Facilitated diffusion: facilitated diffusion involves the movement of molecules down their concentration gradients. It differs from simple diffusion in the fact that a carrier protein or a channel protein within the cell membrane helps them get from one side to the other. This is also a passive process. An example of facilitated diffusion is the movement of glucose molecules into liver cells through glucose transporter proteins embedded in the plasma membrane.
Active transport: when molecules move against their concentration gradients (so from a region of low concentration to a region of high concentration), they do so by active transport. This involves a carrier protein which carries the molecule from one side of the membrane to the other. It is an active process and uses ATP to release energy. An example is the transport of glucose from the villi of the intestine into the bloodstream.
Endocytosis: if substances are too large to cross the membrane, they enter the cell by endocytosis. The cell surrounds the substance and folds its membrane around it. The membrane then pinches off to engulf the substance, which causes a vesicle to form inside the cell containing the ingested substance. This is an active process so will require energy in the form of ATP. An example of endocytosis is when phagocytes carry out phagocytosis, in which the phagocyte engulfs a whole bacterium in order to destroy it.
Exocytosis: when large substances need to leave the cell, such as hormones and digestive enzymes, they do so by exocytosis. These substances will be contained inside vesicles which move towards the plasma membrane and fuse with it. This causes the substances to either be released outside of the cell or they will be inserted straight into the membrane (for example, if the substance is a membrane protein). Exocytosis is an active process which requires ATP.
Extensive microscopic molecular dynamics simulations have been performed to study the effects of short-chain alcohols, methanol and ethanol, on two different fully hydrated lipid bilayer systems (POPC and DPPC) in the fluid phase at 323 K. It is found that ethanol has a stronger effect on the structural properties of the membranes. In particular, the bilayers become more fluid and permeable: ethanol molecules are able to penetrate through the membrane in typical timescales of ∼200 ns, whereas for methanol that timescale is considerably longer, at least of the order of microseconds. A closer examination exposes a number of effects due to ethanol. Hydrogen-bonding analysis reveals that a large fraction of ethanols is involved in hydrogen bonds with lipids. This in turn is intimately coupled to the ordering of hydrocarbon chains: we find that binding to an ethanol decreases the order of the chains. We have also determined the dependence of lipid-chain ordering on ethanol concentration and found that to be nonmonotonous. Overall, we find good agreement with NMR and micropipette studies.
Ethanol disrupts the physical structure of cell membranes. The most fluid membranes, including those that are low in cholesterol, are the most easily disordered by ethanol. Although the membrane-disordering effect is small, there is pharmacological, temporal, and genetic evidence that it is important. Animals that are resistant to ethanol intoxication because of their genetic background or because of previous exposure to ethanol are found to have brain membranes that are not easily disordered in vitro. An exception is the increased behavioral sensitivity in aging animals, which is not matched by changes in their membranes. When animals are treated chronically with ethanol, their membranes become stiffer, a response that can be regarded as adaptive. Ethanol may favor the uptake of cholesterol or saturated fatty acids into membranes, thus reducing its own effect.
