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Eichhornia crassipes: Shedding Light on its Chemical Composition, Biological Activities and Industrial Uses
Published in Mahendra Rai, Shandesh Bhattarai, Chistiane M. Feitosa, Ethnopharmacology of Wild Plants, 2021
Fadia S. Youssef, Noor H. Aysa, Mohamed L. Ashour
The rapid environmental variations and their concomitant effects greatly influence the advances in sustainable international power sources. There is a developing mission to enlarge the stockpile of biomass assets for bioenergy creation. E. crassipes acts as a potential alternative energy source since it is available extensively in freshwater, marine, and aquatic ecosystems throughout the world (Sricoth et al. 2018, Venu et al. 2019). It acts as a promising candidate for fuel ethanol production in tropical countries because of their high availability and high biomass yield (Das et al. 2016, Sayago 2019).
Alcohol, drugs, toxins and post-mortem toxicology
Published in Helen Whitwell, Christopher Milroy, Daniel du Plessis, Forensic Neuropathology, 2021
Colin Smith, Christopher Milroy
Ethanol is an alcohol consumed in alcoholic beverages. It produces neurological dysfunction both directly and secondary to vitamin deficiencies and metabolic dysfunction (Sutherland et al. 2014a). Alcohol is typically consumed orally and rapidly absorbed by the gastrointestinal tract, mostly in the small bowel. It is not bound by plasma proteins, so is rapidly diffused in the blood stream. Because it is essentially not absorbed by fat or bone, its volume of distribution is related to the total body water. As such men have a lower blood ethanol compared with women when the same amount of ethanol is consumed. Alcohol is metabolised to acetaldehyde via three main enzyme pathways: alcohol dehydrogenase (ADH), microsomal ethanol oxidising system (MEOS), which requires the CYP2E1 enzyme system, and peroxisomal catalase, though the latter pathway is not significant in vivo. Non-oxidative pathways also occur. ADH is the main pathway at low concentrations but with chronic use MEOS becomes more important. The rate of metabolism of ethanol is typically 15–18 mg/100 mL per hour but may vary between 10 and 25 mg/100 mL per hour. Alcohol elimination is a zero order process at high concentrations, but this is not the case with very low concentrations. Most ethanol is metabolised in the liver. This results in the production of acetoacetate which is converted to acetate.
Disposition and Metabolism of Drugs of Dependence
Published in S.J. Mulé, Henry Brill, Chemical and Biological Aspects of Drug Dependence, 2019
Ethanol is a clear, colorless, mobile, flammable liquid b. 78.5°C, with pleasant odor and a burning taste. It is miscible with water and organic liquids. The level of blood alcohol associated with coma is usually between 0.45 to 0.55% by weight, the fatal level being 0.60 to 0.90%, which is further lowered to 0.35% in the presence of barbiturates.
Ocular Manifestations After Acute Methanol Poisoning
Published in Neuro-Ophthalmology, 2023
Maamouri Rym, Nabi Wijden, Maamouri Héla, Sassi Héla, Brahmi Nozha, Monia Cheour
In this study we evaluated ocular abnormalities after severe acute methanol poisoning. We assessed ophthalmological findings of 21 patients diagnosed with acute methanol poisoning requiring medical intensive care. All of the patients were young or middle-aged males. The mean blood methanol level was significantly higher in patients without ocular symptoms (p = .03). We hypothesise that the absence of a positive correlation between mean blood methanol level and ocular symptoms may suggest that, even with very low blood levels, ocular toxicity thresholds may be reached. This can be explained by a major sensitivity of ocular structures to methanol-derived toxins. Some have studies demonstrated that the incidence of ocular abnormalities correlated with the volume of methanol consumed,9 while other authors have shown an absence of correlation.10 It is noteworthy that some factors may influence methanol toxicity and enhance its effect like the concomitant ingestion of ethanol or the treatment administered.3,11
Dissolution thermodynamics and preferential solvation of genistein in some (ethanol + water) mixtures at different temperatures
Published in Drug Development and Industrial Pharmacy, 2022
Guanjun Nan, Yanru Huang, Zhengzheng Liu, Yu Liu, Yunzhe Li, Guangde Yang
It has been reported that genistein could be isolated from natural products, such as soybeans [15], the Ginkgo biloba leaves [16], quinoa seeds (Chenopodium quinoa Willd.) [17], and Radix Puerariae lobatae [18]. Many solvents have been employed to extract isoflavonoids, including water, ethanol, methanol, acetone, and acetonitrile [19,20]. Thanks to its non-toxicity, low cost and miscibility with water in all proportions, ethanol is an ideal organic solvent that widely used in the separation and purification process of isoflavonoids [21,22]. Usually, the low solubility of compounds leads to failure in the medication development process. The solubility of drugs in common solvents is helpful for optimal formulation and application of therapeutic dose to enhance absorption and bioavailability. In the pharmaceutical sciences, ethanol is a common cosolvent employed to change aqueous solubility of chemicals and pharmaceuticals. Therefore, it is significant to obtain the solubility data of genistein in the binary system of ethanol and water to obtain comprehensive physicochemical data for the drug.
Treating ethylene glycol poisoning with alcohol dehydrogenase inhibition, but without extracorporeal treatments: a systematic review
Published in Clinical Toxicology, 2022
Jessie Beaulieu, Darren M. Roberts, Sophie Gosselin, Robert S. Hoffman, Valery Lavergne, Knut Erik Hovda, Bruno Megarbane, Derrick Lung, Ruben Thanacoody, Marc Ghannoum
Ethanol also appears efficient and safe when used as monotherapy in the absence of AKI and acidemia. However, there were several failures within the cutoffs identified above [56,67,73,89,123,132]. A subtherapeutic ethanol concentration (from reducing the ethanol infusion rate due to CNS effects) may have contributed to some of these failures [47,67,89,91]. Further evidence of the limitations of ethanol therapy is also demonstrated by patients presenting with end-organ injury despite having co-ingested ethanol and having a therapeutic ethanol concentration on presentation. [157] Additionally, the ADH inhibition from ethanol is weaker than fomepizole [7,8]. Ethanol also carries risks, including altered mental status, hepatitis, pancreatitis and gastritis and hypoglycemia in children [45]. Contrary to fomepizole, the ethylene glycol dose and concentration appear predictive of ethanol failure (Tables 2A and 2B); this may reflect fomepizole’s higher affinity or better efficiency compared to ethanol [158].