Chinese children with autism: A multiple chemical elements profile in erythrocytes

Wu, Jing; Liu, Duojian; Shou, Xiao-Jing; Zhang, Jishui; Meng, Fanchao; Liu, Yaqiong; Han, Song‐Ping; Zhang, Rong; Jia, Jinzhu; Wang, Jingyu; Han, Ji-Sheng

doi:10.1002/aur.1949

Cited by 14 publications

(7 citation statements)

References 68 publications

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“…However, under physiological conditions, PGE 2 is a signaling molecule that plays an important role in brain development, regulating proliferation and differentiation of neuroectodermal stem cells by affecting the Wnt/β-catenin pathway and is thus significant for the expression of genes important for brain development [57]. It is postulated that this is the mechanism behind the role of PGE 2 in neurodevelopmental diseases, for example in ASD [57], which could explain the increased risk of this disorder in children with elevated blood Pb levels [23][24][25][26].…”

Section: Prostanoidsmentioning

confidence: 99%

“…It is linked to numerous metabolic and structural changes in the developing brain (for detailed review see [12][13][14][15]), resulting in various cognitive disorders [16][17][18][19]. Children exposed to Pb in the early stages of development show a high incidence of many neurodevelopmental diseases, such as hyperactivity, emotional symptoms and conduct disorder [20], attention-deficit hyperactivity disorder (ADHD) [21,22], autism spectrum disorder (ASD) [23][24][25][26], and tend to have lower IQs [27,28]. Until recently, the safe blood Pb concentration was believed to be 10 µg/dL [29,30].…”

Section: Introductionmentioning

confidence: 99%

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Pre- and Neonatal Exposure to Lead (Pb) Induces Neuroinflammation in the Forebrain Cortex, Hippocampus and Cerebellum of Rat Pups

Chibowska

Korbecki

Gutowska

et al. 2020

IJMS

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Lead (Pb) is a heavy metal with a proven neurotoxic effect. Exposure is particularly dangerous to the developing brain in the pre-and neonatal periods. One postulated mechanism of its neurotoxicity is induction of inflammation. This study analyzed the effect of exposure of rat pups to Pb during periods of brain development on the concentrations of selected cytokines and prostanoids in the forebrain cortex, hippocampus and cerebellum. Methods: Administration of 0.1% lead acetate (PbAc) in drinking water ad libitum, from the first day of gestation to postnatal day 21, resulted in blood Pb in rat pups reaching levels below the threshold considered safe for humans by the Centers for Disease Control and Prevention (10 µg/dL). Enzyme-linked immunosorbent assay (ELISA) method was used to determine the levels of interleukins IL-1β, IL-6, transforming growth factor-β (TGF-β), prostaglandin E2 (PGE2) and thromboxane B2 (TXB2). Western blot and quantitative real-time PCR were used to determine the expression levels of cyclooxygenases COX-1 and COX-2. Finally, Western blot was used to determine the level of nuclear factor kappa B (NF-κB). Results: In all studied brain structures (forebrain cortex, hippocampus and cerebellum), the administration of Pb caused a significant increase in all studied cytokines and prostanoids (IL-1β, IL-6, TGF-β, PGE2 and TXB2). The protein and mRNA expression of COX-1 and COX-2 increased in all studied brain structures, as did NF-κB expression. Conclusions: Chronic pre-and neonatal exposure to Pb induces neuroinflammation in the forebrain cortex, hippocampus and cerebellum of rat pups.

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Section: Prostanoidsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Pre- and Neonatal Exposure to Lead (Pb) Induces Neuroinflammation in the Forebrain Cortex, Hippocampus and Cerebellum of Rat Pups

Chibowska

Korbecki

Gutowska

et al. 2020

IJMS

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“…Of these, the ASD group showed lower Zn concentrations in 16 studies (31%), and higher Zn concentrations in 10 studies (19%), compared to the control group. Of the total number of included studies, Sweetman et al (2019), Wu et al (2018), and Gentile et al (1983) did not report differences in Zn concentrations between the groups [ 17 , 34 , 45 ]. Of these, Sweetman et al (2019) reported that Zn levels exceeded the limits for reference values, where 38 children (26%) had Zn levels < 10.7 μmol/L (17 in the ASD group [23%] and 21 in the control group [29.2%]) [ 45 ].…”

