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Autism Studies and Related Medical Conditions, January 2009 - TACA

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determined the observed haplotype effect. CONCLUSIONS: Overtransmission of<br />

the GSTP1*A haplotype to case mothers suggests that action in the mother<br />

during pregnancy likely increases the likelihood of AD in her fetus. If this is<br />

confirmed <strong>and</strong> is a result of a gene-environment interaction occurring during<br />

pregnancy, these findings could lead to the design of strategies for prevention or<br />

treatment.<br />

Yao, Y., W. J. Walsh, et al. (2006). "Altered vascular phenotype in autism: correlation<br />

with oxidative stress." Arch Neurol 63(8): 1161-4.<br />

BACKGROUND: <strong>Autism</strong> is a neurologic disorder characterized by impaired<br />

communication <strong>and</strong> social interaction. Results of previous studies showed<br />

biochemical evidence for abnormal platelet reactivity <strong>and</strong> altered blood flow in<br />

children with autism. OBJECTIVE: To evaluate the vascular phenotype in children<br />

with autism. DESIGN AND MAIN OUTCOME MEASURES: Urinary levels of<br />

isoprostane F(2alpha)-VI, a marker of lipid peroxidation; 2,3-dinor-thromboxane<br />

B(2), which reflects platelet activation; <strong>and</strong> 6-keto-prostagl<strong>and</strong>in F(1alpha), a<br />

marker of endothelium activation, were measured by means of gas<br />

chromatography-mass spectrometry in subjects with autism <strong>and</strong> healthy control<br />

subjects. SETTING AND SUBJECTS: Children with a clinical diagnosis of autism<br />

attending the Pfeiffer Treatment Center. RESULTS: Compared with controls,<br />

children with autism had significantly higher urinary levels of isoprostane<br />

F(2alpha)-VI, 2,3-dinor-thromboxane B(2), <strong>and</strong> 6-keto-prostagl<strong>and</strong>in F(1alpha).<br />

Lipid peroxidation levels directly correlated with both vascular biomarker ratios.<br />

CONCLUSION: Besides enhanced oxidative stress, platelet <strong>and</strong> vascular<br />

endothelium activation also could contribute to the development <strong>and</strong> clinical<br />

manifestations of autism.<br />

Yorbik, O., C. Akay, et al. (2004). "Zinc status in autistic children." J Trace Elem Exp<br />

Med 17(2): 101-107.<br />

Yorbik, O., A. Sayal, et al. (2002). "Investigation of antioxidant enzymes in children with<br />

autistic disorder." Prostagl<strong>and</strong>ins Leukot Essent Fatty Acids 67(5): 341-3.<br />

Impaired antioxidant mechanisms are unable to inactivate free radicals that may<br />

induce a number of pathophysiological processes <strong>and</strong> result in cell injury. Thus,<br />

any abnormality in antioxidant defence systems could affect neurodevelopmental<br />

processes <strong>and</strong> could have an important role in the etiology of autistic disorder.<br />

The plasma levels of glutathione peroxidase (GSH-Px) <strong>and</strong> superoxide dismutase<br />

(SOD), <strong>and</strong> erythrocyte levels of GSH-Px were investigated in 45 autistic children<br />

<strong>and</strong> compared with 41 normal controls. Levels of erythrocyte SOD, erythrocyte<br />

<strong>and</strong> plasma GSH-Px were assayed spectrophotometrically. Activities of<br />

erythrocyte SOD, erythrocyte <strong>and</strong> plasma GSH-Px in autistic children were<br />

significantly lower than normals. These results indicate that autistic children have<br />

low levels of activity of blood antioxidant enzyme systems; if similar<br />

<strong>Autism</strong> <strong>Studies</strong> & <strong>Related</strong> <strong>Medical</strong> <strong>Conditions</strong> – <strong>TACA</strong> © Page 102

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