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Managing Crush Injuries on Arrival
Published in Kajal Jain, Nidhi Bhatia, Acute Trauma Care in Developing Countries, 2023
Sarvdeep Singh Dhatt, Deepak Neradi
Mannitol (osmotic diuretic and free radical scavenger) may be used to treat and prevent ARF. It also helps to reduce compartment pressure by osmotic diuresis and decreasing vascular permeability. However, due to possible complications [nephrotoxicity/congestive heart failure (CHF)], its use is controversial and should be started/titrated according to urine output. Furosemide (loop diuretic) should be avoided, as it acidifies urine and promotes myoglobulin precipitation. Hyperkalaemia is an early sign of cardiac arrhythmia and needs early corrective measures. Early administration of 15 g/day of sodium polystyrene sulfonate (potassium binder) can be used to prevent fatal hyperkalaemia due to reperfusion injury. Correction of hypocalcaemia should be avoided, as administered calcium gets trapped in injured muscles and causes metastatic calcification and rebound hypercalcaemia. Calcium should be used only to prevent hyperkalaemic cardiac arrhythmia. Allopurinol (xanthine oxidase inhibitor) given early may be used to protect from reperfusion injury to ischaemic cells by reducing free radical formation. Dialysis is required in hyperkalaemia/metabolic acidosis resistant to medical therapy, volume overload and uraemia. Dialysis is usually required two to three times daily for 2 weeks to restore renal function. Crush victims are at increased risk of sepsis, systemic inflammatory response syndrome (SIRS) or multi-organ failure; therefore, they require intensive care monitoring, aggressive treatment of open injuries and nutritional supplementation.
Replicase
Published in Paul Pumpens, Single-Stranded RNA Phages, 2020
The finding on the Qβ replicase inhibition by polyethylene sulfonate was of a special importance. The polyethylene sulfonate at low concentrations inhibited the initiation, but not elongation, of RNA synthesis by Qβ replicase (Kondo and Weissmann 1972b). It allowed in turn the controlled, stepwise synthesis of RNA by the Qβ enzyme (Bandle and Weissmann 1972). The polyethylene sulfonate affected a step subsequent to the primary binding of Qβ RNA to the replicase and prior to the formation of the first few internucleotide bonds. Therefore, if addition of polyethylene sulfonate to the Qβ RNA-directed Qβ replicase reaction after initiation has taken place, it led to the exclusive formation of free, single-stranded minus strands. Moreover, the inhibition by polyethylene sulfonate could be reversed by the addition of an appropriate quantity of protamine sulfate.
Cleansing of Hair
Published in Dale H. Johnson, Hair and Hair Care, 2018
c. Alkyl Sulfonates. The alkyl sulfonates most commonly used in shampoos are alpha-olefin sulfonates (AOS). They are prepared by sulfonating alpha olefins with sulfur trioxide. Subsequent neutralization produces a mixture of alkene sulfonates and hydroxy alkane sulfonates. The chemical structures of these two sulfonates are as follows: where R is an alkyl chain with 12 to 14 carbons, and M is a cation such as sodium.
Bulk phase resource ratio alters carbon steel corrosion rates and endogenously produced extracellular electron transfer mediators in a sulfate-reducing biofilm
Published in Biofouling, 2019
Gregory P. Krantz, Kilean Lucas, Erica L.- Wunderlich, Linh T. Hoang, Recep Avci, Gary Siuzdak, Matthew W. Fields
One of the confirmed dysregulated metabolites, sulfolactate, was increased 15.7-fold under EAL conditions on 1018 steel (Figure 7). Sulfolactate is a sulfonate compound related to the cysteine/methionine processing pathways in some microorganisms. A complete pathway from cysteine to sulfolactate is not predicted in the Desulfovibrio G20 genome whereas the genome is annotated to contain an aminotransferase that could convert cysteate to sulfopyruvate (E.C. 2.6.1.1; KEGG). However, the genome annotation does not contain an identified enzyme to catalyze the conversion of sulfopyruvate to sulfolactate. The commonly identified enzymes with this activity include sulfolactate dehydrogenase (R and S) and malate dehydrogenase and would provide additional electron acceptor (reduction of sulfopyruvate to sulfolactate) via recycling of cysteine through cysteate and could account for the elevated sulfolactate levels that were detected under EAL conditions. The Desulfovibrio G20 genome is annotated to have a gene that encodes a protein with potential malate dehydrogenase activity (Dde1008, NAD+-linked). Sequence comparisons and biochemical studies have recently expanded the functionality of previously annotated malate and lactate dehydrogenases to have other activities such as sulfolactate dehydrogenase (Muramatsu et al. 2005); however, the potential role of Dde1008 in conversion of sulfopyruvate to sulfolactate is unknown.