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2022, Clinical Nutrition Open Science Show abstractNavigate Down The biological membranes are important for cell structure and function but, during diseased conditions such as diabetes and in chronic alcoholism, they may be impaired. Nitroxidative stress mediated by persistent hyperglycemia is a major complication in diabetics with alcohol abuse. The present study is intended to investigate the antioxidant, anti-diabetic, and hepatoprotective effects of aqueous green tea extract (GTE) against cumulative effects of alcohol and diabetic pathology, focusing liver mitochondrial membranes. Mitochondrial membrane fluidity and membrane Na+/K+ and Mg2+ATPases were measured. Displacement loop (D-loop) of mitochondrial DNA (mt-DNA) was screened by PCR-Sanger's sequencing method. In addition, nuclear and mitochondrial encoded genes were analyzed. Molecular docking studies were performed to screen potential targets using the docking module implemented in Pyrx2010. In the present study, marked mitochondrial-DNA deletions were observed in diabetic-alcohol group which were ameliorated by GTE treatment. Also, GTE restored the alterations in the exacerbated levels of membrane fluidity and activities of Na+/K+ and Mg2+ ATPase to normalcy. ADME properties were evaluated for the ligand, Epigallocatechin 3 Gallate (EGCG) and reference drug, Rosiglitazone (RTG). It showed that, higher binding affinities and energy profiles of EGCG with the active site ofinducible nitric oxide synthase (iNOS) compared to RTG making non-bonded interactions with their active residues and surrounding allosteric residues. The present investigation demonstrated that, EGCG would be a promising next generation anti-diabetic compound as well as anti-inflammatory drug, and may be effectively used in the treatment of hepatopathy induced by double jeopardy of diabetes and alcohol abuse. 2022, Chemosphere Show abstractNavigate Down This study aimed to reveal possible alterations to lipidomic profiles in Sydney rock oysters, Saccostrea glomerata, exposed to estrogenic mixtures (i.e., estrone, E1; 17β-estradiol, E2; estriol, E3; 17α-ethinylestradiol, EE2; bisphenol A, BPA; 4-t-octylphenol, 4-t-OP; and 4-nonylphenol, 4-NP) at “low” and “high” concentrations, typical of those detected in Australian and global receiving waters. A seven-day acute exposure window exhibited significantly lower abundances of many non-polar metabolites in digestive gland, gills, and gonads. Overall, there was a strong effect of the carrier solvent ethanol (despite a low exposure of 0.0002%), with all solvent containing treatments exhibiting lower abundances of lipidic metabolites, especially in the gill and digestive gland. No significant changes of the lipidome were exhibited in the male gonad by estrogenic exposure. However, in the female gonad, significant reductions of phospholipids and phosphatidylcholine were associated with exposure to high estrogenic mixtures. We hypothesise that the decreases in these phospholipids in the female gonad may be attributable to 1) lower algal consumption and thus lower uptake of lipidic building blocks; 2) a reduction of available substrates for phospholipid and phosphatidylcholine synthesis; and/or 3) induction of reactive oxygen species via estrogen metabolism, which may cause lipid peroxidation and lower abundance of phospholipids. 2022, Advances in Neurotoxicology Show abstractNavigate Down Alcohol use disorder is a condition in which the individual keeps drinking alcohol despite repeated attempts to stop or control such behavior, which in turn generates negative social, occupational, and health consequences. Animal models have been developed to reproduce the deleterious effects of excessive ethanol intake, including ethanol-induced conditioned inflammation. There are several mechanisms underlying ethanol-induced toxicity. The excitotoxicity and downstream effects resultant of an imbalance in excitatory/inhibitory currents and the products of ethanol metabolism, in conjunction with the oxidative microenvironment product of oxidative/nitrosative stress rank among the most accepted mechanisms contributing to ethanol-induced neuronal dysfunction. Yet the emergence of mitochondrial dysfunction that decreases ATP along with increases in intracellular Ca2 + concentrations, plus the disruption of the NADH/NAD+ ratio is also relevant. Ferrous Fe overload and the inflammatory damage due to excessive alcohol intake or withdrawal are also key players underlying ethanol-induced neurotoxicity. Furthermore, a relationship between neuroinflammation and oxidative stress is recognized as a result of dopamine metabolism, inadequate functionality of the cystine-glutamate antiporter, mitochondrial dysfunction, and peripheral inflammation, that altogether lead to cell death. On this basis, a few therapeutic approaches have been approved to treat alcohol use disorder, albeit many others are still under scrutiny. The knowledge of the cellular and molecular mechanisms underlying alcohol use disorder is needed to provide new insights that fuel the development of new pharmacologically-relevant treatments. 