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Monographs of Topical Drugs that Have Caused Contact Allergy/Allergic Contact Dermatitis
Published in Anton C. de Groot, Monographs in Contact Allergy, 2021
Lactic acid is a normal intermediate in the fermentation (oxidation, metabolism) of sugar. It may be used in topical drugs, notably with salicylic acid in collodion for the treatment of warts. It is also applied with calcium chloride, magnesium chloride, dextrose monohydrate, sodium chloride, and sodium bicarbonate in replacement solutions in Continuous Renal Replacement Therapy to replace plasma volume removed by ultrafiltration. The sodium salt of racemic or inactive lactic acid (sodium lactate) is a hygroscopic agent used intravenously as a systemic and urinary alkalizer. Topical preparations containing (mostly) 12% ammonium lactate are indicated for the treatment of dry, scaly skin (xerosis) and ichthyosis vulgaris and for temporary relief of itching associated with these conditions. Lactic acid is also used to make cultured dairy products, as a food preservative, and to produce other chemicals (1).
Acinetobacter — Microbiology
Published in E. Bergogne-Bénézin, M.L. Joly-Guillou, K.J. Towner, Acinetobacter, 2020
Most strains are unable to reduce nitrate, which explains the previous designation Bacterium anitratum. Ammonium and nitrate salts can serve as sources of nitrogen (Baumann et al., 1968). The nutritional spectrum can be used for phenotypic assignment of strains to different genomic species (Bouvet and Grimont, 1986; 1987; Bouvet and Jeanjean, 1989; Gerner-Smidt et al., 1991; Gennari and Lombardi, 1993; Kampfer et al., 1993). Strains of several genomic species produce acid from glucose, although usually they do not use this substrate for growth. The acidification of glucose is mediated by a non-specific aldolase which also mediates oxidation of lactose, D-mannose, L-arabinose and D-xylose (Baumann et al., 1968). The aldolase has been shown to be a quinoprotein with pyrroloquinoline quinone (PQQ) as a cofactor (Duine, 1991). No other carbohydrate-acidifying enzymes have been found in Acinetobacter.
Overview of Renal Control of Acid–Base Balance
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The catabolism of protein and oxidation of the constituent amino acids by the liver produces some glutamine. The proximal tubular cells take up glutamine and metabolize it to ammonium ions. The ammonium ions are secreted into the tubular lumen by counter-transport with sodium ions, and bicarbonate diffuses into the peritubular capillaries (Figure 45.3). This is new bicarbonate that is added to the peritubular capillary blood. Ammonium is the protonated form of ammonia. It is an extremely weak acid as it dissociates to ammonia and hydrogen ions.
Purification and characterisation of glutathione reductase from scorpionfish (scorpaena porcus) and investigation of heavy metal ions inhibition
Published in Journal of Enzyme Inhibition and Medicinal Chemistry, 2023
The purification process began with the homogenate preparation step. Ammonium sulphate precipitations in the range of 0–100% were performed on the prepared liver tissue. The GR enzyme precipitated in the intervals of 60–80% during the precipitation procedure. After precipitation, dialysis was performed to remove ions in the medium before affinity chromatography. Following dialysis, purification was performed on a 2′,5′-ADP Sepharose 4B affinity column, and the molecular weight of GR was determined using the SDS polyacrylamide gel electrophoresis. The liver tissue was purified 25.96 times with a yield of 28.277% and its molecular weight was determined to be 25 kDa. Quantitative protein determination was determined by the Bradford method. Ni2+, Mn2+, Cr3+, and Cd2+ heavy metals were applied on the purified enzyme. IC50 values of heavy metals were calculated as 2.4 µM, 30 µM, 135 µM and 206 µM, for Mn2+, Cd2+, Ni2+, and Cr3+, respectively.
Preclinical and clinical developments in enzyme-loaded red blood cells: an update
Published in Expert Opinion on Drug Delivery, 2023
Marzia Bianchi, Luigia Rossi, Francesca Pierigè, Sara Biagiotti, Alessandro Bregalda, Filippo Tasini, Mauro Magnani
Hyperammonemia is mostly caused by chronic liver diseases and congenital defects in the urea cycle’s enzymes. As reviewed in Rossi et al. [8], the excessive ammonium blood concentration is neurotoxic, producing many neurological complications, such as hepatic encephalopathy, convulsions, up to coma and death, and currently available medications are not completely successful. Erythrocyte-bioreactors, containing enzymes that process ammonium, have been proposed to remove this byproduct of many reactions from the blood [11,12,13]; the most promising ones were engineered to co-encapsulate glutamate dehydrogenase (GDH) and alanine aminotransferase (ALT) (Figure 2), thus creating a metabolic pathway where α-ketoglutarate and L-glutamic acid were produced and consumed cyclically [55]. However, the low encapsulation rate of a commonly employed bovine liver GDH made the clinical use of this approach unfeasible. Recently, in Borsakova et al. [56], new bioreactors containing ALT and a non-aggregating new bacterial GDH enzyme from Proteus species at higher loading were produced, and the efficacy of these erythrocytes was demonstrated in vitro. The ammonium consumption rate increased linearly with an increase in encapsulated GDH activity and in accordance with alanine production, which indicated the joint functioning of both encapsulated enzymes. These preliminary results defined the most promising conditions to achieve therapeutic efficacy of such bioreactors and for their future clinical use as treatment to reduce ammonia levels.
Exosome mimetics derived from bone marrow mesenchymal stem cells deliver doxorubicin to osteosarcoma in vitro and in vivo
Published in Drug Delivery, 2022
Jinkui Wang, Mujie Li, Liming Jin, Peng Guo, Zhaoxia Zhang, Chenghao Zhanghuang, Xiaojun Tan, Tao Mi, Jiayan Liu, Xin Wu, Guanghui Wei, Dawei He
Adherent cells were isolated by scraping, and the collected BMSCs were re-suspended in phosphate-buffered saline (PBS) at a concentration of 5 × 106 cells/mL. The Extruder (Avanti Mini-Extruder) was used for two sequential extrusions through a 10-μm and 5-μm polycarbonate membrane filter (Whatman), as in the previous article (Jang et al., 2013). Then super centrifuged at 100,000g for 70 min and re-suspend in 240 mM ammonium sulfate solution. The monodisperse nanoscale EMs were then prepared using a miniature extruder (Avanti Mini-Extruder) through a 1-μm polycarbonate membrane filter (Whatman). Then slide-A-Lyzer Nutritional Cassette (MWCO 20 kDa) was used overnight at room temperature at 2 L PBS (pH7.4) to remove ammonium sulfate outside EMs and form an ammonium sulfate concentration gradient. Then doxorubicin was added to EMs with a concentration of 1010 particles/mL at a final concentration of 0.2–1 mg/mL and incubated at room temperature for 6 h to promote the loading of doxorubicin into EMs. The preparation method of ammonium sulfate was described in previous literature (Guo et al., 2021). A doxorubicin-encapsulating EM (EM-Dox) solution was injected into slide-A-Lyzer Nutritional Cassette (MWCO 20 kDa) and dialyzed in PBS (pH7.4) overnight at room temperature to remove free doxorubicin. We used the same method to prepare the blank EMs using a miniature extruder (Avanti mini-extruder) through a 10-μm, 5-μm, and 1-μm polycarbonate membrane filter (Whatman) for three sequential extrusions.