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      Ammonia Production, Excretion, Toxicity, and Defense in Fish: A Review

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          Abstract

          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 NH+4 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 NH 3, NH+4 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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          Most cited references160

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          The multifunctional fish gill: dominant site of gas exchange, osmoregulation, acid-base regulation, and excretion of nitrogenous waste.

          The fish gill is a multipurpose organ that, in addition to providing for aquatic gas exchange, plays dominant roles in osmotic and ionic regulation, acid-base regulation, and excretion of nitrogenous wastes. Thus, despite the fact that all fish groups have functional kidneys, the gill epithelium is the site of many processes that are mediated by renal epithelia in terrestrial vertebrates. Indeed, many of the pathways that mediate these processes in mammalian renal epithelial are expressed in the gill, and many of the extrinsic and intrinsic modulators of these processes are also found in fish endocrine tissues and the gill itself. The basic patterns of gill physiology were outlined over a half century ago, but modern immunological and molecular techniques are bringing new insights into this complicated system. Nevertheless, substantial questions about the evolution of these mechanisms and control remain.
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            Glutamine: a Trojan horse in ammonia neurotoxicity.

            Mechanisms involved in hepatic encephalopathy still remain to be defined. Nonetheless, it is well recognized that ammonia is a major factor in its pathogenesis, and that the astrocyte represents a major target of its CNS toxicity. In vivo and in vitro studies have shown that ammonia evokes oxidative/nitrosative stress, mitochondrial abnormalities (the mitochondrial permeability transition, MPT) and astrocyte swelling, a major component of the brain edema associated with fulminant hepatic failure. How ammonia brings about these changes in astrocytes is not well understood. It has long been accepted that the conversion of glutamate to glutamine, catalyzed by glutamine synthetase, a cytoplasmic enzyme largely localized to astrocytes in brain, represented the principal means of cerebral ammonia detoxification. Yet, the "benign" aspect of glutamine synthesis has been questioned. This article highlights evidence that, at elevated levels, glutamine is indeed a noxious agent. We also propose a mechanism by which glutamine executes its toxic effects in astrocytes, the "Trojan horse" hypothesis. Much of the newly synthesized glutamine is subsequently metabolized in mitochondria by phosphate-activated glutaminase, yielding glutamate and ammonia. In this manner, glutamine (the Trojan horse) is transported in excess from the cytoplasm to mitochondria serving as a carrier of ammonia. We propose that it is the glutamine-derived ammonia within mitochondria that interferes with mitochondrial function giving rise to excessive production of free radicals and induction of the MPT, two phenomena known to bring about astrocyte dysfunction, including cell swelling. Future therapeutic approaches might include controlling excessive transport of newly synthesized glutamine to mitochondria and its subsequent hydrolysis.
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              Aquaporins with selectivity for unconventional permeants.

              B Wu, E Beitz (2007)
              The aquaporin protein family generally seems to be designed for the selective passage of water or glycerol. Charged molecules, metal ions and even protons are strictly excluded. Recently, particular aquaporin isoforms were reported to conduct unconventional permeants, i.e., the unpolar gases carbon dioxide and nitric oxide, the polar gas ammonia, the oxidative oxygen species hydrogen peroxide, and the metalloids antimonite, arsenite and silicic acid. Here, we summarize the available data on permeability properties and physiological settings of these aquaporins and we analyze which structural features might be connected to permeability for non-water, non-glycerol solutes.
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                Author and article information

                Journal
                Front Physiol
                Front. Physiology
                Frontiers in Physiology
                Frontiers Research Foundation
                1664-042X
                08 August 2010
                04 October 2010
                2010
                : 1
                : 134
                Affiliations
                [1] 1simpleDepartment of Biological Sciences, National University of Singapore Singapore, Republic of Singapore
                [2] 2simpleNatural Sciences and Science Education, National Institute of Education, Nanyang Technological University Singapore, Republic of Singapore
                Author notes

                Edited by: Shigehisa Hirose, Tokyo Institute of Technology, Japan

                Reviewed by: Jim Ballantyne, University of Guelph, Canada; Jonathan M. Wilson, CIMAR, Portugal

                *Correspondence:Yuen K. Ip, Department of Biological Sciences, National University of Singapore, Kent Ridge, Singapore 117543, Republic of Singapore. e-mail: dbsipyk@ 123456nus.edu.sg

                This article was submitted to Frontiers in Aquatic Physiology, a specialty of Frontiers in Physiology

                Article
                10.3389/fphys.2010.00134
                3059970
                21423375
                da7ccc79-06be-4bdb-a143-056da2826dab
                Copyright © 2010 Ip and Chew.

                This is an open-access article subject to an exclusive license agreement between the authors and the Frontiers Research Foundation, which permits unrestricted use, distribution, and reproduction in any medium, provided the original authors and source are credited.

                History
                : 19 June 2010
                : 06 September 2010
                Page count
                Figures: 5, Tables: 0, Equations: 0, References: 194, Pages: 20, Words: 21231
                Categories
                Physiology
                Review Article

                Anatomy & Physiology
                ammonia transporter,fish,ammonia,ammonia excretion,ammonia toxicity,nitrogen metabolism

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