Tail-Oxidized Cholesterol Enhances Membrane Permeability for Small Solutes

Numerous studies have dealt with the cytochemical localization of cytochrome oxidase via cytochrome c. More recent studies have dealt with indicating initial foci of this reaction by altering incubation pH (1) or postosmication procedure (2,3). The following study is an attempt to locate such foci by altering membrane permeability. It is thought that such alterations within the limits of maintaining morphological integrity of the membranes will ease the entry of exogenous substrates resulting in a much quicker oxidation and subsequently a more precise definition of the oxidative reaction.The diaminobenzidine (DAB) method of Seligman et al. (4) was used. Minced pieces of rat liver were incubated for 1 hr following toluene treatment (5,6). Experimental variations consisted of incubating fixed or unfixed tissues treated with toluene and unfixed tissues treated with toluene and subsequently fixed.

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The Effect of Oxidized Cholesterol on the Aorta of Rabbits- Scanning Electron Microscopic Observations

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100054327 ◽

1982 ◽

Vol 40 ◽

pp. 340-341

Author(s):

S. K. Pena ◽

C. B. Taylor ◽

J. Hill ◽

J. Safarik

Keyword(s):

Cholesterol Biosynthesis ◽

Cholesterol Content ◽

Arterial Injury ◽

Electron Microscopic ◽

Aortic Smooth Muscle ◽

Oxidized Cholesterol ◽

Initial Event ◽

Membrane Structure And Function ◽

Scanning Electron Microscopic ◽

And Function

Introduction: Oxidized cholesterol derivatives have been demonstrated in various cell cultures to be very potent inhibitors of 3-hvdroxy-3- methylglutaryl Coenzyme A reductase which is a principle regulator of cholesterol biosynthesis in the cell. The cholesterol content in the cells exposed to oxidized cholesterol was found to be markedly decreased. In aortic smooth muscle cells, the potency of this effect was closely related to the cytotoxicity of each derivative. Furthermore, due to the similarity of their molecular structure to that of cholesterol, these oxidized cholesterol derivatives might insert themselves into the cell membrane, alter membrane structure and function and eventually cause cell death. Arterial injury has been shown to be the initial event of atherosclerosis.

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Sarcolemmal permeability changes during early myocardial anoxia

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100084089 ◽

1978 ◽

Vol 36 (2) ◽

pp. 642-643

Author(s):

M. Ashraf ◽

L. Landa ◽

L. Nimmo ◽

C. M. Bloor

Keyword(s):

Cell Membrane ◽

Membrane Permeability ◽

Coronary Artery Occlusion ◽

Artery Occlusion ◽

Cell Membrane Permeability ◽

Enzyme Release ◽

Sprague Dawley ◽

Sprague Dawley Rats ◽

Sarcolemmal Permeability ◽

Membrane Changes

Following coronary artery occlusion, the myocardial cells lose intracellular enzymes that appear in the serum 3 hrs later. By this time the cells in the ischemic zone have already undergone irreversible changes, and the cell membrane permeability is variably altered in the ischemic cells. At certain stages or intervals the cell membrane changes, allowing release of cytoplasmic enzymes. To correlate the changes in cell membrane permeability with the enzyme release, we used colloidal lanthanum (La+++) as a histological permeability marker in the isolated perfused hearts. The hearts removed from sprague-Dawley rats were perfused with standard Krebs-Henseleit medium gassed with 95% O2 + 5% CO2. The hypoxic medium contained mannitol instead of dextrose and was bubbled with 95% N2 + 5% CO2. The final osmolarity of the medium was 295 M osmol, pH 7. 4.

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