Ammonia toxicity mechanism in fish: Studies on rainbow trout (Salmo gairdneri Rich.)

Arillo, Attilio; Margiocco, C.; Melodia, F.; Mensi, P.; Schenone, G.

doi:10.1016/0147-6513(81)90006-3

Cited by 145 publications

(59 citation statements)

References 41 publications

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“…3A) during acidosis probably represents a detoxification mechanism to prevent ammonia toxicity, thereby maintaining circulating [ammonia] within a homeostatic range (Fromm and Gillette, 1968;Olson and Fromm, 1971;Arillo et al, 1981;Mommsen and Walsh, 1992;Ip et al, 2004). This action has been demonstrated previously in goldfish exposed to high environmental ammonia (Olson and Fromm, 1971;Sinha et al, 2013).…”

Section: Urea Metabolismmentioning

confidence: 87%

Physiological and molecular responses of the goldfish kidney (Carassius auratus) to metabolic acidosis, and potential mechanisms of renal ammonia transport

Lawrence

Wright

Wood

2015

Journal of Experimental Biology

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Relative to the gills, the mechanisms by which the kidney contributes to ammonia and acid-base homeostasis in fish are poorly understood. Goldfish were exposed to a low pH environment (pH 4.0, 48 h), which induced a characteristic metabolic acidosis and an increase in total plasma [ammonia] but reduced plasma ammonia partial pressure (P NH3 ). In the kidney tissue, total ammonia, lactate and intracellular pH remained unchanged. The urinary excretion rate of net base under control conditions changed to net acid excretion under low pH, with contributions from both the NH 4 + (∼30%) and titratable acidity minus bicarbonate (∼70%; TA-HCO 3 − ) components. Inorganic phosphate (P i ), urea and Na + excretion rates were also elevated while Cl − excretion rates were unchanged. Renal alanine aminotransferase activity increased under acidosis. The increase in renal ammonia excretion was due to significant increases in both the glomerular filtration and the tubular secretion rates of ammonia, with the latter accounting for ∼75% of the increase. There was also a 3.5-fold increase in the mRNA expression of renal Rhcg-b (Rhcg1) mRNA. There was no relationship between ammonia secretion and Na + reabsorption. These data indicate that increased renal ammonia secretion during acidosis is probably mediated through Rhesus (Rh) glycoproteins and occurs independently of Na + transport, in contrast to branchial and epidermal models of Na + -dependent ammonia transport in freshwater fish. Rather, we propose a model of parallel H + /NH 3 transport as the primary mechanism of renal tubular ammonia secretion that is dependent on renal amino acid catabolism.

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Section: Urea Metabolismmentioning

confidence: 87%

Physiological and molecular responses of the goldfish kidney (Carassius auratus) to metabolic acidosis, and potential mechanisms of renal ammonia transport

Lawrence

Wright

Wood

2015

Journal of Experimental Biology

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“…results in profound energy (ATP) deficits in the brain (Lutz et al, 2003;Bickler and Buck, 2007), but similar ATP deficits have been reported in mammals (Kosenko et al, 1994) and fishes experiencing hyperammonemia (Arillo et al, 1981;Schenone et al, 1982). During anoxia, the lack of ATP results in a run-down of transmembrane ion gradients due to insufficient ATP delivery to ion pumps such as the Na + /K + -ATPase.…”

Section: Introductionmentioning

confidence: 98%

The relationship between NMDA receptor function and the high ammonia tolerance of anoxia-tolerant goldfish

