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Non-Protein-Bound Iron and 4-Hydroxynonenal Protein Adducts in Autistic Spectrum Disorders

Friday, 3 May 2013: 14:00-18:00
Banquet Hall (Kursaal Centre)
R. Canitano1, A. Pecorelli2, S. Leoncini3, C. De Felice4, C. Signorini3, G. Valacchi5, L. Ciccoli3 and J. Hayek4, (1)University hospital of Siena, Siena, Italy, (2)2Department of Pathophysiology, Experimental Medicine & Public Health, University of Siena, Siena, Italy, (3)Department of Pathophysiology, Experimental Medicine & Public Health, University of Siena, Siena, Italy, (4)University Hospital of Siena AOUS, Siena, Italy, (5)University of Ferrara, Ferrara, Italy
Background:  A potential relationship between oxidative stress (OS) and autism spectrum disorders (ASDs) has been repeatedly explored, nevertheless, the OS contribution in the autism pathogenesis is still not fully elucidated

Objectives:  to evaluate the redox status in ASD

Methods: In this study we investigated for the first time the levels of non-protein-bound iron (NPBI), a pro-oxidant factor, and 4-hydroxynonenal protein adducts (4-HNE-PAs), as a marker of lipid peroxidation-induced protein damage, in children with ASD (n=20, mean age 12.0 ± 6.2 years) .

Results:  Intraerythrocyte and plasma NPBI levels measured by HPLC result significantly increased (1.98- and 3.56-folds) in  patients with ASD, as compared to controls (n=18, mean age 11.7 ± 6.5 years) (p=0.0019 and p<0.0001, respectively). Likewise, immunoblotting analysis shows significantly higher levels of 4-HNE PAs in erythrocyte membranes and in plasma (1.58- and 1.6-folds, respectively) from  patients with ASD (p=0.0043  and p=0.0001, respectively). Antioxidant erythrocyte GSH was slightly decreased (-10.34 %)  in patients (p=0.0215).

Conclusions: Our findings indicate an impairment of the redox status in ASD patients, with a pro-oxidant / antioxidant balance shifted toward the pro-oxidant arm. Increased levels of NPBI could contribute to lipid peroxidation and, consequently, to increased plasma and erythrocyte membranes 4-HNE-PAs, thus amplifying the oxidative damage, potentially contributing to the phenotype of AD.

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