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Autism Studies and Related Medical Conditions, January 2009 - TACA

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permeability. Detoxification of mercury <strong>and</strong> other heavy metals by DMSA/DMPS<br />

chelation can have marked benefit. Documented sulfoxidation-sulfation inadequacies<br />

call for sulfur-sulfhydryl repletion <strong>and</strong> other liver p450 support. Many nutrient<br />

supplements are beneficial <strong>and</strong> well tolerated, including dimethylglycine (DMG) <strong>and</strong> a<br />

combination of pyridoxine (vitamin B6) <strong>and</strong> magnesium, both of which benefit roughly<br />

half of ASD cases. Vitamins A, B3, C, <strong>and</strong> folic acid; the minerals calcium <strong>and</strong> zinc; cod<br />

liver oil; <strong>and</strong> digestive enzymes, all offer benefit… Current pharmaceuticals fail to<br />

benefit the primary symptoms <strong>and</strong> can have marked adverse effects. Individualized, indepth<br />

clinical <strong>and</strong> laboratory assessments <strong>and</strong> integrative parent-physician-scientist<br />

cooperation are the keys to successful ASD management."<br />

112. Kidd PM. An approach to the nutritional management of autism. Altern Ther Health<br />

Med. 2003 Sep-Oct;9(5):22-31 PMID 14526708<br />

Glutathione<br />

113. Wang XF, Cynader MS. Astrocytes provide cysteine to neurons by releasing<br />

glutathione. J Neurochem. 2000 74(4):1434-42. PMID 10737599<br />

"Cysteine is the rate-limiting precursor of glutathione synthesis. Evidence suggests that<br />

astrocytes can provide cysteine <strong>and</strong>/or glutathione to neurons. However, it is still<br />

unclear how cysteine is released <strong>and</strong> what the mechanisms of cysteine maintenance by<br />

astrocytes entail. In this report, we analyzed cysteine, glutathione, <strong>and</strong> related<br />

compounds in astrocyte conditioned medium using HPLC methods. In addition to<br />

cysteine <strong>and</strong> glutathione, cysteine-glutathione disulfide was found in the conditioned<br />

medium. In cystine-free conditioned medium, however, only glutathione was detected.<br />

These results suggest that glutathione is released by astrocytes directly <strong>and</strong> that<br />

cysteine is generated from the extracellular thiol/disulfide exchange reaction of cystine<br />

<strong>and</strong> glutathione: glutathione + cystinecysteine + cysteine-glutathione disulfide.<br />

Conditioned medium from neuron-enriched cultures was also assayed in the same way<br />

as astrocyte conditioned medium, <strong>and</strong> no cysteine or glutathione was detected. This<br />

shows that neurons cannot themselves provide thiols but instead rely on astrocytes. We<br />

analyzed cysteine <strong>and</strong> related compounds in rat CSF <strong>and</strong> in plasma of the carotid artery<br />

<strong>and</strong> internal jugular vein. Our results indicate that cystine is transported from blood to<br />

the CNS <strong>and</strong> that the thiol/disulfide exchange reaction occurs in the brain in vivo.<br />

Cysteine <strong>and</strong> glutathione are unstable <strong>and</strong> oxidized to their disulfide forms under<br />

aerobic conditions. Therefore, constant release of glutathione by astrocytes is essential<br />

to maintain stable levels of thiols in the CNS."<br />

114. Fonnum F, Lock EA. The contributions of excitotoxicity, glutathione depletion <strong>and</strong><br />

DNA repair in chemically induced injury to neurones: exemplified with toxic effects on<br />

cerebellar granule cells. J Neurochem. 2004 Feb;88(3):513-31. PMID: 14720201<br />

<strong>Autism</strong> <strong>Studies</strong> & <strong>Related</strong> <strong>Medical</strong> <strong>Conditions</strong> – <strong>TACA</strong> © Page 334

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