Production Of Glutaric Acid Research Articles

Highly active and selective Cs2.5H0.5PW12O40/SBA-15 composite material in the oxidation of cyclopentane-1,2-diol to glutaric acid by aqueous H2O2

Abstract In the present work, for the first time the Cs 2.5 H 0.5 PW 12 O 40 /SBA-15 catalysts were prepared as highly efficient catalysts for the direct production of glutaric acid (GAC) via selective oxidation of cyclopentane-1,2-diol by using aqueous hydrogen peroxide as the green oxidant. The yield of GAC is higher than 88%. The fresh catalyst and the recovered ones were all characterized by XRD, FT-IR, Raman and 31 P MAS NMR to reveal the structure change during the reaction. XRD results revealed that the Cs 2.5 H 0.5 PW 12 O 40 /SBA-15 catalysts keep the crystalline structure of the as-prepared Cs 2.5 H 0.5 PW 12 O 40 . And it is found that the structure of the Cs 2.5 H 0.5 PW 12 O 40 /SBA-15 catalysts was retained after the reaction, as determined by Raman, FT-IR and 31 P MAS NMR. The new Cs 2.5 H 0.5 PW 12 O 40 /SBA-15 catalyst can be easily recycled after reaction and can be reused six times, indicating its excellent stability.

Mechanism of age-dependent susceptibility and novel treatment strategy in glutaric acidemia type I

Glutaric acidemia type I (GA-I) is an inherited disorder of lysine and tryptophan metabolism presenting with striatal lesions anatomically and symptomatically similar to Huntington disease. Affected children commonly suffer acute brain injury in the context of a catabolic state associated with nonspecific illness. The mechanisms underlying injury and age-dependent susceptibility have been unknown, and lack of a diagnostic marker heralding brain injury has impeded intervention efforts. Using a mouse model of GA-I, we show that pathologic events began in the neuronal compartment while enhanced lysine accumulation in the immature brain allowed increased glutaric acid production resulting in age-dependent injury. Glutamate and GABA depletion correlated with brain glutaric acid accumulation and could be monitored in vivo by proton nuclear magnetic resonance (1H NMR) spectroscopy as a diagnostic marker. Blocking brain lysine uptake reduced glutaric acid levels and brain injury. These findings provide what we believe are new monitoring and treatment strategies that may translate for use in human GA-I.

Reduction of lysine intake while avoiding malnutrition—Major goals and major problems in dietary treatment of glutaryl‐CoA dehydrogenase deficiency

Treatment in glutaryl-CoA dehydrogenase deficiency, an inborn error of metabolism of lysine and tryptophan, is mainly based on restriction of lysine intake, supplementation of carnitine, and an intensification of therapy during intercurrent illnesses. The major principle of dietary treatment is to reduce the production of glutaric acid and 3-hydroxyglutaric acid by restriction of natural protein in general and of lysine in particular. In parallel to development, the growing child learns to utilize different protein sources, shifting the primarily milk-based diet to a mixed diet. The changes in nutritional demands and food composition during the first years of life greatly influence nutritional support for affected patients at different ages. This article highlights frequent pitfalls of dietary treatment for this disease and focuses on particular risks of malnutrition in terms of essential amino acids and micronutrients and/or excess intake of lysine between age 3 months and age 6 years. We conclude from the examples given that restriction of natural protein intake plus application of lysine-free amino acid mixtures minimizes the risk of malnutrition and allows a reliable control of protein and lysine intake and, thus, seems particularly recommendable during the vulnerable period for acute encephalopathic crises. The efficacy of these theoretical and experience-based approaches to dietary treatment of glutaryl-CoA dehydrogenase deficiency should be investigated in detail in prospective clinical studies.

Application of polyethylene glycol-based aqueous biphasic reactive extraction to the catalytic oxidation of cyclic olefins

Glutaric acid and 1,2,3,4-butanetetracarboxylic acid (BTCA) have been synthesized by sodium tungstate catalyzed oxidation of the cyclic olefins: cyclopentene and 1,2,3,6-tetrahydrophthalic anhydride (THPA), using hydrogen peroxide in a polyethylene glycol (PEG)-2000/NaHSO 4 aqueous biphasic system (PEG-ABS). The production of glutaric acid and BTCA was found to increase from the monophasic to the biphasic regimes, and was found to be greatest at short tie-line lengths (TLLs), close to the system’s critical point, yielding glutaric acid and BTCA in 73.1 and 82.5% yield, respectively. The results imply that mutual mixing or contact of the components is important, because the product dicarboxylic acids were found to increase from the monophasic side to the critical point and decrease from the critical point to more divergent regimes. The two reactions were compared with adipic acid synthesis from cyclohexene in terms of the cyclic olefin structure, and the partitioning of the dicarboxylic acid product in the ABS.

