C B Lim

Bio: C B Lim is an academic researcher from National University of Singapore. The author has contributed to research in topics: Urea & Excretion. The author has an hindex of 2, co-authored 2 publications receiving 201 citations.

The marble goby oxyeleotris marmoratus activates hepatic glutamine synthetase and detoxifies ammonia to glutamine during air exposure

Abstract: Ammonia levels in various tissues of the marble goby Oxyeleotris marmoratus remained constant throughout a 72 h period of air exposure. The rate of ammonia excretion in these experimental fish decreased to approximately one-fifth of that of the submerged control. Ammonia was not converted to urea during air exposure because there were no significant increases in urea content in the tissues. Also, urea excretion rate was lowered to one-fiftieth that of the submerged fish. After 24 h of air exposure, there was a significant increase in muscle glutamine content, which peaked at 48 h. The increase in glutamine content could account for the decreases in the amounts of ammonia and urea excretion during air exposure. The specific activities of hepatic glutamate dehydrogenase (amination) and glutamine synthetase in these experimental fish increased threefold and thirtyfold, respectively, in comparison with the submerged controls. Thus, O. marmoratus appears to be the first known teleost that responds to air exposure by activating hepatic glutamine synthetase to detoxify internally produced ammonia.

Reduction in the rates of protein and amino acid catabolism to slow down the accumulation of endogenous ammonia: a strategy potentially adopted by mudskippers (Periophthalmodon schlosseri snd Boleophthalmus boddaerti) during aerial exposure in constant darkness

Abstract: This study was designed to elucidate the strategies adopted by mudskippers to handle endogenous ammonia during aerial exposure in constant darkness. Under these conditions, specimens exhibited minimal locomotory activity, and the ammonia and urea excretion rates in both Periophthalmodon schlosseri and Boleophthalmus boddaerti decreased significantly. As a consequence, ammonia accumulation occurred in the tissues of both species of mudskipper. A significant increase in urea levels was found in the liver of P. schlosseri after 24h of aerial exposure, but no similar increase was seen in the tissues of B. boddaerti. It is unlikely that these two species of mudskipper detoxified ammonia to urea during aerial exposure since B. boddaerti does not possess a complete ornithine-urea cycle (OUC) and, although all the OUC enzymes were present in P. schlosseri, the activity of carbamoyl phosphate synthetase present in the liver mitochondria was too low to render the OUC functional for ammonia detoxification. Peritoneal injection of 15NH4Cl into P. schlosseri showed that this mudskipper was capable of incorporating some of the labelled ammonia into urea in its liver. However, aerial exposure did not affect this capability and did not induce detoxification of the accumulated ammonia to urea. Mudskippers exposed to terrestrial conditions and constant darkness did, however, show significant decreases in the total free amino acid content in the liver and blood, in the case of P. schlosseri and in the muscle of B. boddaerti. No changes in the alanine or glutamine content of the muscle were found in either species. Analyses of the balance between the reduction in nitrogenous excretion and the increase in nitrogenous accumulation further revealed that these two species of mudskipper were capable of reducing their protein and amino acid catabolic rates. Such adaptations constitute the most efficient way to avoid the build-up of internal ammonia, and would render unnecessary the detoxification of ammonia through energetically expensive pathways. This finding may be the first report of a teleost fish showing a reduction in proteolysis and amino acid catabolism in response to aerial exposure.

