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Relevant bibliographies by topics / Propionic acid accumulation

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Academic literature on the topic 'Propionic acid accumulation'

Author: Grafiati

Published: 2 June 2025

Last updated: 31 July 2025

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Journal articles on the topic "Propionic acid accumulation"

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Feliz, Brady, David R. Witt, and Brent T. Harris. "Propionic Acidemia: A Neuropathology Case Report and Review of Prior Cases." Archives of Pathology & Laboratory Medicine 127, no. 8 (2003): e325-e328. http://dx.doi.org/10.5858/2003-127-e325-paancr.

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Abstract Propionic acidemia is a disorder of branch-chain amino acid and odd-chain fatty acid metabolism. The clinical features typically begin shortly after birth, with rare cases presenting in young adulthood. This disorder most commonly is characterized by episodic decompensations with dehydration, lethargy, nausea, and vomiting as well as a risk for neurologic sequelae. The defect is in the propionyl-CoA carboxylase enzyme with a resultant accumulation of toxic organic acid metabolites. Neuropathologic findings in this inborn error of metabolism have not been extensively characterized but

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Inanc, B., S. Matsui, and S. Ide. "Propionic acid accumulation and controlling factors in anaerobic treatment of carbohydrate: effects of H2 and pH." Water Science and Technology 34, no. 5-6 (1996): 317–25. http://dx.doi.org/10.2166/wst.1996.0566.

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Propionic acid is believed to be the most retardative volatile acid appearing in the anaerobic treatment process. However, the mechanisms by which propionic acid accumulates have not been well understood. Several studies and thermodynamical calculations suggest that an increased hydrogen partial pressure in the system is the cause for the accumulation of propionic acid. However, recent findings by the authors and a few other researchers indicated that artificially elevated or reduced hydrogen partial pressure had no discernible effect. Hence, the consensus on the inhibitory effects of hydrogen

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He, Dao-Yao, Yoshiaki Yazaki, Yoko Nishizawa, et al. "Gene Activation by Cytoplasmic Acidification in Suspension-Cultured Rice Cells in Response to the Potent Elicitor, N-Acetylchitoheptaose." Molecular Plant-Microbe Interactions® 11, no. 12 (1998): 1167–74. http://dx.doi.org/10.1094/mpmi.1998.11.12.1167.

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N-Acetylchitoheptaose strongly induces a set of defense reactions in suspension-cultured rice cells including cytoplasmic acidification (K. Kuchitsu, Y. Yazaki, K. Sakano, and N. Shibuya, Plant Cell Physiol. 38:1012-1018, 1997) and the accumulation of mRNAs for two rapidly activated genes, EL2 and EL3 (E. Minami, K. Kuchitsu, D.-Y. He, H. Kouchi, N. Midoh, Y. Ohtsuki, and N. Shibuya, Plant Cell Physiol. 37:563-567, 1996), as well as phenylalanine ammonia-lyase (PAL), chitinase and β-1,3-glucanase. Treatment of cells with propionic acid resulted in the accumulation of the mRNAs for EL2, EL3, an

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Brass, E. P., P. V. Fennessey, and L. V. Miller. "Inhibition of oxidative metabolism by propionic acid and its reversal by carnitine in isolated rat hepatocytes." Biochemical Journal 236, no. 1 (1986): 131–36. http://dx.doi.org/10.1042/bj2360131.

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The present study was designed to study the interaction of propionic acid and carnitine on oxidative metabolism by isolated rat hepatocytes. Propionic acid (10 mM) inhibited hepatocyte oxidation of [1-14C]-pyruvate (10 mM) by 60%. This inhibition was not the result of substrate competition, as butyric acid had minimal effects on pyruvate oxidation. Carnitine had a small inhibitory effect on pyruvate oxidation in the hepatocyte system (210 +/- 19 and 184 +/- 18 nmol of pyruvate/60 min per mg of protein in the absence and presence of 10 mM-carnitine respectively; means +/- S.E.M., n = 10). Howev

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Kido, Jun, Shirou Matsumoto, and Kimitoshi Nakamura. "Carglumic Acid Contributes to a Favorable Clinical Course in a Case of Severe Propionic Acidemia." Case Reports in Pediatrics 2020 (March 9, 2020): 1–5. http://dx.doi.org/10.1155/2020/4709548.

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Propionic acidemia (PA) is manifested as an abnormal accumulation of propionic acid and its metabolites, including methylcitrate, 3-hydroxypropionic acid, and propionylglycine, and is caused by a defect of propionyl-CoA carboxylase. PA is complicated by acute life-threatening metabolic crises, which are precipitated by a catabolic state and result in multiple organ failure or even death, if untreated. A neonate with PA recovered from the first metabolic crisis 3 days after birth but developed a second metabolic crisis during the recovery phase. This patient was considered to have severe PA and

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Inanc, B., S. Matsui, and S. Ide. "Propionic acid accumulation in anaerobic digestion of carbohydrates: an investigation on the role of hydrogen gas." Water Science and Technology 40, no. 1 (1999): 93–100. http://dx.doi.org/10.2166/wst.1999.0021.

