Abstract
Blood-Brain Barrier (BBB) is a dynamic anatomical interface that separates brain parenchyma from blood circulation and is principally constituted by the cerebral microcapillary endothelial cells [1,2]. BBB is composed of distinct structural and functional organization through the presence of inter-endothelial tight junction complexes, abundant expression of nutrient and efflux transporters including metabolically active sites. While the TJ complexes tightly seal the paracellular gaps and contribute to high resistance of BBB [3], the presence of specific nutrient transporters and receptor systems selectively regulate the delivery of metabolic substrates, nutrients and macromolecules to the brain. In addition, efflux transporters belonging to the ABC superfamily prevent the brain permeation of blood-borne neurotoxic chemicals including xenobiotics and eliminates the accumulation of toxic metabolites within the brain parenchyma [1]. Taken together, the BBB serves as a physiological, transport and metabolic barrier that critically regulates ion, molecular and cellular flux into the brain, thus maintaining the CNS microenvironment for optimal neuronal function [2]. Importantly, impairment of BBB integrity by various exogenous or endogenous pathological stimuli involving increased load of oxidative/inflammatory stress in the neurovascular unit, is a potential mechanism underlying the pathogenesis of a host of neurologic and degenerative disorders [3,4].
Highlights
Emerging evidence indicts Tobacco Smoke (TS) as preventable risk factor in the etiology of neurological disorders such as ischemic stroke, silent cerebral infarctions, multiple sclerosis and cerebral aneurysms [8,9,10]
The precise mechanisms implicated in TS induced neuropathogenesis is not completely understood, nicotine-dependent pathways at the cerebrovasculature are believed to partly mediate TS-induced neurotoxicity and stroke
Experimental and clinical evidence assessing the toxicological profiles of these diverse tobacco products at the brain microvasculature is minimally reported to support their safety and availability of such information is deemed to be essential for regulatory bodies to set standards on the tobacco products for improving public health [15]
Summary
Emerging evidence indicts TS (active and passive) as preventable risk factor in the etiology of neurological disorders such as ischemic stroke, silent cerebral infarctions, multiple sclerosis and cerebral aneurysms [8,9,10]. The precise mechanisms implicated in TS induced neuropathogenesis is not completely understood, nicotine-dependent pathways at the cerebrovasculature are believed to partly mediate TS-induced neurotoxicity and stroke Main stream TS was shown to impair BBB dysfunction that was prevented by anti-oxidant supplementation [7], while nicotine exacerbated ischemic stroke and brain edema [12].
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