Ammonia toxicity, tolerance, and excretion

Abstract: Ammonia is an unusual toxicant in that it is produced by, as well as being poisonous to, animals. In aqueous solution ammonia has two species, NH3 and NH4+, total ammonia is the sum of [NH3] + [NH4+] and the pK of this ammonia/ammonium ion reaction is around 9.5. The NH3/NH4+ equilibrium both internally in animals and in ambient water depends on temperature, pressure, ionic strength, and pH; pH is most often of greatest significance to animals. Elevated ammonia levels in the environment are toxic. Temperature has only minor effects on ammonia toxicity expressed as total ammonia in water, and ionic strength of the water can influence ammonia toxicity, but pH has a very marked effect on toxicity. Acid waters ameliorate, whereas alkaline waters exacerbate ammonia toxicity. The threshold concentration of total ammonia ([NH3] + [NH4+]) resulting in unacceptable biological effects in freshwater, promulgated by the EPA (1998), is 3.48 mg N/liter at pH 6.5 and 0.25 mg N/liter at pH 9.0. There is only a relatively small saltwater data set, and a paucity of data on ammonia toxicity in marine environments, particularly chronic toxicity. The national criteria promulgated in the EPA (1989) saltwater document is a criterion continuous concentration (chronic value) of 0.99 mg N/liter total ammonia and a criterion maximum concentration (half the mean acute value) of 6.58 mg N/liter total ammonia, somewhat less than the equivalent freshwater pH 8.0 values of 1.27 and 8.4 mg N/liter total ammonia, respectively. This is consistent with marine species being somewhat more sensitive to ammonia than freshwater species. Toxicity studies are usually carried out on unfed, resting fish in order to facilitate comparison of results. Based on recent studies, however, environmental stresses, including swimming, can have dramatic effects on ammonia toxicity. It is also clear that feeding results in elevated postprandial body ammonia levels. Thus, feeding will probably also exacerbate ammonia toxicity. Fish may be more susceptible to elevated ammonia levels during and following feeding or when swimming. Thus, present ammonia criteria may fail to protect migrating fish and may be inappropriate for fish fed on a regular basis. Most teleost fish are ammonotelic, producing and excreting ammonia by diffusion of NH3 across the gills. They are very susceptible to elevated tissue ammonia levels under adverse conditions. Some fish avoid ammonia toxicity by utilizing several physiologic mechanisms. Suppression of proteolysis and/or amino acid catabolism may be a general mechanism adopted by some fishes during aerial exposure or ammonia loading. Others, like the mudskipper, can undergo partial amino acid catabolism and use amino acids as an energy source, leading to the accumulation of alanine, while active on land. Some fish convert excess ammonia to less toxic compounds including glutamine and other amino acids for storage. A few species have active ornithine—urea cycles and convert ammonia to urea for both storage and excretion. Under conditions of elevated ambient ammonia, the mudskipper P. schlosseri can continue to excrete ammonia by active transport of ammonium ions. There are indications that some fish may be able to manipulate the pH of the body surface to facilitate NH3 volatilization during aerial exposure, or that of the external medium to lower the toxicity of ammonia during ammonia loading. Future investigation of these aspects of “environmental ammonia detoxification” may produce new information on how fish avoid ammonia intoxication.

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

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 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.

Ammonia in estuaries and effects on fish

Abstract: This review aims to explore the biological responses of fish in estuaries to increased levels of environmental ammonia. Results from laboratory and field studies on responses of fish to varying salinity and their responses increased ammonia will he evaluated, although studies which examine responses to ammonia, in relation to varying salinity, pH and temperature together are rare. In a survey of British estuaries the continuous measurement of total ammonia showed values that ranged from background levels increasing up to c. 10 mg N l -1 although higher values have been noted sporadically. In outer estuaries pH values tended to stabilize towards sea water values (e.g. c. pH 8). Upper reaches of estuaries are influenced by the quality of their fresh waters sources which can show a wide range of pH and water quality values depending on geological, climatic and pollution conditions. In general the ammonia toxicity (96 h LC 50 ) to marine species (e.g. 0.09-3.35 mg l -1 NH 3 ) appears to be roughly similar to freshwater species (e.g. 0.068-2.0 mg l -1 NN 3 ). Ammonia toxicity is related to differences between species and pH rather than to the comparatively minor influences of salinity and temperature. In the marine environment the toxicity of ionized ammonia (NH 4 + ) should be considered. The water quality standard for freshwater salmonids of 21 μg I -1 NH 3 -N was considered to be protective for most marine fish and estuarine fish although the influence of cyclical changes in pH, salinity and temperature were not considered. During ammonia exposures, whether chronic or episodic, estuarine fish may be most at risk as larvae or juveniles, at elevated temperatures, if salinity is near the seawater value and if the pH value of the water is decreased. They are also likely to be at risk from ammonia intoxication in waters of low salinity, high pH and high ammonia levels. These conditions are likely to promote ammonia transfer from the environment into the fish, both as ionized and unionized ammonia, as well as promoting ammonia retention by the fish. Fish are more likely to be prone to ammonia toxicity if they are not feeding, are stressed and if they are active and swimming. Episodic or cycling exposures should also be considered in relation to the rate at which the animal is able to accumulate and excrete ammonia and the physiological processes involved in the transfer of ammonia. In the complex environment of an estuary, evaluation of ammonia as a pollutant will involve field and laboratory experiments to determine the responses of fish to ammonia as salinity and temperature vary over a period of time. It will also be necessary to evaluate the responses of a variety of species including estuarine residents and migrants.

Hormonally controlled chloride movement across Drosophila tubules is via ion channels in stellate cells

Abstract: Anion conductance across theDrosophila melanogaster Malpighian (renal) tubule was investigated by a combination of physiological and transgenic techniques. Patch-clamp recordings identified cluster...