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Plasma concentrations of aspartic acid were elevated 30 min after 1000 mg/kg L-aspartate (oral or i.p.) to 15-day-old and adult mice. Thereafter, plasma concentrations rapidly declined exponentially with a half-life of approximately 0.2 h in both age groups. Aspartic acid plasma concentrations were not appreciably altered after the oral or ip administration of 10 and 100 mg/kg L-aspartate. 
60 - 85 % of the administered 14C-L-aspartate was exhaled as CO2 in young and in adult mice within 5 h p.a., for the i.p. and the oral routes and for the 3 doses used: 10, 100 and 1000 mg/kg bw. A reduced metabolism was observed in the first 30 min p.a. in the high dose group.
Human cells normally handle large quantities of the dicarboxylic amino acid L-aspartic acid, which is an essential part of normal cellular function. Aspartate enters the Krebs cycle and the urea cycle.
Protein in the diet is digested in the gut and the amino acids or small peptides are absorbed. L-aspartate is absorbed from the intestinal lumen by an active transport process. Metabolism occurs during the absorption process of free and protein bound L-aspartate, by transamination, resulting in oxaloacetate, thereby reducing the available amount of L-aspartate in the portal blood.
The rodent appears to metabolize the dicarboxylic amino acids differently than the primate. This may be of significance in determining the susceptibility of the rodent to dicarboxylic amino acid-induced neuronal necrosis, in contrast to the primate, which is not sensitive.

Key value for chemical safety assessment

Bioaccumulation potential:
no bioaccumulation potential

Additional information