DuPont begins glutaric acid production

DuPont begins glutaric acid production

Glutaryl-Coenzyme A Dehydrogenase Deficiency: A Distinct Encephalopathy

Clinical course, diagnostic and therapeutic management, and neurodevelopmental outcome were evaluated in 11 patients with glutaryl-coenzyme A dehydrogenase deficiency. In 9 patients macrocephalus was present at or shortly after birth and preceded the neurological disease. In 7 children an acute illness resembling encephalitis appeared after a period of normal development; 2 had developmental delay and progressive "dystonic cerebral palsy." Later, all 9 displayed typical signs of a disorder of the basal ganglia. In 1 patient with macrocephalus the disorder was diagnosed before the onset of neurological disease; in another it was diagnosed prenatally. Computed tomography and magnetic resonance imaging scans revealed severe generalized cerebral atrophy, most striking in the frontal and temporal lobes in 10 patients. Further deterioration was halted after initiation of treatment consisting of low-protein diets, special formulas low in lysine and tryptophan, and supplements of riboflavin and L-carnitine. Only 1 patient showed a slight clinical improvement. Later, dietary therapy was discontinued in 2 older patients and relaxed in a third without observed adverse effects. Two patients in whom treatment could be initiated before the onset of neurological symptoms have developed normally. However, duration of follow-up (6 and 29 months) does not yet allow classification of glutaryl-coenzyme A dehydrogenase deficiency as a treatable disorder. Total body production of glutaric acid, reflected in the daily urinary output, was efficiently reduced by therapeutic measures. Levels of glutaric acid in plasma and cerebrospinal fluid remained unchanged, which may in part explain the overall unsatisfactory outcome. All patients presented with a severe secondary deficiency of carnitine.(ABSTRACT TRUNCATED AT 250 WORDS)

Short-chain acids of Pseudomonas species encountered in clinical specimens.

The short-chain acids of 36 strains of Pseudomonas grown on Trypticase soy agar were determined by gas-liquid chromatography. Distinct acid profiles were observed for each of the eight species tested. Propionic, isobutyric, and isovaleric acids were the principal acids detected in media extracts of P. maltophilia, P. cepacia, P. pseudoalcaligenes, P. diminuta, and P. vesiculare. The presence and relative amounts of the isobutyric and isovaleric acids clearly distinguished P. maltophilia, P. pseudoalcaligenes, and P. cepacia from other species. P. diminuta could be distinguished from P. vesiculare by the production of glutaric acid; P. testosteroni was the only species tested which produced relatively large amounts of phenylacetic acid.

Short-Chain Acids of Pseudomonas Species Encountered in Clinical Specimens

The short-chain acids of 36 strains of Pseudomonas grown on Trypticase soy agar were determined by gas-liquid chromatography. Distinct acid profiles were observed for each of the eight species tested. Propionic, isobutyric, and isovaleric acids were the principal acids detected in media extracts of P. maltophilia, P. cepacia, P. pseudoalcaligenes, P. diminuta, and P. vesiculare. The presence and relative amounts of the isobutyric and isovaleric acids clearly distinguished P. maltophilia, P. pseudoalcaligenes, and P. cepacia from other species. P. diminuta could be distinguished from P. vesiculare by the production of glutaric acid; P. testosteroni was the only species tested which produced relatively large amounts of phenylacetic acid.

The keto acid metabolism of Corynebacterium diphtheriae growing in submerged culture.

SUMMARY: The keto acid production of Corynebacterium diphtheriae (strain CN2000) growing in submerged culture in complex medium was investigated. Pyruvic acid production followed a pattern in which there was a very rapid production of acid which reached a peak about 12 hr. after inoculation. The acid concentration decreased rapidly after 12 hr. and the final pyruvic acid concentration appeared to be very variable. The source of the pyruvic acid is believed to be lactic acid, the concentration of which decreased rapidly as pyruvic acid increased. The presence in the medium of sufficient iron to abolish toxin production completely did not affect the pattern of pyruvic acid production. a-Ketoglutaric acid production in the cultures appeared to vary in a random manner. C. diphtheriae strain G12/6 produced a maximum yield of pyruvic acid after only 6 hr. growth but was otherwise similar to strain CN2000. C. diphtheriae strain SM1 gave a maximum production of pyruvic acid after 24 hr. but in the presence of 3 μg. Fe/ml. production was more rapid and was like that found for strain CN2000. No correlation was found between toxin production and the production of pyruvic acid or a-keto glutaric acid.