Blood-brain barrier stress-induced

Gilgun-Sherki Y., Melamed E., and Offen D. (2001). Oxidative stress induced-neurodegenerative diseases the need for antioxidants that penetrate the blood brain barrier. Neuropharmacology 40 959-975. 

Another method of neurotoxicant entry into the CNS is by exploitation of a compromised blood-brain barrier. Aluminum itself compromises the blood-brain barrier and reactive species, both directly and indirectly, can open the barrier. Blood-borne inflammation, possibly through the release of reactive oxygen species, is widely known to create a leaky blood-brain barrier. This allows inflammatory cells, endotoxins, and neurotoxicants to enter the CNS. Inflammation within the brain itself also affects blood-brain barrier permeability, an aspect that potentially links psychological stress to increased susceptibility to neurotoxicants. It has been shown that inflammatory responses are induced in animals under stressful conditions, such as electrical shock, restraint, or adverse social interactions. 

Perhaps the main peroxide-induced alterations, within cells and tissues, are those that affect calcium and sodium homeostasis. Na, K-ATPase, which is considered as the core of the sodium pump , is strongly affected by peroxides, and especially by lipid hydroperoxides [137-139]. This implies that oxidative stress will usually be associated with cellular edema . Alternatively, activation of the Na, K-ATPase of vascular endothelia, such as the blood-brain barrier, will result in extracellular edema on the antiluminal side of the endothelium, due to massive influx of sodium ions [119]. 

Skultetyova, L, Tokarev, D., and Jezova, D., Stress-induced increase in blood-brain barrier permeability in control and monosodium glutamate-treated rats. Brain Res. Bull, 45(2), 175, 1998. 

Sharma, H. S., Nyherg, F, Cervos-Navarro, J., and Dey, P. K. (1992). Histamine modulates heat stress-induced changes in blood-brain barrier permeability, cerebral blood flow, brain oedema and serotonin levels An experimental study in conscious young rats. Neuroscience 50, 445-454. 

Abou-Donia, M.B., Khan, W.A., Suliman, H.B., and Abdel-Rehman, A.A. (2001). Sarin-induced increase in blood-brain barrier (BBB) permeability is augmented by coexposure with stress, pyridostigmine bromide (PB), DEET, and permethrin in rats. Conference on Illness Among Gulf War Veterans A Decade of Scientific Research, Alexandria, VA, January 24—26, 2001, p. 140. 

Shear stress induces larger amounts of elastin in cells and inhibits tissue calcification. Occludin, a transmembrane protein that forms tight junctions between cells, and is the main contributor to the blood-brain barrier (an obstacle to free passage of complex molecules into the central nervous system), is present in lesser amounts at high shear stress values (about 10% less at 20-30 dynes/cm ). 

Potential modes of action for lead neurotoxicity include oxidative stress, inhibition of enzymes needed for energy production, decreased levels of neurotransmitters and altered neurotransmitter release, and increased permeability of the blood-brain barrier (EPA 2012). Ultimately, lead-induced neurotoxicity in adults consists of changes in brain stracture and neurochemistry, including white-matter changes, reduction in gray matter, and alterations in brain metabolites. 

HIV-1 gpl20-induced injury to the blood-brain barrier role of metaUoproteinases 2 and 9 and relationship to oxidative stress. J Neuropathol Exp Neurol 69 801-816... 

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