Zinc deficiency exacerbates loss in blood-brain barrier integrity induced by hyperoxia measured by dynamic MRI.
ABSTRACT Using dynamic Magnetic Resonance Imaging (dMRI), blood-brain barrier (BBB) permeability (k(PSrho)) and tissue interstitial leakage space (v(e)) were evaluated in zinc-deficient (ZnDF) male weanling Wistar rats following 3 days exposure to hyperoxia (85% O2). Temporal monitoring of T1-weighted MR image changes, following a bolus intravenous injection of gadolinium-DTPA, allowed estimation of BBB integrity. Three-day exposure of hyperoxia caused a marginal loss of BBB integrity, reflected in a slight increase in kPSrho and v(e), observed in both the animals fed adequate zinc (ZnAL) and pair-fed controls (ZnPF). However, zinc deficiency resulted in a significant increase in both kPSrho and v(e), indicating a severely disturbed BBB. In addition MR-visible free water was elevated in ZnDF brains following hyperoxia treatment indicating that a loss of BBB integrity may be associated with neuronal edema. The diminished BBB integrity may be free-radical mediated as the ratio of oxidized to reduced glutathione (GSSG:GSH) was significantly elevated.
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Article: Oxidative stress in autism.[Show abstract] [Hide abstract]
ABSTRACT: STATEMENT OF PURPOSE: Indirect markers are consistent with greater oxidative stress in autism. They include greater free-radical production, impaired energetics and cholinergics, and higher excitotoxic markers. Brain and gut, both abnormal in autism, are particularly sensitive to oxidative injury. Higher red-cell lipid peroxides and urinary isoprostanes in autism signify greater oxidative damage to biomolecules. A preliminary study found accelerated lipofuscin deposition--consistent with oxidative injury to autistic brain in cortical areas serving language and communication. Double-blind, placebo-controlled trials of potent antioxidants--vitamin C or carnosine--significantly improved autistic behavior. Benefits from these and other nutritional interventions may be due to reduction of oxidative stress. Understanding the role of oxidative stress may help illuminate the pathophysiology of autism, its environmental and genetic influences, new treatments, and prevention. OBJECTIVES: Upon completion of this article, participants should be able to: 1. Be aware of laboratory and clinical evidence of greater oxidative stress in autism. 2. Understand how gut, brain, nutritional, and toxic status in autism are consistent with greater oxidative stress. 3. Describe how anti-oxidant nutrients are used in the contemporary treatment of autism.Alternative therapies in health and medicine 11(1):19. · 1.14 Impact Factor
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ABSTRACT: Despite volumes of international research, the etiology of chronic fatigue syndrome (CFS) remains elusive. There is, however, considerable evidence that CFS is a disorder involving the central nervous system (CNS). It is our hypothesis that altered permeability of the blood-brain barrier (BBB) may contribute to ongoing signs and symptoms found in CFS. To support this hypothesis we have examined agents that can increase the blood-brain barrier permeability (BBBP) and those that may be involved in CFS. The factors which can compromise the normal BBBP in CFS include viruses, cytokines, 5-hydroxytryptamine, peroxynitrite, nitric oxide, stress, glutathione depletion, essential fatty acid deficiency, and N-methyl-D-aspartate overactivity. It is possible that breakdown of normal BBBP leads to CNS cellular dysfunction and disruptions of neuronal transmission in CFS. Abnormal changes in BBBP have been linked to a number of disorders involving the CNS; based on review of the literature we conclude that the BBB integrity in CFS warrants investigation.Medical Hypotheses 09/2001; 57(2):231-7. DOI:10.1054/mehy.2001.1306 · 1.15 Impact Factor