine evoked a delayed swelling after 10 min of exposure. The effect of glutamine was concentration-dependent, with half-maximal and maximal effects at ∼ 0.1 and 0.5 mM. Glutamine in hypoosmotic solution induced a dissipation of the mitochondrial membrane potential. The effects on the mitochondrial membrane potential and the glial soma size were reduced by (i) agents which inhibit the transfer of glutamine into mitochondria and its hydrolysis there, (ii) inhibition of the mitochondrial permeability transition, (iii) inhibitors of oxidative-nitrosative stress, and (iv) inhibitors of phospholipase A(2) and cyclooxygenase. Glutamine-induced glial swelling was also prevented by ATP and adenosine, acting at adenosine A(1) receptors. The data suggest that hypoosmolarity accelerates the swelling-inducing effect of glutamine on retinal glial cells, and that swelling induction by glutamine is mediated by inducing oxidative-nitrosative stress, inflammatory lipid mediators, and mitochondrial dysfunction.

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“…27,28) Neuroprotective effect of trolox is further supported by its protective effect in amyloid b-mediated neurotoxicity, 29) and interleukin (IL-1b) induced neurodegeneration. 30) In addition to protective effects in neurotoxicity models, trolox counteracted the toxic effects of S-morpholinosydnonimine (SIN-1), a peroxynitrite donor in lung epithelial cells, 31) and in arrhythmias in isolated heart preparations. 32) Consistent with the earlier reports, we have also observed significant increase in the level of MDA in ischemic animals indicating oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of Trolox in Global Cerebral Ischemia in Gerbils

Gupta

Sharma

2006

Biological & Pharmaceutical Bulletin

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Stroke is the third leading cause of death and a major cause of long-term disability in industrialized countries. Dramatic reduction of oxygen in stroke may lead to ischemia of the whole brain (global ischemia) or of defined cerebral territories (focal ischemia) depending on the cerebral artery occluded.1) Global cerebral ischemia is commonly an outcome of a range of clinical conditions, which comprises cardiac arrest, closed head injury, coronary artery bypass surgery etc. The most affected brain area as a consequence of global ischemia is CA1 neurons of the hippocampus. Neuronal death in global ischemia precedes 1-3 d after insult, a process referred as delayed neuronal death. 2-4)The pathophysiological mechanisms leading to neuronal injury in ischemic stroke are complex and multifactorial. Ischemia induced brain damages are accompanied by biochemical alterations and neurological sequelae.1) There are substantial experimental evidences that reactive oxygen species (ROS) are produced in the brain during ischemia and reperfusion injury.5) ROS such as superoxide radical, hydroxyl radical and hydrogen peroxide contributes to ischemic brain damage.5) Superoxide can react with nitric oxide to form peroxynitrite, a potent oxidant. It has been proposed that many of the toxic effects of nitric oxide are due to the generation of peroxynitrite. Peroxynitrite can directly react with target biomolecules like DNA, protein, via one or two electron oxidations. 5-7)Antioxidants such as (Ϫ)-epigallocatechin gallate, melatonin, curcumin, FeTMPyP and FeTPPS have been demonstrated to ameliorate neuronal damage in cerebral ischemic reperfusion injury. 3,[8][9][10][11] Antioxidant activity of trolox (6-hydroxy-2,5,7,8-tetramethyl chroman-2-carboxylic acid) a cellpermeable, water-soluble derivative of vitamin E has been established in vitro and in vivo conditions. 12-15) However its neuroprotective effects have not been investigated in global cerebral ischemia. Therefore, in the present study, the neuroprotective potential of trolox was investigated in bilateral carotid artery occlusion induced global cerebral ischemia in Mongolian gerbils. MATERIALS AND METHODS AnimalsAdult male Mongolian gerbils (Meriones unguiculatus) weighing 60-80 g were obtained from Central Animal Facility (CAF), NIPER for this study. They were provided with standard diet and water ad libitum and were maintained at 22Ϯ2°C and a 12 : 12 h light : dark cycle. All the procedures used in this study were approved by Institutional Animal Ethics Committee (IAEC), NIPER.Materials Trolox was purchased from Calbiochem Inc., U.S.A. Cresyl violet and malondialdehyde were purchased from Sigma Chemical Company, U.S.A. Rest of the chemicals were of analytical grade and were purchased from commercial suppliers.Treatment Schedule Gerbils were divided into sham, vehicle-treated ischemic and trolox-treated (3, 10, 30 mg/kg i.p.) ischemic groups. Phosphate buffer saline (pH 7.4) was used as a vehicle for trolox. Trolox was administered 30 min before occlusion.Induction of Transie...

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Interactions between Nitric Oxide and Arachidonic Acid in Lung Epithelial Cells: Possible Roles for Peroxynitrite and Superoxide

Cited by 6 publications

References 67 publications

GABA and Glutamate Uptake and Metabolism in Retinal Glial (Müller) Cells

GABA and Glutamate Uptake and Metabolism in Retinal Glial (Müller) Cells

Synergistic action of hypoosmolarity and glutamine in inducing acute swelling of retinal glial (Müller) cells

Neuroprotective Effects of Trolox in Global Cerebral Ischemia in Gerbils

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