BACKGROUND: Neurological disturbances have been implicated with aspartame (ASP) consumption and the cholinergic system with acetylcholinesterase (AChE) seems actively involved. AIM: To evaluate the effect of ASP and its metabolites on rat hippocampal AChE activity. METHODS: Hippocampal homogenate or pure enzyme AChE (eel E. electricus) was incubated with the sum or each of ASP components, phenylalanine (Phe), aspartic acid (asp) and methanol (MeOH) for 1h at 37 degrees C. AChE activity was measured spectrophotometrically. RESULTS: Incubation of rat tissue or pure enzyme with the sum of ASP metabolites in concentrations in CSF (the concentrations were calculated according to the CSF/plasma concentration ratios) following 150 or 200mgkg(-1) of ASP consumption, resulted in significant enzyme activity reductions of 25 and 31% for hippocampal AChE and 11% (p<0.01) and 19% for pure enzyme, respectively. Aspartic acid concentrations of 0.42 or 0.56mM significantly reduced the enzyme activities by 13 and 20% for hippocampal AChE and 15 and 18% for pure enzyme, respectively. Phe concentrations of 0.042 or 0.083mM decreased the enzyme activity by 12% (p<0.01) and 20% (p<0.001) for hippocampal AChE and 15 and 18% (p<0.001) for pure enzyme, respectively. Methanol concentrations of 0.60 or 0.80mM remarkably inhibited hippocampal AChE by about 18 and 22% and pure enzyme by about 14 and 20%, respectively. CONCLUSIONS: Low concentrations of ASP components had no effect on hippocampal and pure AChE activity, whereas high or toxic concentrations remarkably decreased both enzyme activities. Muscarinic symptoms may be related to the latter concentrations of ASP metabolites.
BACKGROUND:Neurological disturbances have been implicated with aspartame (ASP) consumption and the cholinergic system with acetylcholinesterase (AChE) seems actively involved. AIM: To evaluate the effect of ASP and its metabolites on rat hippocampal AChE activity. METHODS: Hippocampal homogenate or pure enzyme AChE (eel E. electricus) was incubated with the sum or each of ASP components, phenylalanine (Phe), aspartic acid (asp) and methanol (MeOH) for 1h at 37 degrees C. AChE activity was measured spectrophotometrically. RESULTS: Incubation of rat tissue or pure enzyme with the sum of ASP metabolites in concentrations in CSF (the concentrations were calculated according to the CSF/plasma concentration ratios) following 150 or 200mgkg(-1) of ASP consumption, resulted in significant enzyme activity reductions of 25 and 31% for hippocampal AChE and 11% (p<0.01) and 19% for pure enzyme, respectively. Aspartic acid concentrations of 0.42 or 0.56mM significantly reduced the enzyme activities by 13 and 20% for hippocampal AChE and 15 and 18% for pure enzyme, respectively. Phe concentrations of 0.042 or 0.083mM decreased the enzyme activity by 12% (p<0.01) and 20% (p<0.001) for hippocampal AChE and 15 and 18% (p<0.001) for pure enzyme, respectively. Methanol concentrations of 0.60 or 0.80mM remarkably inhibited hippocampal AChE by about 18 and 22% and pure enzyme by about 14 and 20%, respectively. CONCLUSIONS: Low concentrations of ASP components had no effect on hippocampal and pure AChE activity, whereas high or toxic concentrations remarkably decreased both enzyme activities. Muscarinic symptoms may be related to the latter concentrations of ASP metabolites.