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Journal of Child Neurology, Vol. 19, No. 6, 413-417 (2004)
DOI: 10.1177/088307380401900603
© 2004 SAGE Publications

Polymorphisms in Xenobiotic Metabolism Genes and Autism

Fatema J. Serajee, MD

Department of Pediatrics, Wayne State University, Detroit, MI

Rafiqun Nabi, PhD

Department of Pediatrics, Wayne State University, Detroit, MI

Hailang Zhong, BS

Department of Pediatrics, Wayne State University, Detroit, MI

A.H.M. Mahbubul Huq, MD, PhD

Department of Pediatrics, Wayne State University, Detroit, MI, ahuq{at}med.wayne.edu, Department of Neurology Wayne State University. Detroit, MI

Autism is a neurodevelopmental syndrome defined by deficits in social reciprocity and communication and by unusual repetitive behaviors. Although there is an underlying genetic predisposition, the etiology of autism is currently unknown. A recent increase in prevalence suggests that genetically determined vulnerability to environmental exposure might contribute to the causation of autism. We performed family-based association studies of polymorphisms in metal-regulatory transcription factor 1(MTF1 ), a multispecific organic anion transporter (ABCC1), proton-coupled divalent metal ion transporters (SLCI IA3 and SLC11A2), paraoxonase 1 (PON1), and glutathione S-transferase (GSTP1) genes in 196 autistic disorder families. There was deviation from the expected pattern of transmission for polymorphisms in MTF1 (Single nucleotide polymorphism database reference identification number, dbSNP rs3790625, P = .02) and divalent metal ion transporter SLCI IA3 (dbSNP rs2304704, P = .07) genes. Although these results might represent chance finding, further investigations of genetic variations of metal metabolism in autism are warranted. (J Child Neurol 2004;19:413-417).


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