2021, Phytochemistry Letters Show abstractNavigate Down This article has been withdrawn: please see Elsevier Policy on Article Withdrawal (//www.elsevier.com/locate/withdrawalpolicy). This article has been withdrawn at the request of the editor and publisher. The publisher regrets that an error occurred which led to the premature publication of this paper. This error bears no reflection on the article or its authors. The publisher apologizes to the authors and the readers for this unfortunate error. 2021, Optics and Laser Technology Show abstractNavigate Down Nickel-titanium (nitinol) is a biocompatible shape memory alloy with hyperelasticity and biocompatibility property. A three-dimensional heat diffusion model was used in conjunction with phase explosion theory to explain the formation of core-shell nanoparticles of nitinol. The diffusion model was used to evaluate the melt-pool temperature in the ablation region, while the phase explosion theory was used to estimate the thermophysical expansion and subsequent fragmentation of molten and vaporized nitinol. The mathematical parameters were formulated in conjunction with the experimental results of pulsed laser ablation of core-shell nitinol nanoparticles of various sizes. The model was further employed to predict the sizes of the nanoparticles produced at other higher fluences and the results were experimentally validated. 2021, Food Bioscience Show abstractNavigate Down Soursop (Annona muricata L.) is a highly perishable fruit and is often rejected by the market due to external injury or rapid aging process that leads to unacceptable senescence for further processing. A previous study has optimised the alcoholic fermentation of soursop to produce soursop wine using an alternative fermentative starter culture. Therefore, this study was aimed to produce soursop vinegar using an acetous fermentation and investigate the physicochemical, toxicity and organoleptic properties. Soursop vinegar showed significantly (p ≤ 0.05) higher acetic acid (3.5 ± 0.3%), total phenolic content (220 ± 20 ppm gallic acid equivalence) and FRAP (ferric reducing antioxidant power) activity (222 ± 2 μM ascorbic acid equivalence), with lower pH, sugar, ethanol and DPPH (2,2-diphenyl-1-picrylhydrazyl) free radical scavenging activity while retaining ascorbic acid, compared to those of soursop wine. A toxicity assay carried out using the fish embryos toxicity (FET) showed that the median lethality concentration (LC50) for fish embryos was 11.8 mg/mL, which was considered as non-toxic. Meanwhile, toxicity with human liver tissue (HepG2) using the MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay suggested that the cells’ survivability increased when the concentration of soursop vinegar was ≤6.25%. Sensory evaluation was carried out using quantitative descriptive analysis and the soursop vinegar was less sour and sweeter than commercial vinegar. This study offers an alternative way of reducing wastage of soursop fruit by the conversion of soursop into vinegar using a combination of alternative alcoholic and acetous fermentations.Cited by (72)
Arrow Up and RightView all citing articles on ScopusAlcohol exacerbated biochemical and biophysical alterations in liver mitochondrial membrane of diabetic male wistar rats – A possible amelioration by green tea
Estrogenic mixtures induce alterations in lipidomic profiles in the gonads of female oysters
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Alcohol exacerbated biochemical and biophysical alterations in liver mitochondrial membrane of diabetic male wistar rats – A possible amelioration by green tea
Thermo-physical modeling and experimental validation of core-shell nanoparticle fabrication of nickel-titanium (nitinol) alloy
