. The Biological bulletin. Biology; Zoology; Biology; Marine Biology. I E Q O/ I D. O /o o 12 WATER 12 %, 8 34 14 .31 I FIGURE 5. A proposed mechanism explaining the differential effects of NH3 and NH4+ on A/, rosenbergii larvae cultured in solutions of different pH. The values for blood salinity, pH, and total ammonia were estimated from literature data as described in the text. These condi- tions are assumed to be typical of larvae prior to addition of high ambient ammonia. The water ammonia levels are incipient lethal concentrations derived for the three pH values tested. Am-
. The Biological bulletin. Biology; Zoology; Biology; Marine Biology. I E Q O/ I D. O /o o 12 WATER 12 %, 8 34 14 .31 I FIGURE 5. A proposed mechanism explaining the differential effects of NH3 and NH4+ on A/, rosenbergii larvae cultured in solutions of different pH. The values for blood salinity, pH, and total ammonia were estimated from literature data as described in the text. These condi- tions are assumed to be typical of larvae prior to addition of high ambient ammonia. The water ammonia levels are incipient lethal concentrations derived for the three pH values tested. Am- monia in water of high pH exists in relatively large quantities as unionized NH3, which rapidly diffuses into larvae, increasing blood ammonia to toxic levels. In low pH solutions ammonia exists almost totally as NH4+. This ion is shown to compete with Na in active transport pro- cesses and toxicity ensues from osmoregulatory failure. monia found toxic at high pH about mg/liter or 10% exists as NHs. This level exceeds that postulated for the blood by about four-fold, and consequently NH:i would diffuse into animals. At a blood pH " the molecule would be pro- tonated to NH4+, thereby maintaining the NHS diffusion gradient inward. Body concentrations of ammonia would rise if alternate routes of excretion could not expel this surplus, and toxicity follow, perhaps via a mode described by Campbell (1973). Toxicity might include elevation of blood pH as NH3 is protonated and a decrease in substrate for the tricarboxylic acid cycle as excess ammonia reverses the usual oxidation of glutamate (Campbell, 1973). Toxicity clue to inward dif- fusion of at high pH is rapid and caused mortality among test larvae in 2-18 hr(). The deleterious effect of high ambient ammonia levels on an alternate route of ammonia excretion from the blood (nondiffusion) is the second component of the model. It is proposed that inhibition of sodium influx is a major factor contribut- ing
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Keywords: ., bookauthorlilliefrankrat, booksubjectbiology, booksubjectzoology
