Oxidants, Antioxidants, and Delayed Language Correlations in Children with Autism

Special Article – Communication Disorders and Rehabilitation

Phys Med Rehabil Int. 2017; 4(6): 1134.

Oxidants, Antioxidants, and Delayed Language Correlations in Children with Autism

Azab SN¹*, Saber AS² and Mostafa HA¹

¹Department of Otorhinolaryngology, Faculty of Medicine, Beni- Suef University, Egypt

²Department of Otorhinolaryngology, Faculty of Medicine, Ain Shams University, Egypt

*Corresponding author: Safinaz Nagib Azab, Department of Otorhinolaryngology, Faculty of Medicine, Beni- Suef University, Egypt

Received: October 21, 2017; Accepted: November 15, 2017; Published: November 22, 2017


Autism is complexes behaviorally known as neurodevelopmental disorder characterized by significant deterioration in social interaction, mental abilities language development and other communicative abilities. It is deemed a multicauses disorder that is affected by genetic, immunological and environmental factors and inclusive oxidative stress. Aim of such study was to estimate level of antioxidant enzyme coenzyme Q10 and level of malondialdehyde (MDA) in children with autism and correlate these results with their language and behavior pattern. The study included 30 Egyptian children with autism and 30 normal children as control group. Their ages ranged between 3 to 6 years. Diagnosis was done using DSM-V and ADI-R. Cases were classified into high and low functioning autism using CARS. We compared plasma levels of coenzyme Q10 and MDA in children with autism and controls. Our results showed significant increased MDA and decreased coenzyme Q10 in autistic children compared to controls. On the other hand, Increased MDA and decreased coenzyme Q10 were not related to severity of autistic features and language abilities among autistic children group. Regarding language abilities of autistic children, there was positive correlation between IQ and total language age and negative correlation between CARS and total language age.


Autism and its affined spectrum of disorders (ASD) are neurodevelopmental disorders distinguished by fundamental feebleness in social interaction, difficulty with communication, and restrictive and repetitive conducts [1]. Mitochondrial disorders are one of the most joint metabolic diseases in children. Mitochondrial diseases occur in a subset of autism cases and are usually caused by genetic abnormality or mitochondrial respiratory pathway anomalisms. They have also been correlated with developmental retraction and retardation in ASD comprehensive missing language expertise, hyperactivity, unusual social interaction, limited interests, stereotypical demeanors, seizures, and self-detrimental behaviors [2]. The free radicals are produced endogenously through oxidative metabolism and energy fabrication by mitochondria where the electron transport chain in mitochondria is a first provenance of reactive oxygen species (ROS) production [3]. ROS have the ability to rush pivotal components of the cell, as polyunsaturated fatty acids, proteins, and nucleic acid. These reflections can modify fundamental membrane properties such as enzyme activities, fluidity, ion transport, protein synthesis and protein cross-linking finally resulting in cell death [4]. Neuronal cells are extremely susceptible to oxidative stress due to the high rate of oxygen distribution and consumption in the brain [5]. Mitochondrial Coenzyme Q functions comprise arranger of electron transport in the respiratory chain, extraditing electrons from complex I, complex II, and passing them to complex III, and relocate protons from fatty acids to matrix. As an alternative Coenzyme Q function is possible in organization of permeability transition pore opening and nutrition absorption through the Voltage Dependent Anion Channel of outer mitochondrial membrane. Ubiquinol supportive therapy may improve brain mitochondrial function and ATP production and affect brain oxidative stress [6].

Aim of the Work

The aim of the study was to estimate level of antioxidant enzyme coenzyme Q10 and malondialdehyde in children with autism and correlate these results with their behavior and language.

Materials and Methods


The present study included 60 children aged 3–6 years, 30 children of them were diagnosed as autism (patients Group) and a comparable 30 normally developed children served as (control Group), both groups were matching regarding age and gender. Caregivers consent was obtained for all the studied cases and controls. The cases were recruited from Beni-Suef University Hospital and subjected to detailed history taking including three generation pedigrees construction, detailed peri- and postnatal history, similarly affected cases and other family findings. Thorough clinical examination with special emphasis on vocal tract examination and psychometric evaluation using Stanford Binet intelligence scale fifth edition [7] were done. Language assessment protocol [8] was applied in Phoniatric Unit in addition to EEG were applied for all autistic cases. Diagnosis of the cases were confirmed using Autism Diagnostic Interview-Revised (ADI-R) [9] and Clinical interview based on Diagnostic and Statistical Manual of Mental Disorders, 4the edition (DSM-IV) [10] in the Autistic Children Clinic, National Research Center, Cairo, Egypt. Severity was assessed using the childhood autism rating scale CARS [11].

Blood sampling

Venous blood sample was collected from all patients and controls into vacationer tubes containing EDTA. We measured plasma MDA as an indicator of lipid peroxidation status in all autistic children and control subjects according to the method described by Chauhan et al. 2004 [12] and plasma concentrations of both the total and the reduced CoQ10 (ubiquinol) according to the method described by Jiang et al., 2004 [13] using Elisa system.

Statistical analysis

Data were expressed as mean ± SD. Statistical significance was determined using an Cross tabulation test, student t- test and fisher’s exact test. A probability value of P less than 0.05 was considered statistically significant. Bivariate comparisons were examined using Pearson’s and Spearman’s correlation coefficients for parametric and nonparametric variables. P values less than 0.05 was considered statistically significant.


The results showed no significant difference in mean of age of cases compared to control groups (P value is >0.05). Parental consanguinity variation between patient and control groups was measured by Cross tabulation test with no significant difference and the parental age of patient group was older than parental age of control group with highly significant statistical difference (P value <0.01). The percentage of electroencephalogram (EEG) changes among patient group (10% =3 out of 30 children in the patient group have EEG findings) (Table 1). Table 1 showed the percentage of family history with similar condition or other neuropsychiatric cases among patient group. Table 2 showed that the mean of intelligence quotient in patient group was significantly decreased compared to control group. The mean score of total language age among patient group is lower than control group with high significant difference while mean of CARS is higher in patient group than in control group. The average score of intelligence quotient and of total language in patient group was lower than control group. The mean score of CARS is greater in patient groupthan control group (Table 2).