Biological Water and Its Role in the Effects of Alcohol1

Klemm, W. R.

doi:10.1016/s0741-8329(97)00130-4

Cited by 54 publications

(65 citation statements)

References 93 publications

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“…We have gathered evidence for dipolar magnetic coupling between water and EtOH in bovine serum albumin phantoms (Estilaei et al, 1999), in rat brain and in rat brain suspensions (Govindaraju et al, 1997). These findings suggest a dipolar mechanism for MT with the involvement of "biological water" (Klemm, 1998) in the exchange process.…”

Section: Magnetization Transfermentioning

confidence: 87%

“…Indirect evidence for the existence of both macromoleculeassociated and free EtOH, however, comes from our MT experiments (see subsequent discussion). Studies have shown that EtOH is likely to be found on the hydrophilic membrane surface or in protein pockets (Barry and Gawrisch, 1994;Chiou et al, 1992;Hitzeman et al, 1986;Klemm, 1998;Moxon et al, 1991;Rottenberg, 1987Rottenberg, , 1992 or, less likely, in the core of biological membranes, which show a relatively low partition coefficient for short chain alcohols such as EtOH (Barry and Gawrisch, 1994;Chiou et al, 1992;Klemm, 1998;Metcalfe et al, 1968;Rottenberg, 1992). The amount of macromoleculeassociated EtOH in membranes has been described to range from 6% to 90%, depending on the type of membrane investigated (Grenell, 1975;Kelly-Murphy et al, 1984;Nie et al, 1989;Rottenberg et al, 1981;Sarasua et al, 1989), and to be affected by chronic alcohol exposure (Beauge et al, 1985;Chin and Goldstein, 1977;Kelly-Murphy et al, 1984;Littleton and John, 1977;Rottenberg et al, 1981Rottenberg et al, , 1987Sarasua et al, 1989;Wood et al, 1987;reviewed in Rottenberg, 1992).…”

Section: Relaxationmentioning

confidence: 99%

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Ethanol in Human Brain by Magnetic Resonance Spectroscopy: Correlation With Blood and Breath Levels, Relaxation, and Magnetization Transfer

Fein

Meyerhoff

2000

Alcoholism: Clinical and Experimental Research

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Background-Proton magnetic resonance spectroscopy ( 1 H MRS) allows measurement of alcohol in the human brain after alcohol consumption. However, the quantity of alcohol that can be detected in the brain by 1 H MRS pulse sequences has been controversial, with values ranging from about 24% to 94% of the temporally concordant blood alcohol concentrations. The quantitation of brain alcohol is critically affected by the kinetics of alcohol uptake and elimination, by the relaxation times of the protons that give rise to the brain alcohol signal, and by the specifics of both pulse sequence timing and radio frequency pulse applications.

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Section: Magnetization Transfermentioning

confidence: 87%

Section: Relaxationmentioning

confidence: 99%

Ethanol in Human Brain by Magnetic Resonance Spectroscopy: Correlation With Blood and Breath Levels, Relaxation, and Magnetization Transfer

Fein

Meyerhoff

2000

Alcoholism: Clinical and Experimental Research

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“…Specifically, we posit that EtOH causes widespread intracellular water extravasation leading to shrinkage of brain cells and their process. EtOH influences a variety of CNS metabolic processes, but appears to initially affect water movement (Klemm, 1998) by acutely effecting a hyperosmotic environment (Champion et al, 1975). In situations characterized by hyperosmolarity, responses include loss of intracellular water (Pollock and Arieff, 1980) and brain cell shrinkage (Cserr et al, 1987).…”

Section: Discussionmentioning

confidence: 99%

A Mechanism of Rapidly Reversible Cerebral Ventricular Enlargement Independent of Tissue Atrophy

