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Molecular Mechanisms for Statin Pleiotropy and Possible Clinical Relevance in Cardiovascular Disease
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2020
Brian Yu, Nikola Sladojevic, James K. Liao
The primary mechanism of action for all statins is competitive inhibition of HMG-CoA reductase, the rate-limiting enzyme in the synthesis of cholesterol. HMG-CoA reductase catalyzes a four-electron deacetylation, converting HMG-CoA to L-mevalonate and coenzyme A (Fig. 10.1). Lovastatin, simvastatin, and pravastatin are fungal-derived inhibitors of HMG-CoA reductase (type 1 statins), while fluvastatin, atorvastatin, rosuvastatin, and pitavastatin are synthetically derived (type 2 statins) (Endo, 2010). There are three main structures within each compound (Fig. 10.2): (1) the HMG-like moiety mimicking HMG-CoA (in the form of a lactone ring); (2) a hydrophobic ring structure that plays a role in binding of statin to HMG-CoA reductase; (3) side groups on the rings that alter solubility and pharmacokinetic properties (Istvan, 2003). For instance, atorvastatin, simvastatin, lovastatin, and fluvastatin are relatively lipophilic, while rosuvastatin and pravastatin are relatively hydrophilic due to the polar methyl sulfasomidine group and hydroxyl group, respectively. Lipophilic statins can cross cell membranes by cell diffusion, while rosuvastatin and pravastatin require organic anion-transporting polypeptide 1B1 transporters, and are therefore more selective for hepatic tissues (Schachter, 2005). However, hydrophilic statins also exert extrahepatic effects in animals and human studies. It is likely there are yet unknown mechanisms for hydrophilic statins to enter non-hepatic cells, explaining their action on cell types such as endothelial cells.
Medicinal Mushrooms
Published in Anil K. Sharma, Raj K. Keservani, Surya Prakash Gautam, Herbal Product Development, 2020
Temitope A. Oyedepo, Adetoun E. Morakinyo
Over the years, researchers have discovered that certain mushrooms, especially Pleurotus, have the ability to lower cholesterol (Bobek et al., 2001). Further work has discovered statins, the secondary metabolites, as the most likely compound responsible for this action (Alam et al., 2011). Lovastatin (mevinolin) is a statin that occurs in most of the basidiomycetes just like many other fungi. It is a powerful inhibitor of HMG-CoA reductase, the main rate-limiting enzyme in cholesterol production. Lovastatin analysis could serve as another marker for species with elevated levels of this compound. This should, however, be merged with the fact that quite high amounts of mushroom powder would be necessary to effect any action (Lo et al., 2012).
Nanomaterials: Tools, Technology, and Methodology of Nanotechnology-Based Biomedical Systems for Diagnostics and Therapy
Published in Shaker A. Mousa, Raj Bawa, Gerald F. Audette, The Road from Nanomedicine to Precision Medicine, 2020
Christian Schmidt, Joachim Storsberg
Here, three molecules of acetyl-coenzyme A (abbreviated as Ac-CoA) are used to form 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) in the presence of HMG-CoA synthase and the release of two reduced forms of CoA. The HMG-CoA reductase then catalyzes the generation of mevalonate, which now serves as the source for the biogeneration of IPP and subsequent downstream synthesis products [29, 30].
High yield production of lipid and carotenoids in a newly isolated Rhodotorula mucilaginosa by adapting process optimization approach
Published in Biofuels, 2023
Ravi Gedela, Ashish Prabhu, Venkata Dasu Veeranki, Pakshirajan Kannan
In oleaginous yeast, the hydrophilic substrate is consumed via the de novo pathway, and the lipid accumulation proceeds with the depletion of nitrogen compound, which in turns activate AMP deaminase. This activity leads toa series of cascade reactions, which disturbs the TCA cycle in mitochondria and splits the ATP-citrate lyase and acetyl-CoA and oxaloacetate. Further, the acetyl CoA is carboxylated in to malonyl CoA which is the first step of lipid synthesis, and then followed a by series of enzymatic reactions catalyzed by a complex of fatty acid synthases, which ultimately leads to the synthesis of triacyl glycerol. Further in yeast such as Rhodoturula sp that is capable of synthesizing carotenoids, which initiates by the conversion of acetyl CoA to 3 hydroxyl-3 methylglutaryl-CoA catalyzed by 3 hydroxyl-3 methylglutaryl-CoA synthase. Consequently, the HMG- CoA is reduced to mevalonic acid by HMG-CoA reductase and the cascade of reaction takes place for the production of isopentenyl diphosphate (IPP), which is further subjected to an isomerization reaction to form dimethylallyl pyrophosphate (DMAPP), and the addition of 3 molecules of IPP to DMAPP results in geranylgeranyl pyrophosphate (GGPP). The GGPP undergoes a condensation reaction catalyzed by phytoene synthase to form phytoene and finally converted to β-carotene [18]. The biochemical pathway for the formation of lipids and carotenoids in Rhodotorula sp is depicted in Figure S1 (Supplementary Material).
Reproductive outcomes in rat female offspring from male rats co-exposed to rosuvastatin and ascorbic acid during pre-puberty
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Gabriel Adan Araujo Leite, Thamiris Moreira Figueiredo, Tainá Louise Pacheco, Marina Trevizan Guerra, Janete Aparecida Anselmo-Franci, Wilma De Grava Kempinas
Among the lipid-lowering drugs, statins are considered effective due to their efficient reduction of total cholesterol in the blood (Endres 2006; Istvan 2003; Tandon et al. 2005). Statins decrease cholesterol concentrations by inhibiting the enzyme 3-hydroxy-3-methylglutharyl coenzyme A reductase (HMG-CoA reductase) (Istvan and Deisenhofer 2001; Jiménez and Ferre 2011) and preventing the conversion of HMG-CoA to mevalonate, thus reducing intermediate isoprenoids and cholesterol formation (Adam and Laufs 2008; Istvan 2003). The incidence rate of statin prescription to treat hypercholesterolemia in the pediatric population represents 63% of all pharmacotherapies (Liberman, Berger, and Lewis 2009); however, there are no apparent available data specifically for rosuvastatin prescription.
Development and in vitro appraisal of Soluplus® and/or Carbopol® 971 buccoadhesive patches releasing atorvastatin
Published in The Journal of Adhesion, 2022
Aseel Abu-Rumman, Rana Abu-Huwaij, Rania Hamed
An elevated plasma cholesterol level (hypercholesterolemia) is one of the most common causes of death worldwide and can be correlated with a high risk of several diseases such as myocardial infarction, atherosclerosis, or stroke.[1] Statins or 3-hydroxy-3-methylglutaryl-coenzyme (HMG-CoA) reductase competitive inhibitors are the most potent antihyperlipidemic agents, which effectively lower low-density lipoprotein in a dose-dependent manner, by approximately 35–61% with maximal doses, and 20–38% with initial doses .[2]