Acute ammonia toxicity and the protective effects of methionine sulfoximine on the swamp eel, Monopterus albus

Abstract

The objectives of this study were to examine how the swamp eel, Monopterus albus, defended against acute ammonia toxicity derived from the intraperitoneal injection with a sublethal dose (10 micromol g(-1) fish) of ammonium acetate (CH(3)COONH(4)) followed by 24 hr of emersion, and to elucidate the mechanisms of acute ammonia toxicity with respect to glutamine accumulation in the brain using L-methionine S-sulfoximine [MSO; a glutamine synthetase inhibitor]. When confronted with a sublethal dose of CH(3)COONH(4) followed by emersion, only a small fraction of the exogenous ammonia was excreted, and ammonia contents in various organs, especially the brain, increased transiently to high levels. Increased glutamine synthesis and decreased amino acid catabolism in and outside the brain were involved in the defence against acute ammonia toxicity. When injected with a lethal dose (16 micromol g(-1) fish) of CH(3)COONH(4) followed by emersion, ammonia (approximately 30 micromol g(-1) tissue), but not glutamine ( approximately 5 micromol g(-1) tissue), accumulated to extraordinarily high levels in the brain of succumbed fish. Hence, glutamine accumulation in the brain might not be the major mechanism of acute ammonia toxicity in M. albus. MSO (100 microg g(-1) fish) had a partial protective effect in fish injected with a lethal dose of CH(3)COONH(4). However, this effect was unrelated to the suppression of glutamine synthesis and accumulation in the brain. Instead, MSO suppressed the rate of ammonia buildup in the brain, possibly through its effects on glutamate dehydrogenase therein.

Skeletal Muscle and the Effects of Ammonia Toxicity in Fish, Mammalian, and Avian Species: A Comparative Review Based on Molecular Research

“…Studies on mudskippers [ 3 ] found that high levels of ammonia induced high levels of glutamine in the brain but not death, indicating that the mechanism for toxicity in the brain of fish could differ from that of mammals. Similar findings were reported for the African sharptooth catfish [ 2 ] and the swamp eel [ 119 ]. NH 4 + has also been shown to be able to substitute for K + in K + ion channels in neurons, affecting the membrane potential and excitability of the neuron and could account for the hyperexcitability and convulsions observed in hyperammonemic fish [ 120 , 121 ].…”

Excretory nitrogen metabolism and defence against ammonia toxicity in air‐breathing fishes

“…Furthermore, after 144 h of exposure to environmental ammonia, the glutamine contents in the muscle and liver reached 10·84 and 17·06 µmol g −1 , which happened to be the highest known for fishes. Monopterus albus also has high tolerance of acute ammonia toxicity and detoxifies exogenous ammonia to glutamine (Tng et al , ). Furthermore, an intraperitoneal injection of ammonium acetate into M .…”

Detoxification Pathways in Response to Environmental Ammonia Exposure of the Cuttlefish, Sepia pharaonis: Glutamine and Urea Formation

“…After 6 h of ammonia exposure, the level of GSase activity in the gills of the crab, P. trituberculatus , increased by 1.87‐ and 2.48‐fold in the 5 and 5 mg/L ammonia treatment groups, respectively, and the level of GDH activity increased significantly within the first 12 h (Liu et al ). Similar studies have also revealed that the activities of GSase and GDH are higher in response to ammonia exposure (Murray et al ; Wright et al ; Tng et al ). The level of GSase and GDH activities exhibited a notable dose‐dependent relationship with the ammonia exposure concentration in this study, and the increase in the GDH or GSase activities was also accompanied by an increase in the glutamine content, as reported in other marine animals (Wee et al ; Hegazi et al ; Wang et al ).…”