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Monolayers and Multilayers
Published in Victor M. Starov, Nanoscience, 2010
Hernán Ritacco, Iván López-Montero, Francisco Monroy, Francisco Ortega, Ramón G. Rubio
Phosphatydilcholines (PC) and phosphatydilethanolamines (PE) are zwitter ionic lipids while phosphatidylglicerol (PG) and phosphatydilserines (PS) have a net negative charge. PS is practically exclusive of the inner plasma membranes, being intimately related to maintaining a membrane potential, responsible for gating membrane transporters among other important essential functions of the membrane. Other nonchained lipids, like cholesterol (Chol), acting as small bricks, may fill in the gaps formed by kinks, so contributing to the structural stability of the bilayer. Cholesterol, in contrast, is not present in the plasma membrane of older organism as bacteria. Its structural effects are believed to be performed by other, apparently more complex, phospholipids, such as cardiolipin, which contains four hydrocarbon chains linked to a biglycerol polar head. Sphingolipids [sphingomyelin (SM) being the most important], constitute the second family of membrane lipids with hydrocarbon chains. The only difference with phospholipids is the presence of an amide group instead of a glycerol as a linker between the phosphate group and the hydrocarbon chains. The preferred lengths of these chains are similar to those of the phospholipids but, contrarily to those, sphingolipids are mostly saturated. These lipids are present in cholesterol-rich domains, named rafts, which are believed to play a crucial role not only in the function of transmembrane proteins but also in membrane mechanics. A lipid raft can be considered a disk-shaped bilayer aggregate, floating inside the continuous lipid bilayer, and made of a specialized lipid formula to favor the native folding of the membrane proteins. The mechanical role of rafts is yet a matter of debate. They are believed to be local reservoirs of condensed lipids, necessary for protein function, but if homogenously distributed could give rise to an unacceptably high viscosity of the membrane.
Environmental chemicals and adverse pregnancy outcomes: Placenta as a target and possible driver of pre- and postnatal effects
Published in Critical Reviews in Environmental Science and Technology, 2023
Jing Li, Adrian Covaci, Da Chen
Moreover, the regulation of PPARs signaling pathways by environmental chemicals may induce lipid metabolism in placental cells. TPhP can disturb lipid metabolism, increase the production of triglycerides, fatty acids, and phosphatidic acid, decrease the levels of phosphatidylethanolamine, phosphatidylserine, and sphingomyelin, and induce endoplasmic reticulum stress and cell apoptosis (Wang et al., 2021). Di(2-ethylthexyl) phthalate (DEHP) and MEHP are also known to disturb lipid synthesis in several organs and are high affinity ligands of the PPARγ (Melnick, 2001). In rat trophoblastic cells, DEHP and its metabolites (MEHP and 2-ethylhexanoic acid) increased the expression of PPARs (i.e., α, β, and γ) and disrupted fatty acid balance, which could lead to IUGR and impaired cognitive function (Xu et al., 2005). Also, MEHP induced an important change of JEG-3 cells lipidome, especially in glycerolipids and glycerophospholipids, with a marked accumulation of triacylglycerols (Petit et al., 2018), and inhibited human extravillous trophoblast HTR-8/SVneo cells invasion via the PPARγ pathway (Gao et al., 2017), which provides an insight in the mechanisms of DEHP-associated early pregnancy loss.
Unified Dosimetry Quality Audit Index: an integrated Monte Carlo model-based quality assurance ranking for radiotherapy treatment of glioblastoma multiforme
Published in Radiation Effects and Defects in Solids, 2023
Praveen Kumar C, Lalit M. Aggarwal, Saju Bhasi, Neeraj Sharma
CCWM521 within the phantom synthesised as white matter comprised of water, lipids and oligodendrocyte networks which provide energy substrates to axons. Composition was calculated from major constituent components for lipid assay as sphingomyelin, cerebroside, cholesterol, choline glycerophosphate, ethanolamine glycerophosphate and water content as 80.8%. Calculated elemental composition was C = 0.36792, H = 0.7818362, N = 0.048609, O = 1.5448296, Na = 0.000321856, P = 0.039558, S = 0.004, K = 0.005473762, with computed mean excitation energy = 49.1 eV and the density value assigned to the modest 1.093 g/cm3. The frontal part of the corpus callosum, genu width of 1.328 cm was assigned to the slab presuming photon beam direction incident onto the frontal lobe.
Longitudinal metabolic alterations in plasma of rats exposed to low doses of high linear energy transfer radiation
Published in Journal of Environmental Science and Health, Part C, 2021
Tixieanna Dissmore, Andrew G DeMarco, Meth Jayatilake, Michael Girgis, Shivani Bansal, Yaoxiang Li, Khyati Mehta, Vijayalakshmi Sridharan, Kirandeep Gill, Sunil Bansal, John B Tyburski, Amrita K Cheema
Complex cellular responses triggered by exposure to non-lethal doses of ionizing radiation may lead to changes in metabolomic profiles depending on radiation type and dose.18–22 In this study, we report the results from a rat model aimed at delineating longitudinal alterations in the plasma metabolome after exposure to 0.5 Gy of 1H (250 MeV) or 16O (600 MeV/n) radiation. The dysregulated metabolites included certain classes of lipids such as phosphatidylethanolamine (PE), ceramide, sphingomyelin (SM) and lysophosphatidic acid (LPA). Pro-inflammatory cytokines and oxidative stress may stimulate the generation of SMs, from the ceramide response to sphingomyelin synthase in the Golgi apparatus.23 Dysregulation observed in SM(24:1) at the 3-month time point may indicate some degree of neuronal damage.24 Additionally, we found a significant increase in eicosapentaenoyl PAF C-16 after exposure to 0.5 Gy of 1H at 12 the month time point, which may be because of ionizing radiation-mediated oxidation of phospholipids. Radiation-induced peroxidation of fatty acids may indicate cellular damage at various levels.25,26 Lastly, we observed decreased levels of LPA(18:0) after exposure to 1H and 16O at 12 months. Previously it has been reported that inflammatory prostaglandins Phosphatidylcholine (PC) generates lysophosphatidylcholine (LPC) and lysophosphatidic acid (LPA) through the actions of Pla2) and phospholipase D (Pld) that is further converted to Phosphatidic acid (PA). Decreased levels of LPA may suggest increased levels of PA that can directly stimulate G protein-coupled receptor activation of mTor through resulting in increased cell proliferation.27