Roles of intestinal glutamate dehydrogenase and glutamine synthetase in environmental ammonia detoxification in the euryhaline four-eyed sleeper, Bostrychus sinensis.
This study aimed to examine the hypothesis that intestinal glutamate dehydrogenase (GDH) and glutamine synthetase (GS) could be involved in ammonia detoxification in the euryhaline Bostrychus sinensis exposed to ammonia in a hyperosmotic environment, whereby drinking was essential for osmoregulation. Our results indicate that there was a significant increase in ammonia content in the intestine of B. sinensis exposed to 15 mmol l(-1) NH(4)Cl in seawater (pH 7.0) for 6 days. There were also significant increases in the amination and deamination activities and protein abundance of intestinal GDH. The GDH amination/deamination ratio remained unchanged, indicating that there could be increases in the turnover of glutamate. However, the difference between the amination and deamination activities increased 2-fold, implying that there could be an increase in glutamate formation in the intestine. Since the intestinal glutamate content remained unchanged, excess glutamate formed might have been channeled into other amino acids and/or transported to other organs. Indeed, the intestinal glutamine content increased significantly by 2-fold, with a significant increase in the activity and protein abundance of intestinal GS. Since the magnitude of glutamine accumulation in the intestine was lower than those in liver and muscle, which lacked changes in GDH activities, intestinal glutamate could have been shuttled to liver and muscle to facilitate increased synthesis of glutamine therein. By contrast, when fish were exposed to a much higher concentration (30 mmol l(-1)) of NH(4)Cl in 5 per thousand water (pH. 7.0), the magnitude of increase in ammonia content in the intestine was less prominent, and there were no changes in activities and kinetic properties of intestinal GDH. Therefore, it can be concluded that the intestine of B. sinensis was involved in the defense against ammonia toxicity during exposure to ammonia in a hyperosmotic medium.
Peh
W Y X
WY
Department of Biological Science, National University of Singapore, Kent Ridge, Singapore 117543, Republic of Singapore.
Chew
S F
SF
Ching
B Y
BY
Loong
A M
AM
Ip
Y K
YK
D000641:Ammonia / Q000032:analysis / Q000378:metabolism* / Q000633:toxicity; D000643:Ammonium Chloride / Q000378:metabolism / Q000633:toxicity; D000818:Animals; D004789:Enzyme Activation / Q000187:drug effects; D005969:Glutamate Dehydrogenase / Q000378:metabolism*; D005974:Glutamate-Ammonia Ligase / Q000378:metabolism*; D018698:Glutamic Acid / Q000378:metabolism; D007422:Intestines / Q000201:enzymology*; D008099:Liver / Q000737:chemistry / Q000201:enzymology; D018482:Muscle, Skeletal / Q000737:chemistry / Q000201:enzymology; D010473:Perciformes / Q000378:metabolism*; D012623:Seawater / Q000737:chemistry; D014874:Water Pollutants, Chemical / Q000032:analysis / Q000378:metabolism* / Q000633:toxicity; D014882:Water-Electrolyte Balance
D014874:Water Pollutants, Chemical; D000643:Ammonium Chloride; D018698:Glutamic Acid; D000641:Ammonia; D005969:Glutamate Dehydrogenase; D005974:Glutamate-Ammonia Ligase