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The function of the fatty-acid oxidation pathway in fibroblast cultures and biomarkers for abnormalities in non-mitochondrial fatty-acid metabolism were not consistently abnormal across the subgroup of ASD children, consistent with the notion that the abnormalities in fatty-acid metabolism found in this subgroup of children with ASD were secondary to TCAC abnormalities

however, this can substantially distort metal coordination geometry[ 107 , 152 ] and prevents valuable information regarding SOD1s native posttranslational modifications from being collected