Clin Invest Med 2009; 32 (1): E13-E19. AbstractPurpose: To investigate the pharmacokinetics of Lcarnitine (LC) and its analogues, acetyl-L-carnitine (ALC) and propionyl -L-carnitine (PLC) in healthy volunteers after single L-carnitine administration. Methods: Liquid L-carnitine (2.0 g) was administered orally as a single dose in 12 healthy subjects. Plasma and urine concentrations of L-carnitine, ALC and PLC were detected by HPLC. Results:The maximum plasma concentration (Cmax) and area under the curve (AUC0-) of L-carnitine was 84.7±25.2 μmol·L -1 ·h and 2676.4±708.3 μmol·L -1 ·h, respectively. The elimination half-life of L-carnitine and the time required to reach the Cmax (Tmax) was 60.3±15.0 and 3.4±0.46 h, respectively. The Cmax of ALC (12.9±5.5 μmol·L -1 ) and PLC (5.08±3.08 μmol·L -1 ) was lower than Lcarnitine (P<0.01), so as the AUC0-(166.2±77.4 and 155.6±264.2μmol·L -1 ·h, respectively, P<0.01). The half-life of ALC (35.9±28.9h) and PLC (25.7±30.3 h) was also shorter than L-carnitine (P<0.01). The 24h accumulated urinary excretion of L-carnitine, ALC and PLC were 613.5±161.7, 368.3±134.8 and 61.3±37.8μmol, respectively. Conclusion: L-carnitine has a greater maximum plasma concentration than ALC and PLC. L-carnitine also has a longer half-life than ALC and PLC. These data may have important implications in the designing of dosing regimens for L-carnitine or its analogues, such as ALC or PLC.L-carnitine (3-hydroxy-4-N-trimethylammonium butyrate) is an endogenous compound mainly derived from food stuff, such as meat and dairy products. [1][2][3] It is also synthesized in the human, in the liver and kidneys, from the essential amino acids lysine and methionine. [1][2][3] In humans, the endogenous carnitine pool, which comprises free L-carnitine and a range of short-, medium-and long-chain esters, such as acetyl-L-carnitine (ALC) and propionyl-L-carnitine (PLC), is maintained by absorption of L-carnitine from dietary sources, biosynthesis within the body and extensive renal tubular reabsorption from glomerular filtrate. [1][2][3] L-carnitine has important roles in intermediary metabolism, including the transport of long chain fatty acids across the mitochondrial inner membrane; more than 90% of the human body's store is present in skeletal and cardiac muscle. 1,2 L-carnitine is an essen-ORIGINAL RESEARCH

The degree of brain development can be expressed by the levels of brain brain-derived neurotrophic factor (BDNF). BDNF plays an irreplaceable role in the process of neuronal development, protection, and restoration. The aim of the present study was to evaluate the effects of boric acid supplementation in water on the ostrich chick neuronal development. One-day-old healthy animals were supplemented with boron in drinking water at various concentrations, and the potential effects of boric acid on brain development were tested by a series of experiments. The histological changes in brain were observed by hematoxylin and eosin (HE) staining and Nissl staining. Expression of BDNF was analyzed by immunohistochemistry, quantitative real-time PCR (QRT-PCR), and enzyme linked immunosorbent assay (ELISA). Apoptosis was evaluated with Dutp-biotin nick end labeling (TUNEL) reaction, and caspase-3 was detected with QRT-PCR. The results were as follows: (1) under the light microscope, the neuron structure was well developed with abundance of neurites and intact cell morphology when animals were fed with less than 160 mg/L of boric acid (groups II, III, IV). Adversely, when boric acid doses were higher than 320 mg/L(groups V, VI), the high-dose boric acid neuron structure was damaged with less neurites, particularly at 640 mg/L; (2) the quantity of BDNF expression in groups II, III, and IV was increased while it was decreased in groups V and VI when compared with that in group I; (3) TUNEL reaction and the caspase-3 mRNA level showed that the amount of cell apoptosis in group II, group III, and group IV were decreased, but increased in group V and group VI significantly. These results indicated that appropriate supplementation of boric acid, especially at 160 mg/L, could promote ostrich chicks' brain development by promoting the BDNF expression and reducing cell apoptosis. Conversely, high dose of boric acid particularly in 640 mg/L would damage the neuron structure of ostrich chick brain by inhibiting the BDNF expression and increasing cell apoptosis. Taken together, the 160 mg/L boric acid supplementation may be the optimal dose for the brain development of ostrich chicks.