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Research article Ultrasonics Sonochemistry, Volume 36, 2017, pp. 191-197 Show abstractNavigate Down Effects of low-intensity ultrasound (at different frequency, treatment time and power) on Saccharomyces cerevisiae in different growth phase were evaluated by the biomass in the paper. In addition, the cell membrane permeability and ethanol tolerance of sonicated Saccharomyces cerevisiae were also researched. The results revealed that the biomass of Saccharomyces cerevisiae increased by 127.03% under the optimum ultrasonic conditions such as frequency 28 kHz, power 140 W/L and ultrasonic time 1 h when Saccharomyces cerevisiae cultured to the latent anaphase. And the membrane permeability of Saccharomyces cerevisiae in latent anaphase enhanced by ultrasound, resulting in the augment of extracellular protein, nucleic acid and fructose-1,6-diphosphate (FDP) contents. In addition, sonication could accelerate the damage of high concentration alcohol to Saccharomyces cerevisiae although the ethanol tolerance of Saccharomyces cerevisiae was not affected significantly by ultrasound. Research article International Journal of Food Microbiology, Volume 165, Issue 3, 2013, pp. 265-275 Show abstractNavigate Down Listeria monocytogenes is of particular concern in cold-smoked fish products as it can survive curing and cold-smoking, and can subsequently grow from low numbers to potentially hazardous levels during refrigerated storage. The purpose of this study was to (i) quantify the effects of organic acids, nisin, and their combinations on controlling L. monocytogenes growth on cold-smoked salmon at refrigeration temperatures, (ii) identify synergistic interactions of binary combinations of these antimicrobials, and (iii) determine if results from laboratory growth media can predict antimicrobial efficacy on cold-smoked salmon. Strains representing the genetic diversity of L. monocytogenes lineages I and II were grown in brain heart infusion (BHI) broth as well as on the surface of commercially produced wet-cured, cold-smoked salmon slices at 7 °C. BHI broth and cold-smoked salmon were supplemented with sodium diacetate (SDA, 0.14% water phase (w.p.)), potassium lactate (PL, 2% w.p.), nisin (NI, 50 ppm), and binary combinations of inhibitors at the same levels. Cell densities of L. monocytogenes were measured over time and used to calculate growth parameters, including initial cell density (N0), lag phase (λ), maximum growth rate (μmax), and maximum cell density (Nmax) for each antimicrobial treatment. N0 was significantly lowered by addition of NI with a similar average reduction on salmon (2.02 ± 0.99 log(CFU/g)) and in BHI (1.51 ± 0.83 log(CFU/ml)). Among all antimicrobial treatments, the combination of PL and SDA led to the greatest increase in λ both on salmon (7.1 ± 3.6 days) and in BHI (9.7 ± 3.8 days) when compared to the controls. The combination of PL and SDA had synergistic effects on increasing λ and lowering Nmax both in BHI and on salmon. Among all the treatments tested, the combination of NI and PL led to the greatest reductions in Nmax on salmon. We observed positive correlations between the growth parameters obtained from BHI broth and cold-smoked salmon, indicating that growth of L. monocytogenes in broth, to some extent, qualitatively reflected characteristics of growth on cold-smoked salmon under antimicrobial stresses. Results from BHI could quantitatively predict the variability of growth parameters obtained from salmon for lineage II strains, but not for lineage I strains. Although results from laboratory growth medium may not provide exact predictions of antimicrobial efficacy on cold-smoked salmon, they could be used to rapidly identify effective combinations for further examination on cold-smoked salmon. Research article Chemistry and Physics of Lipids, Volume 221, 2019, pp. 140-144 Show abstractNavigate Down Various experimental data reveal intriguing peculiarities in structural properties of biomimetic membranes. Interestingly, one of the common alterations that is observed at the membrane-water interface underlines the important role of membrane hydration properties. A plausible mechanism of action in the case of many membrane additives seems to be in shifting the water encroachment the way that bilayers absorb more or less water molecules - one of the smallest and often neglected biomolecule. The difference in water interactions with different lipids and cholesterol has been noted at the interface and up to the bilayer center, the ion depending interplay between lipid-water and ion-water hydrations has been shown, and the anaesthetic effect also appears to link tightly to hydration, to discuss but a few examples. Although a complete understanding of the physicochemical processes taking place in biomembranes is not established fully, the understanding of lipid bilayer structural changes as a result of different properties of environment outside and/or inside the membrane provides a foundation for better insights into the structure-function relationships that most certainly take place in complex biomembrane systems. Research article Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, Volume 