Xenobiotic C-sulfonate derivatives; metabolites or metabonates?
Published in Xenobiotica, 2018
In the 1970s reports appeared stating that the major urinary metabolite obtained following the topical application to rats, rabbits and pigs of 2-pyridinethiol-1-oxide (2-mercaptopyridine N-oxide; pyrithione) (Shaw et al., 1950), an antimicrobial agent, was pyridine-N-oxide-2-sulfonic acid (Howlett & Van Abbe, 1975; Min et al., 1970; Wedig et al., 1978). This sulfonic acid was also present in the urine of pigs following intravenous administration (Adams et al., 1976) and detected in rabbit tissues following dermal application (Howlett & Van Abbe, 1975). However, with this compound the sulfur atom was already bonded to a carbon of the pyridine ring before administration and the sulfonic acid metabolite identified was a product of extensive oxygenation of this preexisting sulfur atom and not the result of the addition of a sulfonate group. It was suggested that the dimerization product, 2,2′-(pyridyl-N-oxide) disulfide, identified as a metabolite, was oxidized via the disulfoxide to the disulfone and finally cleaved to yield the sulfonic acid (Figure 1) (Min et al., 1970). Similar pathways have been advocated for glutathione disulfide (Schröder & Eaton, 2009).
Steroid sulfatase inhibitors: the current landscape
Published in Expert Opinion on Therapeutic Patents, 2021
Hanan S. Anbar, Zahraa Isa, Jana J. Elounais, Mariam A. Jameel, Joudi H. Zib, Aya M. Samer, Aya F. Jawad, Mohammed I. El-Gamal
Sulfamate is the universal and the most successful warhead in the structures of STS inhibitors. It causes the inhibitor to act as an irreversible inhibitor of STS enzyme. Other moieties such as sulfonate are much less successful, and the researchers must refrain from using them and stick to sulfamate. N-phosphorylated derivatives are also interesting and worth further deep investigations. In addition, free sulfamate (-O-SO2-NH2) derivatives have been reported to be more potent than any mono- or disubstituted sulfamate (-O-SO2-NHR or -O-SO2-NR2). The insertion of halo substituent ortho to the free sulfamate moiety can contribute to stronger inhibition. We recommend consideration of this in future research projects in the field of design and synthesis of new STS inhibitors. Moreover, the non-steroidal derivatives have less potential to produce estrogenic side effect than steroidal sulfamate analogs. Therefore, the recent studies should focus on the non-steroidal derivatives such as irosustat and most of the recently reported inhibitors. Furthermore, the design of dual STS inhibitor and SERM, tubulin polymerization inhibitor, aromatase inhibitor, or 17β-HSD1 inhibitor can lead to therapeutically efficient synergism. Meanwhile, combination of potent STS inhibitors with SERM, tubulin inhibitors, aromatase inhibitor, or 17β-HSD1 inhibitor can lead to similar result. Lastly, the overall hydrophobicity of the molecule can play a role in cancer cell membrane penetration. The researchers should retain the free sulfamate part and modify the other part of the molecule to achieve this goal keeping in mind the balance between hydrophobicity and hydrophilicity for high drug-like properties.