Kinetics of L-theanine uptake and metabolism in healthy participants are comparable after ingestion of L-theanine via capsules and green tea.

L-Theanine, an amino acid in green tea, is suggested to improve cognition and mood. Therefore, L-theanine is available as a supplement and is now used as an ingredient in functional drinks. Because data on the metabolic fate of L-theanine from human studies are lacking, we investigated the kinetics of L-theanine uptake and its metabolites, ethylamine and glutamic acid, in healthy participants. Within a randomized crossover study, 12 participants ingested a bolus of 100 mg L-theanine via capsules or green tea. On further occasions, 3 participants received 50 and 200 mg L-theanine via capsules. Blood and urine were collected before and up to 24 h postconsumption to determine the concentrations of L-theanine, proteinogenic amino acids, and ethylamine in plasma, erythrocytes, and urine by HPLC. L-Theanine increased in plasma, erythrocytes, and urine with comparable results after both treatments. The maximum plasma concentration of L-theanine occurred 0.8 h after intake of 100 mg L-theanine via capsules (24.3 ± 5.7 µmol/L) and tea (26.5 ± 5.2 µmol/L), respectively. The AUC of L-theanine in plasma increased dose dependently after intake of 50, 100, and 200 mg L-theanine via capsules. Moreover, ethylamine and glutamic acid increased in plasma and were excreted by urine after intake of capsules and tea. In conclusion, L-theanine is rapidly absorbed and seems to be hydrolyzed to ethylamine and glutamic acid. A minor part of L-theanine is retained in erythrocytes. Kinetics and urinary excretion of L-theanine, ethylamine, and glutamic acid are comparable after both treatments. Thus, functional effects of L-theanine intake may result from L-theanine, ethylamine, or glutamic acid.

Translocations as a mechanism for homozygous deletion of 13q14 and loss of the ATM gene in a patient with B-cell chronic lymphocytic leukemia.

Chromosomal aberrations detected by fluorescence in situ hybridization (FISH) on interphase nuclei are important prognostic markers in chronic lymphocytic leukemia (CLL). Deletions in 13q14 and in 11q22.3 are two of the most frequent aberrations in this disease entity (55 and 18%, respectively) and are usually effected by interstitial deletions. Here, we report on the case of a 66-year-old woman with CLL who was analyzed by conventional metaphase cytogenetics as well as fluorescence in situ hybridization. Deletion-specific probes detected a homozygous loss of two anonymous loci in chromosomal band 13q14 in parallel with a heterozygous loss of the ATM gene located in chromosomal band 11q22.3. Karyotype analysis indicated reciprocal but unbalanced translocations involving chromosomes 3, 11, and 13. Deleted sites on 13q14 appeared to be located within the breakpoint regions of the translocations. We show that mechanisms other than interstitial deletions may lead to loss of critical chromosomal regions in CLL.