Oxidative stress in autism: Increased lipid peroxidation and reduced serum levels of ceruloplasmin and transferrin - the antioxidant proteins

Chauhan, Abha; Chauhan, Ved; Brown, W. Ted; Cohen, Ira L.

doi:10.1016/j.lfs.2004.04.038

Cited by 388 publications

(279 citation statements)

References 32 publications

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“…Furthermore, decreased activities of certain antioxidant enzymes including SOD [47] , glutathione peroxidase [47] , catalase [52] , and paraoxonase [53] are found in some individuals with autism. Some ASD children also express increased lipid peroxidation [52,54] , including increased malondialdehyde, which is a marker of oxidative stress and lipid peroxidation [55] . One group of researchers has actually suggested that "oxidative stress (endogenous or environmental) may contribute to the development and clinical manifestations of autism" [46] .…”

Section: Mtd In Autismmentioning

confidence: 99%

“…One group of researchers has actually suggested that "oxidative stress (endogenous or environmental) may contribute to the development and clinical manifestations of autism" [46] . As an example, in one study, clinical regression (loss of previously acquired skills) in some autistic children was associated with lower levels of serum antioxidant enzymes [55] . Oxidative stress may also play a role in the increased male to female ratio observed in autism.…”

Section: Mtd In Autismmentioning

confidence: 99%

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Evidence of Mitochondrial Dysfunction in Autism and Implications for Treatment

Rossignol¹,

Bradstreet²

2008

American J. of Biochemistry and Biotechnology

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Classical mitochondrial diseases occur in a subset of individuals with autism and are usually caused by genetic anomalies or mitochondrial respiratory pathway deficits. However, in many cases of autism, there is evidence of mitochondrial dysfunction (MtD) without the classic features associated with mitochondrial disease. MtD appears to be more common in autism and presents with less severe signs and symptoms. It is not associated with discernable mitochondrial pathology in muscle biopsy specimens despite objective evidence of lowered mitochondrial functioning. Exposure to environmental toxins is the likely etiology for MtD in autism. This dysfunction then contributes to a number of diagnostic symptoms and comorbidities observed in autism including: cognitive impairment, language deficits, abnormal energy metabolism, chronic gastrointestinal problems, abnormalities in fatty acid oxidation, and increased oxidative stress. MtD and oxidative stress may also explain the high male to female ratio found in autism due to increased male vulnerability to these dysfunctions. Biomarkers for mitochondrial dysfunction have been identified, but seem widely under-utilized despite available therapeutic interventions. Nutritional supplementation to decrease oxidative stress along with factors to improve reduced glutathione, as well as hyperbaric oxygen therapy (HBOT) represent supported and rationale approaches. The underlying pathophysiology and autistic symptoms of affected individuals would be expected to either improve or cease worsening once effective treatment for MtD is implemented.

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Section: Mtd In Autismmentioning

confidence: 99%

Section: Mtd In Autismmentioning

confidence: 99%

Evidence of Mitochondrial Dysfunction in Autism and Implications for Treatment

Rossignol¹,

Bradstreet²

2008

American J. of Biochemistry and Biotechnology

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“…Casting a wide net, we included demographic characteristics, diagnostic measures, symptom severity, and exploratory laboratory analyses (prolactin, leptin, and mineral assays). Mineral assays were included because of reports of mineral abnormalities in autism, especially zinc and copper and their ratio (Faber et al 2009) and such related proteins as ferritin and ceruloplasmin (Chauhan et al 2004) and because prolactin, known to be increased by risperidone, has been suspected of increasing ceruloplasmin (DiSilvestro 1986). First, potential moderators (Table 1) and mediators (Table 2) were entered into respective correlation matrices to check for collinearity.…”

mentioning

confidence: 99%

Moderators, Mediators, and Other Predictors of Risperidone Response in Children with Autistic Disorder and Irritability

Arnold

Farmer

Kraemer

et al. 2010

Journal of Child and Adolescent Psychopharmacology

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Objective/Background: The National Institute of Mental Health (NIMH) Research Units on Pediatric Psychopharmacology (RUPP) Autism Network found an effect size of d ¼ 1.2 in favor of risperidone on the main outcome measure in an 8-week double-blind, placebo-controlled trial for irritability in autistic disorder. This paper explores moderators and mediators of this effect. Method: Intention-to-treat (ITT) analyses were conducted with suspected moderators and mediators entered into the regression equations. MacArthur Foundation Network subgroup guidelines were followed in the evaluation of the results. Results: Only baseline severity moderated treatment response: Higher severity showed greater improvement for risperidone but not for placebo. Weight gain mediated treatment response negatively: Those who gained more weight improved less with risperidone and more with placebo. Compliance correlated with outcome for risperidone but not placebo. Higher dose correlated with worse outcome for placebo, but not risperidone. Of nonspecific predictors, parent education, family income, and low baseline prolactin positively predicted outcome; anxiety, bipolar symptoms, oppositional-defiant symptoms, stereotypy, and hyperactivity negatively predicted outcome. Risperidone moderated the effect of change in 5 0 -nucleotidase, a marker of zinc status, for which decrease was associated with improvement only with risperidone, not with placebo.

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“…One of the more destructive free radicals is peroxynitrite, which is generated through a combination of superoxide and NO, both of which are generated in excess with excitotoxicity. Significant elevations in measures of oxidative stress and LPP in autistic children were demonstrated [135,136].…”

Section: The Role Of Mercurymentioning

confidence: 99%

Immune-Glutamatergic Dysfunction as a Central Mechanism of the Autism Spectrum Disorders

Blaylock

Strunecká

2009

CMC

119

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Despite the great number of observations being made concerning cellular and the molecular dysfunctions associated with autism spectrum disorders (ASD), the basic central mechanism of these disorders has not been proposed in the major scientific literature. Our review brings evidence that most heterogeneous symptoms of ASD have a common set of events closely connected with dysregulation of glutamatergic neurotransmission in the brain with enhancement of excitatory receptor function by pro-inflammatory immune cytokines as the underlying mechanism. We suggest that environmental and dietary excitotoxins, mercury, fluoride, and aluminum can exacerbate the pathological and clinical problems by worsening excitotoxicity and by microglial priming. In addition, each has effects on cell signaling that can affect neurodevelopment and neuronal function. Our hypothesis opens the door to a number of new treatment modes, including the nutritional factors that naturally reduce excitotoxicity and brain inflammation.

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Oxidative stress in autism: Increased lipid peroxidation and reduced serum levels of ceruloplasmin and transferrin - the antioxidant proteins

Cited by 388 publications

References 32 publications

Evidence of Mitochondrial Dysfunction in Autism and Implications for Treatment

Evidence of Mitochondrial Dysfunction in Autism and Implications for Treatment

Moderators, Mediators, and Other Predictors of Risperidone Response in Children with Autistic Disorder and Irritability

Immune-Glutamatergic Dysfunction as a Central Mechanism of the Autism Spectrum Disorders

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