1852, Issue 7, 2015, pp. 1400-1409 Show abstractNavigate Down We have explored the mechanisms underlying ethanol-induced mitochondrial dynamics disruption and mitophagy. Ethanol increases mitochondrial fission in a concentration-dependent manner through Drp1 mitochondrial translocation and OPA1 proteolytic cleavage. ARPE-19 (a human retinal pigment epithelial cell line) cells challenged with ethanol showed mitochondrial potential disruptions mediated by alterations in mitochondrial complex IV protein level and increases in mitochondrial reactive oxygen species production. In addition, ethanol activated the canonical autophagic pathway, as denoted by autophagosome formation and autophagy regulator elements including Beclin1, ATG5-ATG12 and P-S6 kinase. Likewise, autophagy inhibition dramatically increased mitochondrial fission and cell death, whereas autophagy stimulation rendered the opposite results, placing autophagy as a cytoprotective response aimed to remove damaged mitochondria. Interestingly, although ethanol induced mitochondrial Bax translocation, this episode was associated to cell death rather than mitochondrial fission or autophagy responses. Thus, Bax required 600 mM ethanol to migrate to mitochondria, a concentration that resulted in cell death. Furthermore, mouse embryonic fibroblasts lacking this protein respond to ethanol by undergoing mitochondrial fission and autophagy but not cytotoxicity. Finally, by using the specific mitochondrial-targeted scavenger MitoQ, we revealed mitochondria as the main source of reactive oxygen species that trigger autophagy activation. These findings suggest that cells respond to ethanol activating mitochondrial fission machinery by Drp1 and OPA1 rather than bax, in a manner that stimulates cytoprotective autophagy through mitochondrial ROS. Research article Biophysical Journal, Volume 104, Issue 5, 2013, pp. 1049-1055 Show abstractNavigate Down Ethanol has a profound impact on biological systems and is moreover used in various medical and nonmedical applications. Its interaction with the lipid part of biological membranes has been the subject of intensive studies, but surprisingly, to our knowledge, no study has examined the influence of ethanol on lipid bilayer nanomechanics. We performed atomic force microscopy-based measurements to assess the influence of ethanol on the nanomechanical properties of fluid supported lipid bilayers. Ethanol significantly reduces membrane stability, bilayer thickness, Young’s modulus, area stretch modulus, and bending stiffness. Altogether, our data suggest that ethanol addition to supported lipid bilayers supports both the hydrophobic and the hydrophilic permeation pathways by a decrease of bilayer thickness and reduced stability, respectively. Research article European Journal of Pharmacology, Volume 789, 2016, pp. 313-318 Show abstractNavigate Down Medical ozone reduced inflammation, IL-1β, TNF-α mRNA levels and oxidative stress in PG/PS-induced arthritis in rats. The aim of this study was to investigate the medical ozone effects in patients with rheumatoid arthritis treated with methotrexate and methotrexate+ozone, and to compare between them. A randomized clinical study with 60 patients was performed, who were divided into two groups: one (n=30) treated with methotrexate (MTX), folic acid and Ibuprophen (MTX group) and the second group (n=30) received the same as the MTX group+medical ozone by rectal insufflation of the gas (MTX+ozone group). The clinical response of the patients was evaluated by comparing Disease Activity Score 28 (DAS28), Health Assessment Questionnaire Disability Index (HAQ-DI), Anti-Cyclic Citrullinated (Anti-CCP) levels, reactants of acute phase and biochemical markers of oxidative stress before and after 20 days of treatment. MTX+ozone reduced the activity of the disease while MTX merely showed a tendency to decrease the variables. Reactants of acute phase displayed a similar picture. MTX+ozone reduced Anti-CCP levels as well as increased antioxidant system, and decreased oxidative damage whereas MTX did not change. Glutathione correlated with all clinical variables just after MTX+ozone. MTX+ozone increased the MTX clinical response in patients with rheumatoid arthritis. No side effects were observed. These results suggest that ozone can increase the efficacy of MTX probably because both share common therapeutic targets. Medical ozone treatment is capable of being a complementary therapy in the treatment of rheumatoid arthritis.Recommended articles (6)
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Presented at the UAEM/IRIEM Research Symposium on Toxicology in San Francisco, California, February 1986.