Wilkie

Pamenter

Duquette

et al. 2011

Journal of Experimental Biology

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SUMMARY Acute ammonia toxicity in vertebrates is thought to be characterized by a cascade of deleterious events resembling those associated with anoxic/ischemic injury in the central nervous system. A key event is the over-stimulation of neuronal N-methyl-D-aspartate (NMDA) receptors, which leads to excitotoxic cell death. The similarity between the responses to acute ammonia toxicity and anoxia suggests that anoxia-tolerant animals such as the goldfish (Carassius auratus Linnaeus) may also be ammonia tolerant. To test this hypothesis, the responses of goldfish were compared with those of the anoxia-sensitive rainbow trout (Oncorhynchus mykiss Walbaum) during exposure to high external ammonia (HEA). Acute toxicity tests revealed that goldfish are ammonia tolerant, with 96 h median lethal concentration (LC50) values of 199 μmol l–1 and 4132 μmol l–1 for NH3 and total ammonia ([TAmm]=[NH3]+[NH4+]), respectively. These values were ∼5–6 times greater than corresponding NH3 and TAmm LC50 values measured in rainbow trout. Further, the goldfish readily coped with chronic exposure to NH4Cl (3–5 mmol l–1) for 5 days, despite 6-fold increases in plasma [T] to ∼1300 μmol l–1 and 3-fold increases in brain [TAmm] to 6700 μmol l–1. Muscle [TAmm] increased by almost 8-fold from ∼900 μmol kg–1 wet mass (WM) to greater than 7000 μmol kg–1 WM by 48 h, and stabilized. Although urea excretion rates (JUrea) increased by 2–3-fold during HEA, the increases were insufficient to offset the inhibition of ammonia excretion that occurred, and increases in urea were not observed in the brain or muscle. There was a marked increase in brain glutamine concentration at HEA, from ∼3000 μmol kg–1 WM to 15,000 μmol kg–1 WM after 48 h, which is consistent with the hypothesis that glutamine production is associated with ammonia detoxification. Injection of the NMDA receptor antagonists MK801 (0.5–8 mg kg–1) or ethanol (1–8 mg kg–1) increased trout survival time by 1.5–2.0-fold during exposure to 2 mmol l–1 ammonia, suggesting that excitotoxic cell death contributes to ammonia toxicity in this species. In contrast, similar doses of MK801 or ethanol had no effect on ammonia-challenged (8–9.5 mmol l–1TAmm) goldfish survival times, suggesting that greater resistance to excitotoxic cell death contributes to the high ammonia-tolerance of the goldfish. Whole-cell recordings measured in isolated brain slices of goldfish telencephalon during in vitro exposure to 5 mmol l–1 or 10 mmol l–1TAmm reversibly potentiated NMDA receptor currents. This observation suggested that goldfish neurons may not be completely resistant to ammonia-induced excitotoxicity. Subsequent western blot and densitometric analyses revealed that NMDA receptor NR1 subunit abundance was 40–60% lower in goldfish exposed to 3–5 mmol l–1TAmm for 5 days, which was followed by a restoration of NR1 subunit abundance after 3 days recovery in ammonia-free water. We conclude that the goldfish brain may be protected from excitotoxicity by downregulating the abundance of functional NMDA receptors during periods when it experiences increased internal ammonia.

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“…Relatively stable blood lactate and glucose concentrations indicate that high external levels of ammonia had no major effect on the general physiology of the ammocoetes. Further, despite a large buildup of internal ammonia, the experimental ammocoetes did not exhibit the hyperactivity normally associated with the onset of ammonia toxicity (Arillo et al 1981).…”

Section: Ammonia Detoxification and Internal Storagementioning

confidence: 99%

Nitrogenous waste excretion by the larvae of a phylogenetically ancient vertebrate: the sea lamprey (Petromyzon marinus)

Wilkie¹,

Wang²,

Walsh³

et al. 1999

Can. J. Zool.

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Larval sea lampreys (Petromyzon marinus) (ammocoetes) excreted significant quantities of urea, which composed 15-20% of the total nitrogenous waste excreted. Compared with teleosts of similar size, ammonia and urea excretion rates (J Amm and J Urea , respectively) in ammocoetes were relatively low, reflecting the low metabolic rate of these burrow-dwelling suspension feeders. Analyses of liver enzymes indicated that ammocoetes had all the enzymes necessary to produce urea via uricolysis, but not those of the ornithine-urea cycle (OUC). Further, exposure to 2 mmol·L -1 total ammonia for 5 d was accompanied by a 3-fold elevation of J Urea , but did not lead to greater OUC activity. Internal ammonia levels increased markedly, however, exceeding 2000 µmol·L -1 in plasma and 5000 µmol·L -1 in muscle after the 5-d exposure period. This high resistance to internal ammonia accumulation was related to the very high glutamine synthetase activities measured in ammocoete brains. The excretion and production of urea by ammocoetes demonstrates for the first time that agnathans are capable of producing physiologically relevant amounts of urea. Given the ancient origins and conserved evolution of lampreys, these observations also suggest that at least some of the early jawless vertebrates were able to produce and excrete urea.

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Ammonia toxicity mechanism in fish: Studies on rainbow trout (Salmo gairdneri Rich.)

Cited by 145 publications

References 41 publications

Physiological and molecular responses of the goldfish kidney (Carassius auratus) to metabolic acidosis, and potential mechanisms of renal ammonia transport

Physiological and molecular responses of the goldfish kidney (Carassius auratus) to metabolic acidosis, and potential mechanisms of renal ammonia transport

The relationship between NMDA receptor function and the high ammonia tolerance of anoxia-tolerant goldfish

Nitrogenous waste excretion by the larvae of a phylogenetically ancient vertebrate: the sea lamprey (Petromyzon marinus)

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