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Rose, Christopher F.

doi:10.1023/a:1021945515514

Cited by 65 publications

(11 citation statements)

References 56 publications

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“…In brain tissue of mammals the high accumulation of glutamine as a result of the ammonia intoxication process, is suggested to induce oxidative stress [17], [74]. Elevation in glutamine level can cause astrocyte swelling, and/or activation of N -methyl-D-aspartate type glutamate (NMDA) receptors [75]–[78]. The over-activation of NMDA receptors incites excess production of ROS and reactive nitrogen species [79].…”

Section: Discussionmentioning

confidence: 99%

Anti-Oxidative Defences Are Modulated Differentially in Three Freshwater Teleosts in Response to Ammonia-Induced Oxidative Stress

et al. 2014

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Oxidative stress and the antioxidant response induced by high environmental ammonia (HEA) were investigated in the liver and gills of three freshwater teleosts differing in their sensitivities to ammonia. The highly ammonia-sensitive salmonid Oncorhynchus mykiss (rainbow trout), the less ammonia sensitive cyprinid Cyprinus carpio (common carp) and the highly ammonia-resistant cyprinid Carassius auratus (goldfish) were exposed to 1 mM ammonia (as NH4HCO3) for 0 h (control), 3 h, 12 h, 24 h, 48 h, 84 h and 180 h. Results show that HEA exposure increased ammonia accumulation significantly in the liver of all the three fish species from 24 h–48 h onwards which was associated with an increment in oxidative stress, evidenced by elevation of xanthine oxidase activity and levels of hydrogen peroxide (H2O2) and malondialdehyde (MDA). Unlike in trout, H2O2 and MDA accumulation in carp and goldfish liver was restored to control levels (84 h–180 h); which was accompanied by a concomitant increase in superoxide dismutase (SOD), catalase (CAT), ascorbate peroxidase activity and reduced ascorbate content. Many of these defence parameters remained unaffected in trout liver, while components of the glutathione redox cycle (reduced glutathione, glutathione peroxidase and glutathione reductase) enhanced to a greater extent. The present findings suggest that trout rely mainly on glutathione dependent defensive mechanism while carp utilize SOD, CAT and ascorbate as anti-oxidative sentinels. Hepatic cells of goldfish appear to utilize each of these protective systems, and showed more effective anti-oxidative compensatory responses towards HEA than carp, while trout were least effective. The present work also indicates that HEA exposure resulted in a relatively mild oxidative stress in the gills of all three species. This probably explains the almost complete lack of anti-oxidative responses in branchial tissue. This research suggests that oxidative stress, as well as the antioxidant potential clearly differ between salmonid and cyprinid species.

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Section: Discussionmentioning

confidence: 99%

Anti-Oxidative Defences Are Modulated Differentially in Three Freshwater Teleosts in Response to Ammonia-Induced Oxidative Stress

et al. 2014

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“…For this to occur in vivo, NH 4 ϩ /NH 3 fluctuations at the astrocyte membrane in the millimolar range would have to arise; however, precise temporal NH 4 ϩ /NH 3 transients in vivo data are not available. Ammonia fluctuations and subsequently cytosolic alkaline shifts are larger at the onset of ALF, suggesting that a deregulation of glutamate release by ammonia from astrocytes may be an early phenomenon and in addition one of the sources leading to this increased extracellular brain glutamate/glutamatergic dysfunction consistently found in different models of ALF (45).…”

Section: Ammonia-triggered Release Of Ca 2ϩ From Intracellular Er Stomentioning

confidence: 99%

Acute Insult of Ammonia Leads to Calcium-dependent Glutamate Release from Cultured Astrocytes, an Effect of pH

