Differential effects on phospholipid phase transitions produced by structurally related long-chain alcohols

Pringle, Michael J.; Miller, Keith W.

doi:10.1021/bi00582a018

Cited by 70 publications

(27 citation statements)

References 48 publications

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“…It is well known that the volatile anesthetics are soluble in lipid compartments of subjects exposed to volatile anesthetics [6,7,8]. Although no longer accepted as a model of general anesthetic action to induce amnesia and analgesia, the Meyer-Overton hypothesis postulated that the anesthetic molecules dissolve into membrane lipids and interact at hydrophobic sites [6, 21].…”

Section: Discussionmentioning

confidence: 99%

“…Although no longer accepted as a model of general anesthetic action to induce amnesia and analgesia, the Meyer-Overton hypothesis postulated that the anesthetic molecules dissolve into membrane lipids and interact at hydrophobic sites [6, 21]. In fact, the volatile anesthetics are known to cause perturbation of membrane structures through a nonspecific interaction with membrane lipid bilayers or affect the activity of cellular enzymes by binding to appropriate sites of membrane-bound proteins [6, 8]. The physical state of the phospholipids in biological membranes is important in determining their susceptibility to the activation of a lipid-requiring enzyme.…”

Section: Discussionmentioning

confidence: 99%

“…Disruption of the plasma lipid bilayer by volatile anesthetics has been described with resultant changes in plasma membrane phospholipid anatomy [6,7,8]. Additionally, it is known that the disruption of the plasma lipid bilayer resulting in translocation of phosphatidylserine (PS) from the inner leaflet to the outer leaflet of the plasma membrane (membrane externalization) results in the release of the potent anti-inflammatory/antinecrotic molecule growth factor β1 (TGF-β1) via ligation of PS receptors in adjacent macrophages [9,10,11,12,13].…”

Section: Introductionmentioning

confidence: 99%

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TGF-Beta1 Release by Volatile Anesthetics Mediates Protection against Renal Proximal Tubule Cell Necrosis

Lee

Kim

et al. 2007

Am J Nephrol

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Background/Aims:We have previously demonstrated that clinically utilized volatile anesthetics protect against renal ischemia reperfusion injury in rats in vivo and reduce necrosis in vitro via activation of ERK and Akt and by upregulating HSP70. In this study, we further deciphered the upstream cellular signaling mechanism(s) of volatile anesthetic-mediated antinecrotic effects in vitro. We hypothesized that volatile anesthetics perturb the structure of the plasma membrane lipid bilayer, causing externalization of phosphatidylserine (PS) to the outer surface on renal tubule cells leading to the increased generation of transforming growth factor-β1 (TGF-β1), a cytokine with antinecrotic properties. Methods and Results: In human proximal tubule (HK-2) cell culture, 16-hour exposure to volatile anesthetics (isoflurane, halothane, sevoflurane) caused membrane externalization of PS detected by positive annexin-V staining and increased the release of TGF-β1 into the cell culture media. Exogenous TGF-β1 induced protection and neutralizing TGF-β1 antibody prevented the cytoprotection by volatile anesthetics against hydrogen peroxide-induced HK-2 cell necrosis. Conclusions: Volatile anesthetics induce a cytoprotective signaling cascade in proximal tubule cells via membrane externalization of PS initiating TGF-β1-mediated cytoprotection.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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TGF-Beta1 Release by Volatile Anesthetics Mediates Protection against Renal Proximal Tubule Cell Necrosis

Lee

Kim

et al. 2007

Am J Nephrol

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“…It has been reported (Eliasz et al, 1976;Lee, 1976;Jain & Wu, 1977;Pringle & Miller, 1979;Kamaya et al, 1984) that shorter alkyl-chain l-alkanols depressed whereas longer ones elevated the main transition temperature of phospholipid membranes. The crossover from depression to elevation of the transition temperature occurred at about the chainlength of 10 to 12 carbon atoms.…”

Section: Introductionmentioning

confidence: 98%

Dose-dependent nonlinear response of the main phase-transition temperature of phospholipid membranes to alcohols

