Applications of amino acid derivatization with 6-aminoquinolyl-N-hydroxysuccinimidyl carbamate. Analysis of feed grains, intravenous solutions and glycoproteins.
ABSTRACT Primary and secondary amines are rapidly labelled by 6-aminoquinolyl-N-hydroxysuccinimidyl carbamate to form highly fluorescent asymmetric urea derivatives which are readily amenable to analysis by liquid chromatography. Derivatization consists of a simple, one-step procedure, and the resulting labelled amines can be analyzed without further cleanup. The adducts are extremely stable with no discernible loss in response after storage for one week at room temperature, making the reagent an ideal candidate for pre-column amino acid analysis. Chromatographic methods for protein hydrolysates have been developed for the analysis of samples containing many unusual amino acids including a number of cysteine derivatives, collagen hydrolysates containing hydroxyproline and hydroxylysine, performic acid oxidized samples and glycoprotein hydrolysates containing glucosamine and galactosamine. Samples with potentially interfering matrix components such as hydrolyzed feed grains and intravenous solutions are readily analyzed and are quantified with average per cent relative standard deviations in the 1-2% range. Comparative data on these samples are in good agreement with either ion-exchange amino acid analysis or label information.
Article: Response of European sea bass (Dicentrarchus labrax) to graded levels of methionine (total sulfur amino acids) in soya protein-based semi-purified diets.[show abstract] [hide abstract]
ABSTRACT: The dietary methionine (Met) and total sulfur amino acid (TSAA) requirements of European sea bass (Dicentrarchus labrax) (initial body weight 13.4 (SD 0.2) g) were estimated in a 12-week dose-response experiment. Seven isonitrogenous (7.6 % DM) and isoenergetic (gross energy, 21.2 MJ/kg DM) diets, based on soya protein and crystalline L-amino acids containing graded levels of L-Met (1.6-16.2 g/kg) at a constant cysteine (4 g/kg) level and a fish meal-based diet, were fed each to triplicate groups of fifty fish kept in 250 litre tanks in a thermoregulated (23 +/- 0.5 degrees C) seawater system. The Met and TSAA-deficient diet resulted in higher mortality, impaired feed intake and growth relative to the other treatments (P < 0.01). No signs of lens opacity due to limiting Met intake were observed and no feed intake or growth depression occurred at the highest level of dietary TSAA. Met and TSAA requirements for optimal N deposition or weight gain as fitted with the broken-line model resulted in estimated values of 8.0 and 12.0 g/kg diet (for example, 1.8 and 2.7 % dietary protein) and 9.1 and 13.1 g/kg diet (for example, 2.0 and 3.0 % dietary protein), respectively. Plasma levels of Met, homocysteine and cysteine increased in response to excess dietary TSAA, corroborating requirement estimates from growth data. N gain resulted in a linear function of TSAA consumption at marginal Met (TSAA) intake. The TSAA intake needed to maintain N balance resulted in a value of 20.0 mg TSAA/kg average body weight0.75 per d, which represents 23 % of the total (maintenance+accretion) requirement.The British journal of nutrition 04/2010; 104(5):664-73. · 3.45 Impact Factor
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ABSTRACT: The association of α-amino-β-methylaminopropionic acid (BMAA) with elevated incidence of amyotrophic lateral sclerosis/Parkinson's disease complex (ALS/PDC) was first identified on the island of Guam. BMAA has been shown to be produced across the cyanobacterial order and its detection has been reported in a variety of aquatic and terrestrial environments worldwide, suggesting that it is ubiquitous. Various in vivo studies on rats, mice, chicks and monkeys have shown that it can cause neurodegenerative symptoms such as ataxia and convulsions. Zebrafish research has also shown disruption to neural development after BMAA exposure. In vitro studies on mice, rats and leeches have shown that BMAA acts predominantly on motor neurons. Observed increases in the generation of reactive oxygen species (ROS) and Ca(2+) influx, coupled with disruption to mitochondrial activity and general neuronal death, indicate that the main mode of activity is via excitotoxic mechanisms. The current review pertaining to the neurotoxicity of BMAA clearly demonstrates its ability to adversely affect neural tissues, and implicates it as a potentially significant compound in the aetiology of neurodegenerative disease. When considering the potential adverse health effects upon exposure to this compound, further research to better understand the modes of toxicity of BMAA and the environmental exposure limits is essential.International Journal of Environmental Research and Public Health 09/2011; 8(9):3728-46. · 1.61 Impact Factor