Effect of alcohols on the permeability of blood-brain barrier

Gulati, Anil; Nath, Chandishwar; Shanker, K.; Srimal, R. C.; Dhawan, K.N.; Bhargava, K. P.

doi:10.1016/0031-6989(85)90054-2

Cited by 40 publications

(17 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…11 used here were well below those observed to alter the transcellular permeability of BMEC monolayers (unpublished observations, P.M. Reardon and K.L. Audus) and the BBB in vivo (30). The viability of cell preparations in both the fluorescence and transcellular studies assessed by trypan blue exclusion was not altered by 21-aminosteroid exposure (data not shown).…”

supporting

confidence: 58%

21-aminosteroid and 2-(aminomethyl)chromans inhibition of arachidonic acid-induced lipid peroxidation and permeability enhancement in bovine brain microvessel endothelial cell monolayers

Shi

Cavitt

Audus

1995

Free Radical Biology and Medicine

View full text Add to dashboard Cite

Abstract:Studies were conducted to demonstrate 21-aminosteroid distribution into the hydrophobic or lipid domains of biological membranes, a presumed site at which these compounds inhibit lipid peroxidation. Bovine brain microvessel endothelial cells (BMECs) were labeled with diphenylhexatriene fluorophores and interactions with cell membranes characterized with fluorescence anisotropy and lifetimes. Two 21-aminosteroids (U-74500A and U74006F) were shown to preferentially alter the fluorescence anisotropy and lifetime parameters of the diphenylhexatriene probe distributing into membranes throughout the BMECs. Little or no effect of the compounds on the fluorescence parameters of the diphenylhexatriene probe the localized on the surface of BMEC plasma membranes. By contrast, cholesterol used as a positive control altered substantially the fluorescence parameters of BMECs labeled with either diphenylhexatriene probe. Results suggest 21-aminosteroid-induced changes in the molecular packing order and drug:fluorescent probe interactions in membrane hydrophobic (or lipid) domains throughout the BMEC. Concentrations of 21-aminosteroids altering the fluorescence parameters of diphenylhexatriene labeled BMECs correspond to those concentrations of 21-aminosteroids effective in vitro in inhibition lipid peroxidation. Evidence for 21-aminosteroid association with the hydrophobic domains in brain microvessel endothelial cells. Free Rad. Biol. Med. 11, 361-371. PMID: 1797623. Publisher's official version: http://dx

show abstract

supporting

confidence: 58%

21-aminosteroid and 2-(aminomethyl)chromans inhibition of arachidonic acid-induced lipid peroxidation and permeability enhancement in bovine brain microvessel endothelial cell monolayers

Shi

Cavitt

Audus

1995

Free Radical Biology and Medicine

View full text Add to dashboard Cite

show abstract

“…However, the effects of alcohol on the permeability of the BBB in adult mammals have been inconsistent. Earlier studies, mostly in the 1980's, showed three types of results: increased permeability with evidence of structural damage (Karwacka, 1980;Gulati et al, 1985;Stewart et al, 1988;Borisenko, 1990); no change induced by alcohol (Hemmingsen et al, 1980;Hillbom and Tervo, 1981;Phillips, 1981;Phillips and Cragg, 1982); and even a protective and beneficial effect (Neilly and Lin, 1986). The conflicting results are not easily reconciled by dose, duration, or other pharmacological factors, whereas a detrimental effect of alcohol on tight junction proteins and alcohol-induced oxidative stress on endothelium was evident in a cell-culture system (Haorah et al, 2005b).…”

Section: Discussionmentioning

confidence: 99%

Increased Leptin Permeation across the Blood–Brain Barrier after Chronic Alcohol Ingestion

