Distribution of D-amino acids in vinegars and involvement of lactic acid bacteria in the production of D-amino acids

Levels of free D-amino acids were compared in 11 vinegars produced from different sources or through different manufacturing processes. To analyze the D- and L-amino acids, the enantiomers were initially converted into diastereomers using pre-column derivatization with o-phthaldialdehyde plus N-acethyl-L-cysteine or N-tert-butyloxycarbonyl-L-cysteine. This was followed by separation of the resultant fluorescent isoindol derivatives on an octadecylsilyl stationary phase using ultra-performance liquid chromatography. The analyses showed that the total D-amino acid level in lactic fermented tomato vinegar was very high. Furthermore, analysis of the amino acids in tomato juice samples collected after alcoholic, lactic and acetic fermentation during the production of lactic fermented tomato vinegar showed clearly that lactic fermentation is responsible for the D-amino acids production; marked increases in D-amino acids were seen during lactic fermentation, but not during alcoholic or acetic fermentation. This suggests lactic acid bacteria have a greater ability to produce D-amino acids than yeast or acetic acid bacteria

Oral Administration of D-aspartate, but not of L-aspartate, Reduces Food Intake in Chicks

In the present study, we determined the effects of oral administration of L- and D-aspartate (L-Asp and D-Asp) on food intake over a period of2haftertheadministration, as well as its effects on the concentration of L- and D-Asp in the brain and plasma. Chicks were orally administered different levels (0, 3.75, 7.5 and 15 mmol/kg body weight) of L-Asp (Experiment 1) and D-Asp (Experiment 2). Administration of several doses of L-Asp linearly increased the concentration of L-Asp, but not of D-Asp, in plasma. Oral L-Asp somewhat modified the levels of L- and D-Asp levels in the telencephalon, but not in the diencephalon. However, food intake was not significantly changed with doses of L-Asp. On the other hand, D-Asp strongly and dose-dependently inhibited food intake over a period of 2 h after the administration. Oral D-Asp clearly increased D-Asp levels in the plasma and diencephalon, but no significant changes in L-Asp were detected. Brain monoamine contents were only minimally influenced by L- or DAsp administration. We conclude that D-Asp may act as an anorexigenic factor in the diencephalon. Key words: brain, D-Aspartate, food intake, L-Aspartate, neonatal chick, plasm