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.
- SourceAvailable from: Renee Dufault
[Show abstract] [Hide abstract]
- "Increased hyperactivity is associated with the development of educational difficulties especially in reading . In rats, zinc deficiency along with oxidative stress predisposes the brain to damage by disruption of the blood-brain barrier  and prenatal zinc deficiency has pronounced effects on postnatal metallothionein metabolism, which can persist into adulthood . With respect to consumption of high fructose corn syrup and adverse effect, Molteni et al. , found that a high fat, HFCS diet reduced brain-derived neurotrophic factor (BDNF) neuronal plasticity, and learning in rats. "
ABSTRACT: Among dietary factors, learning and behavior are influenced not only by nutrients, but also by exposure to toxic food contaminants such as mercury that can disrupt metabolic processes and alter neuronal plasticity. Neurons lacking in plasticity are a factor in neurodevelopmental disorders such as autism and mental retardation. Essential nutrients help maintain normal neuronal plasticity. Nutritional deficiencies, including deficiencies in the long chain polyunsaturated fatty acids eicosapentaenoic acid and docosahexaenoic acid, the amino acid methionine, and the trace minerals zinc and selenium, have been shown to influence neuronal function and produce defects in neuronal plasticity, as well as impact behavior in children with attention deficit hyperactivity disorder. Nutritional deficiencies and mercury exposure have been shown to alter neuronal function and increase oxidative stress among children with autism. These dietary factors may be directly related to the development of behavior disorders and learning disabilities. Mercury, either individually or in concert with other factors, may be harmful if ingested in above average amounts or by sensitive individuals. High fructose corn syrup has been shown to contain trace amounts of mercury as a result of some manufacturing processes, and its consumption can also lead to zinc loss. Consumption of certain artificial food color additives has also been shown to lead to zinc deficiency. Dietary zinc is essential for maintaining the metabolic processes required for mercury elimination. Since high fructose corn syrup and artificial food color additives are common ingredients in many foodstuffs, their consumption should be considered in those individuals with nutritional deficits such as zinc deficiency or who are allergic or sensitive to the effects of mercury or unable to effectively metabolize and eliminate it from the body.Behavioral and Brain Functions 10/2009; 5(1):44. DOI:10.1186/1744-9081-5-44 · 2.00 Impact Factor
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 01/2005; 11(1):19. · 1.14 Impact Factor