&lt;p&gt;The Relationship Between the Level of Copper, Lead, Mercury and Autism Disorders: A Meta-Analysis&lt;/p&gt;

Mohammadabadi, Hamed Jafari; Rahmatian, Aryoobarzan; Sayehmiri, Fatemeh; Rafiei, M R

doi:10.2147/phmt.s210042

Cited by 18 publications

(6 citation statements)

References 24 publications

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“…These studies show that ASD subjects are more vulnerable to mercury compounds than TDC subjects due to the presence of higher levels of mercury compounds in different body tissues such as nails, hair, blood, and urine in the former group. Further, levels of mercury in the body tissues correlate with the severity of symptoms [ 1 , 11 , 12 ]. Mercury compounds may cause neurodevelopmental and systemic changes through different mechanisms, which include inactivation of antioxidants, oxidative stress, neuronal damage, and loss of neuronal connectivity [ 1 , 49 ].…”

Section: Discussionmentioning

confidence: 99%

“…Several studies have shown associations between heavy metal environmental exposure and the etiology of ASD. Heavy metals like mercury and lead have been shown to be positively linked to higher incidence/prevalence of ASD [ 10 , 11 , 12 , 13 ]. These observations suggest that genetic, epigenetic, and environmental factors in combination produce the phenotype of ASD.…”

Section: Introductionmentioning

confidence: 99%

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Thioredoxin 1 and Thioredoxin Reductase 1 Redox System Is Dysregulated in Neutrophils of Subjects with Autism: In Vitro Effects of Environmental Toxicant, Methylmercury

Alshehri,

Ahmad,

Albekairi

et al. 2023

Toxics

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Autism spectrum disorder (ASD) is a complex developmental disorder in children that results in abnormal communicative and verbal behaviors. Exposure to heavy metals plays a significant role in the pathogenesis or progression of ASD. Mercury compounds pose significant risk for the development of ASD as children are more exposed to environmental toxicants. Increased concentration of mercury compounds has been detected in different body fluids/tissues in ASD children, which suggests an association between mercury exposure and ASD. Thioredoxin1 (Trx1) and thioredoxin reductase1 (TrxR1) redox system plays a crucial role in detoxification of oxidants generated in different immune cells. However, the effect of methylmercury and the Nrf2 activator sulforaphane on the Trx1/TrxR1 antioxidant system in neutrophils of ASD subjects has not been studied previously. Therefore, this study examined the effect of methylmercury on Trx1/TrxR1 expression, TrxR activity, nitrotyrosine, and ROS in neutrophils of ASD and TDC subjects. Our study shows that Trx1/TrxR1 protein expression is dysregulated in ASD subjects as compared to the TDC group. Further, methylmercury treatment significantly inhibits the activity of TrxR in both ASD and TDC groups. Inhibition of TrxR by mercury is associated with upregulation of the Trx1 protein in TDC neutrophils but not in ASD neutrophils. Furthermore, ASD neutrophils have exaggerated ROS production after exposure to methylmercury, which is much greater in magnitude than TDC neutrophils. Sulforaphane reversed methylmercury-induced effects on neutrophils through Nrf2-mediated induction of the Trx1/TrxR1 system. These observations suggest that exposure to the environmental toxicant methylmercury may elevate systemic oxidative inflammation due to a dysregulated Trx1/TrxR1 redox system in the neutrophils of ASD subjects, which may play a role in the progression of ASD.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Thioredoxin 1 and Thioredoxin Reductase 1 Redox System Is Dysregulated in Neutrophils of Subjects with Autism: In Vitro Effects of Environmental Toxicant, Methylmercury

Alshehri,

Ahmad,

Albekairi

et al. 2023

Toxics

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“…In the meantime, the clinical presentation of ASD is clearly varying and can present as a collection of health issues and comorbidities [ 8 , 9 ], not limited to neurodevelopmental, language, or social challenges [ 10 , 11 , 12 , 13 , 14 , 15 ]. Comorbidities include immune dysregulation [ 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 ], gastrointestinal issues such as diarrhea, constipation, and dysbiosis, mitochondrial dysfunction [ 24 , 25 , 26 , 27 ], poor detoxification [ 28 ], inflammation [ 29 ], food sensitivities, evidence of environmental toxicants [ 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 , 40 , 41 , 42 ], retained reflexes [ 43 , 44 ], and other structural or functional challenges.…”

Section: Introductionmentioning

confidence: 99%

Reversal of Autism Symptoms among Dizygotic Twins through a Personalized Lifestyle and Environmental Modification Approach: A Case Report and Review of the Literature