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This paper describes the experimental investigation into the accumulation of propionic acid under artificially lowered or elevated hydrogen gas levels. Vacuum operation at 0.13, 0.5, and 0.75 atm on the headspace of the reactors, and a selective permeable Teflon membrane placed in the liquid phase, were used to provide low hydrogen concentrations. In the elevated hydrogen concentration experiments, first, hydrogen gas (20% H2 + 80% N2) was bubbled into a batch CSTR reactor. Second, purer H2 gas (80% H2 + 20% CO2) was overpressurized at 2 atm in vials. Suspended cultures were used in all the ex

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7

Morland, Cecilie, Anne-Sofie Frøland, Mi Nguyen Pettersen, et al. "Propionate enters GABAergic neurons, inhibits GABA transaminase, causes GABA accumulation and lethargy in a model of propionic acidemia." Biochemical Journal 475, no. 4 (2018): 749–58. http://dx.doi.org/10.1042/bcj20170814.

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Propionic acidemia is the accumulation of propionate in blood due to dysfunction of propionyl-CoA carboxylase. The condition causes lethargy and striatal degeneration with motor impairment in humans. How propionate exerts its toxic effect is unclear. Here, we show that intravenous administration of propionate causes dose-dependent propionate accumulation in the brain and transient lethargy in mice. Propionate, an inhibitor of histone deacetylase, entered GABAergic neurons, as could be seen from increased neuronal histone H4 acetylation in the striatum and neocortex. Propionate caused an increa

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Kuley, Esmeray, Gulsun Özyurt, Ilyas Özogul, et al. "The Role of Selected Lactic Acid Bacteria on Organic Acid Accumulation during Wet and Spray-Dried Fish-Based Silages. Contributions to the Winning Combination of Microbial Food Safety and Environmental Sustainability." Microorganisms 8, no. 2 (2020): 172. http://dx.doi.org/10.3390/microorganisms8020172.

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Organic acid contents of acidified and fermented fish silages made from gibel carp (Caracius gibelio) and klunzinger’s ponyfish (Equulites klunzingeri) fishes, and from fish processing residues or by-products, were determined and studied. The silages were undertaken in wet and spray-dried fish-based raw-materials for 3 weeks at room temperature (ca. 25 °C). Selected lactic acid bacteria (LAB) of Enterococcus gallinarum, Lactobacillus brevis, Lactobacillus plantarum, Pediococcus acidilactici, and Streptococcus spp. were employed to produce fermented fish-based silages, while acidified silage wa

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WANG, L., Q. ZHOU, and F. LI. "Avoiding propionic acid accumulation in the anaerobic process for biohydrogen production." Biomass and Bioenergy 30, no. 2 (2006): 177–82. http://dx.doi.org/10.1016/j.biombioe.2005.11.010.

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Espinosa, A., L. Rosas, K. Ilangovan, and A. Noyola. "Effect of trace metals on the anaerobic degradation of volatile fatty acids in molasses stillage." Water Science and Technology 32, no. 12 (1995): 121–29. http://dx.doi.org/10.2166/wst.1995.0473.

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A laboratory UASB reactor was fed with cane molasses stillage at organic loadings from 5 to 21.5 kg COD/m3 d. With an organic load of 17.4 kg COD/m3 d, an accumulation of VFA, principally propionic acid, was observed due to little bioavailability or lack of trace metals (Fe, Ni, Co and Mo). Associated to this, the performance of the UASB reactor was low (44% COD removal efficiency), with an alkalinity ratio above 0.4. The addition of Fe (100 mg/l), Ni (15 mg/l), Co (10 mg/l) and Mo (0.2 mg/l) to the influent reduced significantly the level of propionic acid (5291mg/l to 251 mg/l) and acetic ac

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Dissertations / Theses on the topic "Propionic acid accumulation"

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Goswami, Vandana. "Improvement in propionic acid accumulation from lactose by propionibacterium acidipropionici." Thesis, 1999. http://localhost:8080/xmlui/handle/12345678/2731.

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Book chapters on the topic "Propionic acid accumulation"

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Manoli I. and Venditti C.P. "Disorders of Branched Chain Amino Acid Metabolism." In Metabolic Diseases. IOS Press, 2017. https://doi.org/10.3233/978-1-61499-718-4-117.

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The three essential branched-chain amino acids (BCAAs), leucine, isoleucine and valine, share the first enzymatic steps in their metabolic pathways, including a reversible transamination followed by an irreversible oxidative decarboxylation to coenzyme-A derivatives. The respective oxidative pathways subsequently diverge and at the final steps yield acetyl- and/or propionyl-CoA that enter the Krebs cycle. Many disorders in these pathways are diagnosed through expanded newborn screening by tandem mass spectrometry. Maple syrup urine disease (MSUD) is the only disorder of the group that is assoc

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