Alcohol-induced oxidative stress in brain endothelial cells causes blood-brain barrier dysfunction
- PMID: 16204625
- DOI: 10.1189/jlb.0605340
Alcohol-induced oxidative stress in brain endothelial cells causes blood-brain barrier dysfunction
Abstract
Brain microvascular endothelial cells (BMVEC) connected by tight junctions (TJ) form a tight monolayer at the blood-brain barrier (BBB). We investigated the idea that BBB dysfunction seen in alcohol abuse is associated with oxidative stress stemming from ethanol (EtOH) metabolism in BMVEC. Exposure to EtOH induced catalytic activity/expression of EtOH-metabolizing enzymes, which paralleled enhanced generation of reactive oxygen species (ROS). EtOH-mediated oxidative stress led to activation of myosin light chain (MLC) kinase, phosphorylation of MLC and TJ proteins, decreased BBB integrity, and enhanced monocyte migration across BBB. Acetaldehyde or ROS donors mimicked changes induced by EtOH in BMVEC. Thus, oxidative stress resulting from alcohol metabolism in BMVEC can lead to BBB breakdown in alcohol abuse, serving as an aggravating factor in neuroinflammatory disorders.
Similar articles
-
Involvement of ROS in BBB dysfunction.Free Radic Res. 2009 Apr;43(4):348-64. doi: 10.1080/10715760902751902. Epub 2009 Feb 24. Free Radic Res. 2009. PMID: 19241241 Review.
-
Alcohol-induced oxidative stress.Life Sci. 2007 Jun 27;81(3):177-87. doi: 10.1016/j.lfs.2007.05.005. Epub 2007 May 21. Life Sci. 2007. PMID: 17570440 Review.
-
Inhibition of the myosin light chain kinase prevents hypoxia-induced blood-brain barrier disruption.J Neurochem. 2007 Jul;102(2):501-7. doi: 10.1111/j.1471-4159.2007.04506.x. Epub 2007 Apr 10. J Neurochem. 2007. PMID: 17419808
-
Alcohol-induced blood-brain barrier dysfunction is mediated via inositol 1,4,5-triphosphate receptor (IP3R)-gated intracellular calcium release.J Neurochem. 2007 Jan;100(2):324-36. doi: 10.1111/j.1471-4159.2006.04245.x. J Neurochem. 2007. PMID: 17241155
-
Ethanol-induced activation of myosin light chain kinase leads to dysfunction of tight junctions and blood-brain barrier compromise.Alcohol Clin Exp Res. 2005 Jun;29(6):999-1009. doi: 10.1097/01.alc.0000166944.79914.0a. Alcohol Clin Exp Res. 2005. PMID: 15976526
Cited by
-
Alcohol and stress exposure across the lifespan are key risk factors for Alzheimer's Disease and cognitive decline.Neurobiol Stress. 2024 Jan 4;29:100605. doi: 10.1016/j.ynstr.2024.100605. eCollection 2024 Mar. Neurobiol Stress. 2024. PMID: 38268931 Free PMC article.
-
The Influence of Arsenic Co-Exposure in a Model of Alcohol-Induced Neurodegeneration in C57BL/6J Mice.Brain Sci. 2023 Nov 24;13(12):1633. doi: 10.3390/brainsci13121633. Brain Sci. 2023. PMID: 38137081 Free PMC article.
-
Ameliorative effect of diazepam against ethanol-induced mitochondrial disruption in brains of the mice.Toxicol Rep. 2023 Oct 24;11:405-412. doi: 10.1016/j.toxrep.2023.10.014. eCollection 2023 Dec. Toxicol Rep. 2023. PMID: 37955036 Free PMC article.
-
The influence of physiological and pathological perturbations on blood-brain barrier function.Front Neurosci. 2023 Oct 23;17:1289894. doi: 10.3389/fnins.2023.1289894. eCollection 2023. Front Neurosci. 2023. PMID: 37937070 Free PMC article. Review.
-
Reactive Oxygen Species Are Central Mediators of Vascular Dysfunction and Hypertension Induced by Ethanol Consumption.Antioxidants (Basel). 2023 Sep 29;12(10):1813. doi: 10.3390/antiox12101813. Antioxidants (Basel). 2023. PMID: 37891892 Free PMC article. Review.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Miscellaneous