D’Adamo,

Nelson,

Miller

et al. 2024

JPM

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The prevalence of autism has been increasing at an alarming rate. Even accounting for the expansion of autism spectrum disorder diagnostic (ASD) criteria throughout the 1990’s, there has been an over 300% increase in ASD prevalence since the year 2000. The often debilitating personal, familial, and societal sequelae of autism are generally believed to be lifelong. However, there have been several encouraging case reports demonstrating the reversal of autism diagnoses, with a therapeutic focus on addressing the environmental and modifiable lifestyle factors believed to be largely underlying the condition. This case report describes the reversal of autism symptoms among dizygotic, female twin toddlers and provides a review of related literature describing associations between modifiable lifestyle factors, environmental exposures, and various clinical approaches to treating autism. The twins were diagnosed with Level 3 severity ASD “requiring very substantial support” at approximately 20 months of age following concerns of limited verbal and non-verbal communication, repetitive behaviors, rigidity around transitions, and extensive gastrointestinal symptoms, among other common symptoms. A parent-driven, multidisciplinary, therapeutic intervention involving a variety of licensed clinicians focusing primarily on addressing environmental and modifiable lifestyle factors was personalized to each of the twin’s symptoms, labs, and other outcome measures. Dramatic improvements were noted within several months in most domains of the twins’ symptoms, which manifested in reductions of Autism Treatment Evaluation Checklist (ATEC) scores from 76 to 32 in one of the twins and from 43 to 4 in the other twin. The improvement in symptoms and ATEC scores has remained relatively stable for six months at last assessment. While prospective studies are required, this case offers further encouraging evidence of ASD reversal through a personalized, multidisciplinary approach focusing predominantly on addressing modifiable environmental and lifestyle risk factors.

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“…These findings suggest that MeHg, when given at a non-apoptotic dose in vivo, perturbs cortical neurogenesis in the fetal period, leading to long-lasting impacts on neuro-performance. On the other hand, the epidemiological evidence for the relationship between MeHg exposure and ASD remains inconclusive [11][12][13][14][15], and the underlying mechanism between prenatal MeHg exposure and postnatal ASD onset is unknown. Therefore, deciphering the underlying cellular and molecular mechanisms that mediate MeHg-induced abnormal neurodevelopment (premature neuronal differentiation) will provide new insights into how non-genetic factors such as environmental chemical exposure contribute to ASD etiology.…”

Section: Introductionmentioning

confidence: 99%

Reduction of Glyoxalase 1 Expression Links Fetal Methylmercury Exposure to Autism Spectrum Disorder Pathogenesis

Leung,

Loan,

et al. 2024

Toxics

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Glyoxalase 1 (Glo1) is an essential enzyme to detoxify methylglyoxal (MGO), a cytotoxic byproduct of glycolysis. Accumulating studies have shown an important role of Glo1 in regulating cortical development and neurogenesis, potentially contributing to the pathogenesis of autism spectrum disorder (ASD) when impaired. We have previously shown that prenatal exposure to non-apoptotic low-dose methylmercury (MeHg), an environmental pollutant, induces premature cortical neurogenesis and ASD-like behaviors in a rodent model. In this study, we aimed to determine the underlying molecular mechanisms that mediate prenatal MeHg-induced premature neuronal differentiation and abnormal neurodevelopment. Using single-cell RNA sequencing (scRNA-seq) and real-time quantitative PCR (RT-qPCR), we found that prenatal MeHg exposure at a non-apoptotic dose significantly reduced Glo1 gene expression in embryonic cultured radial glia precursors (RGPs). In cultured RGPs, the knockdown of Glo1 expression increased neuronal production at the expense of the cultured RGPs population, while overexpression of Glo1 restored MeHg-induced neuronal differentiation back to normal levels. Furthermore, we found that co-treatment with both MeHg and multiple MGO scavengers or a CREB inhibitor (iCREB) mitigated MeHg-induced premature neuronal differentiation, reinforcing the role of Glo1 and CREB in mediating MeHg-induced neuronal differentiation. Our findings demonstrate a direct link between MeHg exposure and expression of an ASD risk gene Glo1 in cortical development, supporting the important role of gene–environment interaction in contributing to the etiology of neural developmental disorders, such as ASD.

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<p>The Relationship Between the Level of Copper, Lead, Mercury and Autism Disorders: A Meta-Analysis</p>

Cited by 18 publications

References 24 publications

Thioredoxin 1 and Thioredoxin Reductase 1 Redox System Is Dysregulated in Neutrophils of Subjects with Autism: In Vitro Effects of Environmental Toxicant, Methylmercury

Thioredoxin 1 and Thioredoxin Reductase 1 Redox System Is Dysregulated in Neutrophils of Subjects with Autism: In Vitro Effects of Environmental Toxicant, Methylmercury

Reversal of Autism Symptoms among Dizygotic Twins through a Personalized Lifestyle and Environmental Modification Approach: A Case Report and Review of the Literature

Reduction of Glyoxalase 1 Expression Links Fetal Methylmercury Exposure to Autism Spectrum Disorder Pathogenesis

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