Pan

Barron

Hsuchou

et al. 2007

Neuropsychopharmacol

View full text Add to dashboard Cite

Leptin, a polypeptide mainly produced in the periphery, crosses the blood-brain barrier (BBB) by receptor-mediated transport to exert multiple central nervous system actions including decreased food intake. The reciprocal interactions between leptin transport and alcohol drinking are not clear. In this study, we tested whether alcohol increases leptin entry into brain and, if this occurs, whether it is a consequence of a generalized increase in the permeability of the BBB. BBB permeability to albumin, the increased permeation of which indicates BBB disruption, as well as to leptin was measured after alcohol ingestion. CD1 and B6 mice ingested a 5% liquid alcohol diet or its isocaloric control for 2 weeks. Alcohol ingestion resulted in increased blood-alcohol levels, decreased blood-leptin concentrations, and increased permeation of radioactively labeled leptin across the BBB as shown by in situ perfusion. Although the increased influx of the vascular marker albumin into brain showed partial disruption of the BBB, the influx of 125 I-leptin still could be suppressed by excess unlabeled leptin, indicating persistence of its saturable transport system. When given a choice of either alcohol or control diet, even the alcohol-preferring B6 mice showed a significantly greater preference for the control liquid diet, and there was no evidence of BBB disruption or alterated leptin transport. Furthermore, acute alcohol intoxication induced by intraperitoneal injection of 20% alcohol did not result in BBB disruption or increased leptin permeation 4 h later. Thus, partial disruption of the BBB and increased permeation of leptin in both CD1 and B6 mice were only induced by chronic alcohol ingestion. The results showing increased leptin permeation across the BBB lead to the speculation that leptin may serve as a homeostatic feeding signal in these mice.

show abstract

“…It is well established that the interaction of ethanol with cellular membranes has a profound effect on various cellular functions. Ethanol has been reported to increase the fluidity of nerve cell membranes (Edelfors & Ravn-Jonsen 1990) and has been implicated to change the permeability of blood-brain barrier by increasing the lipid solubility of membranes (Gulati et al 1985).…”

Section: Discussionmentioning

confidence: 99%

Impaired Energy Metabolism after Co-Exposure to Leadand Ethanol

Verma

Dua

Gill

2005

Basic Clin Pharmacol Toxicol

View full text Add to dashboard Cite

Abstract:The neurotoxic effects of lead are controlled by a number of nutritional, physiological and environmental factors. One such factor, ethanol, might affect the neurotoxicity of lead by regulating its absorption and distribution. However, there is little information regarding the possible biochemical mechanism by which ethanol might be affecting the state of neuronal functions in lead-exposed individuals. Therefore, the present investigation involved the effect of alcohol (3 g/kg body weight, intragastrically, for 8 weeks) on lead-induced (50 mg/kg body weight, intragastrically, for 8 weeks) mitochondrial dysfunction in adult rat brain. Ethanol was found to enhance the toxic effects of lead in terms of decreased cellular energy reserves (ATP levels). Co-exposure to lead and ethanol caused marked decline in the rate of mitochondrial respiration as compared to lead alone. Further the activies of various components of the electron transport chain, viz. NADH dehydrogenase, succinate dehydrogenase and cytochrome oxidase depicted a significant decrease in the lead and ethanol co-exposed rats as compared to the lead-treated group. The results of the present study reflect that ethanol makes adult rat brain more vulnerable to the neurotoxic effects of lead in terms of altered mitochondrial energy metabolism.

show abstract

Effect of alcohols on the permeability of blood-brain barrier

Cited by 40 publications

References 11 publications

21-aminosteroid and 2-(aminomethyl)chromans inhibition of arachidonic acid-induced lipid peroxidation and permeability enhancement in bovine brain microvessel endothelial cell monolayers

21-aminosteroid and 2-(aminomethyl)chromans inhibition of arachidonic acid-induced lipid peroxidation and permeability enhancement in bovine brain microvessel endothelial cell monolayers

Increased Leptin Permeation across the Blood–Brain Barrier after Chronic Alcohol Ingestion

Impaired Energy Metabolism after Co-Exposure to Leadand Ethanol

Contact Info

Product

Resources

About