Rose

Kresse

Kettenmann

2005

Journal of Biological Chemistry

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104

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Hyperammonemia is a key factor in the pathogenesis of hepatic encephalopathy (HE) as well as other metabolic encephalopathies, such as those associated with inherited disorders of urea cycle enzymes and in Reye's syndrome. Acute HE results in increased brain ammonia (up to 5 mM), astrocytic swelling, and altered glutamatergic function. In the present study, using fluorescence imaging techniques, acute exposure (10 min) of ammonia (NH 4 ؉ /NH 3 ) to cultured astrocytes resulted in a concentration-dependent, transient increase in [Ca 2؉ ] i . This calcium transient was due to release from intracellular calcium stores, since the response was thapsigargin-sensitive and was still observed in calcium-free buffer. Using an enzyme-linked fluorescence assay, glutamate release was measured indirectly via the production of NADH (a naturally fluorescent product when excited with UV light). Hyperammonemia consequently leads to increased concentrations of ammonia, up to 5 mM, in the brain. This high level of brain ammonia is a key factor in the pathogenesis of central nervous system dysfunction in acute and chronic liver failure. The nature and severity of the central nervous system disorder mainly depend upon the degree and acuteness of the onset of hyperammonemia (1). Acute liver failure (ALF) 1 resulting from viral infections or toxic liver injury is a life-threatening condition where hepatic encephalopathy (HE) develops rapidly and mortality rates are high due to brain stem herniation caused by increased intracranial pressure, a fatal consequence of cytotoxic brain edema. Excess ammonia is toxic to the brain resulting in deleterious effects, by both direct and indirect mechanisms, on cerebral metabolism and neurotransmission.Over the past 10 years, there has been an increasing body of evidence demonstrating that ammonia toxicity is involved in alterations of glutamatergic synaptic regulation which is implicated in the pathophysiology of HE in ALF. Several reports have consistently described increased extracellular concentrations of brain glutamate in different models of experimental ALF (2-5); however, neither the cell type nor the underlying release mechanisms have been identified. One possible explanation for the increased extracellular glutamate may be ammonia's inhibitory effects on the glutamate transporter system in astrocytes. It has been shown that ammonia inhibits glutamate uptake into astrocytes in vitro (6) and decreases protein and gene expression of the glutamate transporter GLT-1 (EAAT-2) in the frontal cortex of rats with ALF (7). The role of ammonia in the glutamatergic dysfunction demonstrated in HE is supported with a positive correlation between extracellular brain concentrations of glutamate and arterial ammonia concentrations in ALF in rats (4). In addition, using mild hypothermia as a treatment in rats with ALF, extracellular brain glutamate concentrations were normalized concomitantly with a lowering of brain ammonia (8).Glutamate has been demonstrated to be an important signaling molecule for neuro...

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“…Because fishes have less advanced central nervous systems than higher vertebrates, this may explain why fishes are more tolerant of ammonia than mammals (Evans et al, 2005). Several theories (glutamatergic dysfunction, glutamine accumulation leading to astrocyte swelling, activation of N -methyl- d -aspartate-type (NMDA) glutamate receptors) have been proposed to address the mechanisms of acute ammonia toxicity in mammalian brains (Brusilow, 2002; Felipo and Butterworth, 2002; Rose, 2002), but they have yet to be confirmed in fish.…”

Section: Impediment Of Ammonia Excretion Ammonia-loading and Mechanmentioning

confidence: 99%

“…In mammals, high levels of brain ammonia (1–3 mmol l −1 ) lead to glutamatergic dysfunction (Felipo and Butterworth, 2002; Rose, 2002) which remains as the leading candidate in the pathogenesis of hepatic encephalopathy in acute liver failure. However, many tropical air-breathing fishes (see Ip et al, 2004b; Chew et al, 2006b for reviews) can tolerate high levels of environmental ammonia, and these environmental tolerance correlate well with their high tolerance of ammonia at the cellular and sub-cellular levels (Ip et al, 2005a).…”

Section: Passage Of Ammonia Across the Blood–brain Barrier And Into Bmentioning

confidence: 99%

Ammonia production, excretion, toxicity, and defense in fish: a review

2010

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Many fishes are ammonotelic but some species can detoxify ammonia to glutamine or urea. Certain fish species can accumulate high levels of ammonia in the brain or defense against ammonia toxicity by enhancing the effectiveness of ammonia excretion through active NH4+transport, manipulation of ambient pH, or reduction in ammonia permeability through the branchial and cutaneous epithelia. Recent reports on ammonia toxicity in mammalian brain reveal the importance of permeation of ammonia through the blood–brain barrier and passages of ammonia and water through transporters in the plasmalemma of brain cells. Additionally, brain ammonia toxicity could be related to the passage of glutamine through the mitochondrial membranes into the mitochondrial matrix. On the other hand, recent reports on ammonia excretion in fish confirm the involvement of Rhesus glycoproteins in the branchial and cutaneous epithelia. Therefore, this review focuses on both the earlier literature and the up-to-date information on the problems and mechanisms concerning the permeation of ammonia, as NH3, NH4+ or proton-neutral nitrogenous compounds, across mitochondrial membranes, the blood–brain barrier, the plasmalemma of neurons, and the branchial and cutaneous epithelia of fish. It also addresses how certain fishes with high ammonia tolerance defend against ammonia toxicity through the regulation of the permeation of ammonia and related nitrogenous compounds through various types of membranes. It is hoped that this review would revive the interests in investigations on the passage of ammonia through the mitochondrial membranes and the blood–brain barrier of ammonotelic fishes and fishes with high brain ammonia tolerance, respectively.

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Cited by 65 publications

References 56 publications

Anti-Oxidative Defences Are Modulated Differentially in Three Freshwater Teleosts in Response to Ammonia-Induced Oxidative Stress

Anti-Oxidative Defences Are Modulated Differentially in Three Freshwater Teleosts in Response to Ammonia-Induced Oxidative Stress

Acute Insult of Ammonia Leads to Calcium-dependent Glutamate Release from Cultured Astrocytes, an Effect of pH

Ammonia production, excretion, toxicity, and defense in fish: a review

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