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Evaluation of Oxidative Stress in Biological Samples Using the Thiobarbituric Acid Reactive Substances Assay
Published on: May 12, 2020
Oxidative stress indices in ASD children in Sub-Sahara Africa
Ishiaq Olayinka Omotosho1, Adekunbi Olufunke Akinade2, Ikeoluwa Abiola Lagunju3
1Department of Chemical Pathology, Neurotoxicology Unit, University of Ibadan, Ibadan, Nigeria. ishiaqomotosh@yahoo.co.uk.
Insights
Children with autism spectrum disorder (ASD) show reduced essential metals (Mg, Zn) and increased lead (Pb), linked to oxidative stress. This imbalance may affect neuronal function, contributing to ASD characteristics.
Area of Science:
- Biochemistry
- Neuroscience
- Environmental Health
Background:
- Autism spectrum disorder (ASD) pathogenesis is complex, with genetics, epigenetics, and oxidative stress implicated.
- Oxidative stress involves an imbalance between free radicals and antioxidants, potentially contributing to ASD.
- Essential metals (Mg, Zn, Cu) and toxic metals (Pb) may play a role in ASD development and oxidative stress.
Purpose of the Study:
- To investigate the levels of essential metals (Mg, Zn, Cu) and toxic metal (Pb) in children with ASD.
- To assess oxidative stress markers (MDA, TPP, TAC, OSI) in children with ASD.
- To explore the relationship between metal levels and oxidative stress in ASD pathogenesis.
Main Methods:
- Recruited 25 children with ASD and 25 neuro-typical (NT) controls.
- Analyzed metal concentrations using ICP-MS.
- Determined oxidative stress markers (MDA, TPP, TAC) and calculated OSI.
Main Results:
- Children with ASD had significantly lower TPP and TAC, and higher MDA compared to NT controls.
- ASD group showed significantly increased Pb and reduced Mg, Zn, and Cu levels.
- A negative correlation was found between Mg and OSI in NT children.
Conclusions:
- Reduced Mg and Zn, with increased Pb, may contribute to inadequate antioxidant capacity in ASD.
- This oxidative imbalance could lead to neuronal transduction abnormalities, causing cognitive and speech deficits in ASD.
- Metal-oxidative stress interactions offer a potential etiological pathway for ASD.
Background:
The pathogenesis of autism spectrum disorder (ASD) remains a medical challenge even in the developed world. Although genetics and epigenetic factors have been variously indicted as major causes of the disorder, development of oxidative stress especially in the formative years of children has equally gained prominence as an etiological basis of the disorder. Oxidative stress is characterized by the production of excessive amounts of free radicals, decreased levels of antioxidants with the attendant imbalance in oxidant/antioxidant ratio. This study was designed to determine the levels of essential metals [magnesium (Mg), zinc (Zn), and copper (Cu)] and toxic metal, lead (Pb), and generation of oxidative stress by their abnormal interaction.
Method:
Twenty-five children clinically diagnosed for ASD according to DSM-IV-TR and 25 neuro-typical (NT) children (controls), (aged 5.96 ± 1.40 years and 6.18 ± 2.59 years respectively) were recruited for this study. Essential and toxic metals were analyzed using induction-coupled plasma-mass spectrometry (ICP-MS); oxidative stress markers [malondialdehyde (MDA), total plasma peroxidase (TPP), and total antioxidant capacity (TAC)] were determined using appropriate biochemical methods. Oxidative stress index (OSI) was calculated.
Results:
The levels of TPP and TAC were significantly reduced while MDA was higher in ASD compared to NT. Although OSI was higher in ASD, the difference was not significant. Pb (lead) concentration was significantly increased while Mg, Zn, and Cu levels were reduced significantly in ASD compared to NT. A significant negative correlation between Mg and OSI (r = - 0.438; p = 0.029) was observed in NT.
Conclusion:
Reduction in Zn and Mg levels with a concurrent increase in Pb in children with ASD in this study may be the basis of inadequate TAC manifesting as increased MDA and reduced TPP levels. The attendant imbalance in oxidant/antioxidant ratio may result in abnormality in neuronal transduction leading to the abnormal cognitive and speech functions characteristic of ASD.

