Journal ArticleDOI
Oxidative stress in autism
Abha Chauhan,Ved Chauhan +1 more
TLDR
Increases in oxidative stress with membrane lipid abnormalities, inflammation, aberrant immune response, impaired energy metabolism and excitotoxicity, leading to clinical symptoms and pathogenesis of autism is proposed.About:
This article is published in Pathophysiology.The article was published on 2006-08-01. It has received 569 citations till now. The article focuses on the topics: Autism & Oxidative stress.read more
Citations
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Journal ArticleDOI
Urinary oxidative stress markers in children with autism
TL;DR: The study reveals that the urinary levels of oxidativestress markers can be considered as the measure of oxidative stress index in autistic children and the significant correlation between the severity of autism with urinary lipid peroxidation products also support the use of oxidative Stress markers and antioxidants as biomarkers of autism.
Journal ArticleDOI
Developmental vitamin D deficiency and autism: Putative pathogenic mechanisms.
TL;DR: The potential neurobiological mechanisms linking prenatal vitamin D deficiency and autism are reviewed and also what future research targets must now be addressed are discussed.
Journal ArticleDOI
A focus on homocysteine in autism.
TL;DR: Monitoring of homocysteine levels in body fluids of autistic children can provide information on genetic and physiological diseases, improper lifestyle (including dietary habits), as well as a variety of pathological conditions.
Journal ArticleDOI
Autism spectrum disorders may be due to cerebral toxoplasmosis associated with chronic neuroinflammation causing persistent hypercytokinemia that resulted in an increased lipid peroxidation, oxidative stress, and depressed metabolism of endogenous and exogenous substances
TL;DR: Data presented in this review suggest that environmental triggering factors caused reactivation of latent cerebral toxoplasmosis because of changes in intensity of latent central nervous system T. gondii infection/inflammation and finally resulted in development of ASD.
Journal ArticleDOI
Differential recruitment of coregulators to the RORA promoter adds another layer of complexity to gene (dys) regulation by sex hormones in autism
TL;DR: The studies demonstrate the direct involvement of androgen receptor (AR) and estrogen receptor (ER) in the regulation of RORA by male and female hormones, respectively, and that the promoter region between −10055 bp and −2344 bp from the transcription start site of R ORA is required for the inverse hormonal regulation.
References
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Book ChapterDOI
Role of free radicals and catalytic metal ions in human disease: an overview.
TL;DR: The chapter discusses the metabolism of transition metals, such as iron and copper, and the chelation therapy that is an approach to site-specific antioxidant protection.
Journal ArticleDOI
Nitric oxide: a cytotoxic activated macrophage effector molecule.
TL;DR: The results suggest that nitric oxide is the precursor of nitrite/nitrate synthesized by cytotoxic activated macrophages and, via formation of iron-nitric oxide complexes and subsequent degradation of Iron-sulfur prosthetic groups, an effector molecule.
Journal ArticleDOI
The mitochondrial death/life regulator in apoptosis and necrosis
TL;DR: The acquisition of the biochemical and ultrastructural features of apoptosis critically relies on the liberation of apoptogenic proteases or protease activators from mitochondria.
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Neuroglial activation and neuroinflammation in the brain of patients with autism
Diana L. Vargas,Caterina Nascimbene,Caterina Nascimbene,Chitra Krishnan,Andrew W. Zimmerman,Andrew W. Zimmerman,Carlos A. Pardo +6 more
TL;DR: It is indicated that innate neuroimmune reactions play a pathogenic role in an undefined proportion of autistic patients, suggesting that future therapies might involve modifying neuroglial responses in the brain.
Journal ArticleDOI
Biological effects of the superoxide radical.
TL;DR: Can the superoxide radical exert deleterious effects independent of participating with H2O2 in the production of the hydroxyl radical?