Zahr

Mayer

Rohlfing

et al. 2013

Neuropsychopharmacol

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Ventricular enlargement, a common in vivo marker of aging, disease, and insult, is presumed to reflect atrophy of surrounding brain regions. Pathological mechanisms underlying ventricular enlargement, however, are likely specific to the condition under investigation. Here, multimodal imaging, incorporating structural magnetic resonance imaging (MRI), MR spectroscopy (MRS), and diffusion weighted imaging (DWI), was used in rats exposed to binge ethanol (EtOH) to provide insight into a mechanism of reversible ventricular enlargement. During intoxication, MRI revealed expansion of ventricles, but volume changes in dorsal or ventral hippocampi, caudateputamen, or thalamus were not detectible. MRS of whole-brain parenchyma showed decreases in N-acetylasparate (NAA) and tissue water T2, and increases in choline-containing compounds (Cho). DWI showed decreased diffusivity selective to the thalamus. All MR parameters returned to baseline with 7 days of recovery. Rapid recovery of ventricular volume and the absence of detectable tissue volume reductions in brain regions adjacent to ventricles argue against atrophy as a mechanism of ventricular expansion. Decreased tissue water T2 and decreased thalamic diffusivity suggest lower tissue water content and a role for both NAA and Cho, as osmolytes is proposed. Together, these data support a model of fluid redistribution during acute EtOH intoxication and recovery to account for rapid ventricular volume changes.

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“…One of the proposed modes of action of ethanol on biological macromolecules and membranes involves the replacement of hydrogen-bonded water by ethanol (1,2). Based on the hydrogen bonding capability of both water and ethanol, it is postulated that they compete for hydrogen bonding sites on the surface of lipids and proteins.…”

mentioning

confidence: 99%

Effect of Ethanol and Osmotic Stress on Receptor Conformation

Mitchell

Litman

2000

Journal of Biological Chemistry

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The combined effects of ethanol and osmolytes on both the extent of formation of metarhodopsin II (MII), which binds and activates transducin, and on acyl chain packing were examined in rod outer segment disc membranes. The ethanol-induced increase in MII formation was amplified by the addition of neutral osmolytes. This enhancement was linear with osmolality. At 360 milliosmolal, the osmolality of human plasma, 50 mM ethanol was 2.7 times more potent than at 0 osmolality, demonstrating the importance of water activity in in vitro experiments dealing with ethanol potency. Ethanol disordered acyl chain packing, and increasing osmolality enhanced this acyl chain disordering. Prior osmotic stress data showed a release of 35 ؎ 2 water molecules upon MII formation. Ethanol increases this number to 49 water molecules, suggesting that ethanol replaces 15 additional water molecules upon MII formation. Amplification of ethanol effects on MII formation and acyl chain packing by osmolytes suggests that ethanol increases the equilibrium concentration of MII both by disordering acyl chain packing and by disrupting rhodopsin-water hydrogen bonds, demonstrating a direct effect of ethanol on rhodopsin. At physiologically relevant levels of osmolality and ethanol, about 90% of ethanol's effect is due to disordered acyl chain packing.One of the proposed modes of action of ethanol on biological macromolecules and membranes involves the replacement of hydrogen-bonded water by ethanol (1, 2). Based on the hydrogen bonding capability of both water and ethanol, it is postulated that they compete for hydrogen bonding sites on the surface of lipids and proteins. Thus, this action of ethanol is equally applicable to mechanisms of ethanol action involving both lipid-mediated and direct protein interactions. The general importance of changes in hydration in enzyme activity is widely acknowledged (3, 4), but there is little detailed knowledge regarding how replacement of water by ethanol in specific protein-water hydrogen bonds might alter protein conformational equilibria or function. In addition, the physical properties of the surrounding phospholipid bilayer are known to modulate membrane function. Ethanol-induced changes in phospholipid hydrogen bonding have been observed to change acyl chain packing in pure lipid bilayers (5-7). Thus, the function of integral membrane receptors could be especially susceptible to the disruption of hydrogen-bonded water by ethanol.Thorough examination of the interplay between ethanol and hydration in modulating membrane receptor function requires the ability to separately analyze the effects of ethanol on both protein structure and bilayer physical properties and to be able to correlate the observed changes. Previously, we examined the effects of ethanol (8) and a series of n-alkanols (9) on both the MI 1 -MII conformational equilibrium and acyl chain packing in the surrounding bilayer. In the present work, the effects of ethanol on the MI-MII equilibrium and acyl chain packing are reexamined as a functi...

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Biological Water and Its Role in the Effects of Alcohol1

Cited by 54 publications

References 93 publications

Ethanol in Human Brain by Magnetic Resonance Spectroscopy: Correlation With Blood and Breath Levels, Relaxation, and Magnetization Transfer

Ethanol in Human Brain by Magnetic Resonance Spectroscopy: Correlation With Blood and Breath Levels, Relaxation, and Magnetization Transfer

A Mechanism of Rapidly Reversible Cerebral Ventricular Enlargement Independent of Tissue Atrophy

Effect of Ethanol and Osmotic Stress on Receptor Conformation

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