Modeling of glutamic acid production by Lactobacillus plantarum MNZ

Background: L-glutamic acid, the principal excitatory neurotransmitter in the brain and an important intermediate in metabolism acts as a precursor of γ-amino butyric acid (GABA). In the present study, culture condition for enhanced glutamic acid production by Lactobacillus plantarum MNZ was optimized and the influence of such conditions on GABA production was evaluated. Results: Results indicated that glutamic acid increased up to 3-fold (3.35) under the following condition: pH 4.5, temperature 37ºC, 12% (w/v) glucose and 0.7% (w/v) ammonium nitrate; whilst GABA production was enhanced up to 10-fold under the following condition: pH 4.5, temperature 37ºC, 6% (w/v) glucose and 0.7% (w/v) ammonium nitrate. Conclusions: This is the first report for dual biosynthesizing activities of a lactic acid bacterium for the production of glutamic acid and GABA. The results of this study can be further used for developing functional foods rich inglutamic acid and subsequently GABA as a bioactive compound.

Effect of propofol on glutamate and gamma-aminobutyric acid release from rat hippocampal synaptosomes / 华中科技大学学报（医学）（英德文版）

To investigate the effect of propofol on the release of glutamate and gamma-aminobutyric acid (GABA) from rat hippocampal synatosomes, synaptosomes was made from hippocampus and incubated with artificial cerebrospinal fluid (aCSF). With the experiment of Ca(2+)-dependent release of glutamate and GABA, dihydrokainic acid (DHK) and nipectic acid were added into aCSF. For the observation of Ca(2+)-independent release of glutamate and GABA, no DHK, nipectic acid and Ca2+ were added from aCSF. The release of glutamate and GABA were evoked by 20 micromol/L veratridine or 30 mmol/L KCI. The concentration of glutamate and GABA in aCSF was measured by using high-performance liquid chromatography (HPLC). 30, 100 and 300 micromol/L propofol significantly inhibited veratridine-evoked Ca(2+)-dependent release of glutamate and GABA (P 0.05). Veratridine or elevated KCI evoked Ca(2+)-independent release of glutamate and GABA was not affected significantly by propofol (P > 0.05). Propofol could inhibit Ca(2+)-dependent release of glutamate and GABA. However, it has no effect on the Ca(2+)-independent release of glutamate and GABA.

La vitamina K: bioquímica, función y deficiencia: revisión / The vitamin K: biochemistry, function and deficiency: riview

La vitamina K es un cofactor que actúa en la síntesis de los factores de coagulación II, VII, IX y X, de los inhibidores de la coagulación, proteínas C y S, y de proteínas de la matriz ósea. Su forma activa actúa como coenzima en la carboxilación del ácido glutámico de dichas proteínas. La función de los factores dependientes de la vitamina K se realizan mediante la formación de complejos enzimaticos, en los cuales estas proteínas se unen sobre la membrana fosfolipídica a un cofactor proteíco, en presencia de calcio. La insuficiencia de los mecanismos responsables de la gamma-carboxilación del ácido glutámico altera la función hemostática. La deficiencia hereditaria de factores dependientes de vitamina K, los antibióticos y los anticoagulantes orales disminuyen la capacidad de formación de los complejos enzimaticos, por lo que se produce síndrome hemorrágico o trombóticos y alteraciones de la masa ósea que son fácilmente tratadas con administración de preparados de vitamina K. Las causas principales de deficiencia son: falta de reservas hepáticas en recién nacidos, insuficiencia hepática, falta de ingesta, malabsorción, antibioticoterapia y admisnistración de cumarínicos. Para el estudio de la vitamina K se usan métodos indirectos, que miden las proteínas dependientes de su acción, y métodos directos que miden específicamente las quinonas