Kamaya

Lin

1986

J. Membrain Biol.

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The effect of 1-alkanols upon the main phase-transition temperature of phospholipid vesicle membranes between gel and liquid-crystalline phases was not a simple monotonic function of alkanol concentration. For instance, 1-decanol decreased the transition temperature at low concentrations, but increased it at high concentrations, displaying a minimal temperature. This concentration-induced biphasic effect cannot be explained by the van't Hoff model on the effect of impurities upon the freezing point. To explain this nonlinear response, a theory is presented which treats the effect of 1-alkanols (or any additives) on the transition temperature of phospholipid membranes in a three-component mixture. By fitting the experimental data to the theory, the enthalpy of the phase transition delta H* and the interaction energy, epsilon*AB between the additive and phospholipid molecules may be estimated. The theory predicts that when epsilon*AB greater than 2 (where epsilon*AB = epsilon AB/RT0, T0 being the transition temperature of phospholipid), both minimum and maximum transition temperatures should exist. When epsilon*AB = 2, only one inflection point exists. When epsilon*AB less than 2, neither maximum nor minimum exists. The alkanol concentration at which the transition temperature is minimum (Xmin) depends on the epsilon*AB value: the larger the epsilon*AB values, the smaller the Xmin. When epsilon*AB is large enough, Xmin values become so small that the plot delta T vs. X shows positive delta T in almost all alkanol concentrations. The interaction energy between 1-alkanols and phospholipid molecules increased with the increase in the carbon chain-length of 1-alkanols. In the case of the dipalmitoylphosphatidylcholine vesicle membrane, the carbon chain-length of 1-alkanols that caused predominantly positive delta T was about 12.

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“…The transfer ofsmall molecules from aqueous medium into lipid bilayers is a process that is undoubtedly important in biological membranes and has accordingly received much attention in recent years (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17)(18)(19). As discussed by Diamond and Katz (5) and Milgram and Solomon (20), this transfer involves rate processes in addition to the equilibrium distribution of solute between aqueous and lipid phases.…”

mentioning

confidence: 99%

A scanning calorimetric study of small molecule-lipid bilayer mixtures.

Sturtevant¹

1982

Proc. Natl. Acad. Sci. U.S.A.

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The influence of small molecules on the main phase transition of dimyristoyl phosphatidylcholine was observed by high-sensitivity differential scanning calorimetry. The variation with temperature of the excess heat capacity is markedly affected by solid solution formation, which appears to be of frequent occurrence in solutions in lipid bilayers. The experimental results are in some cases in reasonable agreement with ideal solution theory.The transfer ofsmall molecules from aqueous medium into lipid bilayers is a process that is undoubtedly important in biological membranes and has accordingly received much attention in recent years (1-19). As discussed by Diamond and Katz (5) and Milgram and Solomon (20), this transfer involves rate processes in addition to the equilibrium distribution of solute between aqueous and lipid phases. In this paper I consider only the equilibrium distribution involving bilayers formed with pure dimyristoyl phosphatidylcholine (Myr2-PtdCho). It must be kept in mind that, as recently shown by Conrad and Singer (21), much of the transfer data that have been obtained with lipid bilayers may have little or no relevance to protein-containing biological membranes.Differential scanning calorimetric (DSC) evidence has been presented (22) which indicates that the gel-to-liquid-crystal transition, the so-called main transition, of phosphatidylcholines in multilamellar suspensions (liposomes) is a first-order transition. With perfectly ordered bilayers formed from pure lipids this transition would thus be isothermal. However, experimental limitations such as imperfect ordering of the lipid molecules in the bilayer, finite scan rates and calorimetric lags, and the presence of traces of impurities lead to observed transitions that extend over a finite range of temperature. The broadening can usually be approximately expressed in terms of the van't Hoff equation [1] in which a is the extent of the phase transition at temperature T, AHVH is the van't Hoff enthalpy, and R is the gas constant. The publication costs ofthis article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U. S. C. §1734 solely to indicate this fact.

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Differential effects on phospholipid phase transitions produced by structurally related long-chain alcohols

Cited by 70 publications

References 48 publications

TGF-Beta1 Release by Volatile Anesthetics Mediates Protection against Renal Proximal Tubule Cell Necrosis

TGF-Beta1 Release by Volatile Anesthetics Mediates Protection against Renal Proximal Tubule Cell Necrosis

Dose-dependent nonlinear response of the main phase-transition temperature of phospholipid membranes to alcohols

A scanning calorimetric study of small molecule-lipid bilayer mixtures.

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