Section: Resultsmentioning

confidence: 99%

Zinc Status and Autism Spectrum Disorder in Children and Adolescents: A Systematic Review

do Nascimento,

Oliveira Silva,

de Morais

et al. 2023

Nutrients

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Autism Spectrum Disorder (ASD) is a neurodevelopmental disorder, the prevalence of which has increased in children and adolescents over the years. Studies point to deficiency of trace elements as one of the factors involved in the etiology of the disorder, with zinc being one of the main trace elements investigated in individuals with ASD. The aim of this review is to summarize scientific evidence about the relationship between zinc status and ASD in children and adolescents. This review has been registered in the International Prospective Register of Systematic Reviews (registration number CRD42020157907). The methodological guidelines adopted were in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) statement. Studies were selected from an active investigation of the PubMed, Scopus, LILACS, and Google databases to search for observational studies. Fifty-two studies from twenty-two countries were included. The sample sizes ranged from 20 to 2635, and the participants ranged from 2 to 18 years old. Nine types of biological matrices were used, with hair, serum, and plasma being the most frequently used in the evaluation of zinc concentrations. Significant differences in zinc concentrations between the ASD and control groups were observed in 23 studies, of which 19 (36%) showed lower zinc concentrations in the ASD group. The classification of studies according to methodological quality resulted in high, moderate, and low quality in 10, 21, and 21 studies, respectively. In general, we did not observe a significant difference between zinc concentrations of children and adolescents with ASD compared to controls; however, studies point to an occurrence of lower concentrations of Zn in individuals with ASD. This review reveals that more prospective studies with greater methodological rigor should be conducted in order to further characterize this relation.

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“…Metal/elemental disturbances have been associated with NDDs [98], suggesting a role of metal dyshomeostasis in their etiology, albeit with much of the focus of studies on NDDs on peripheral markers rather than the brain. For example, alterations in the levels of metals and/or trace metals in serum or in hair or nails are reported and sometimes correlate with the features or severity of ASD [99][100][101][102][103][104][105][106][107]; the observed metal profiles can differ by sex [108] and geographic location. Alterations in the brain metal levels in ASD have been reported [109,110], as have correlations of trace metal levels with neuroinflammatory markers [111].…”

Section: Evidence For the Involvement Of Metals In Ndds And Ndgdsmentioning

confidence: 99%

Air Pollution-Related Brain Metal Dyshomeostasis as a Potential Risk Factor for Neurodevelopmental Disorders and Neurodegenerative Diseases

2020

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Increasing evidence links air pollution (AP) exposure to effects on the central nervous system structure and function. Particulate matter AP, especially the ultrafine (nanoparticle) components, can carry numerous metal and trace element contaminants that can reach the brain in utero and after birth. Excess brain exposure to either essential or non-essential elements can result in brain dyshomeostasis, which has been implicated in both neurodevelopmental disorders (NDDs; autism spectrum disorder, schizophrenia, and attention deficit hyperactivity disorder) and neurodegenerative diseases (NDGDs; Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and amyotrophic lateral sclerosis). This review summarizes the current understanding of the extent to which the inhalational or intranasal instillation of metals reproduces in vivo the shared features of NDDs and NDGDs, including enlarged lateral ventricles, alterations in myelination, glutamatergic dysfunction, neuronal cell death, inflammation, microglial activation, oxidative stress, mitochondrial dysfunction, altered social behaviors, cognitive dysfunction, and impulsivity. Although evidence is limited to date, neuronal cell death, oxidative stress, and mitochondrial dysfunction are reproduced by numerous metals. Understanding the specific contribution of metals/trace elements to this neurotoxicity can guide the development of more realistic animal exposure models of human AP exposure and consequently lead to a more meaningful approach to mechanistic studies, potential intervention strategies, and regulatory requirements.

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Chinese children with autism: A multiple chemical elements profile in erythrocytes

Cited by 14 publications

References 68 publications

Pre- and Neonatal Exposure to Lead (Pb) Induces Neuroinflammation in the Forebrain Cortex, Hippocampus and Cerebellum of Rat Pups

Pre- and Neonatal Exposure to Lead (Pb) Induces Neuroinflammation in the Forebrain Cortex, Hippocampus and Cerebellum of Rat Pups

Zinc Status and Autism Spectrum Disorder in Children and Adolescents: A Systematic Review

Air Pollution-Related Brain Metal Dyshomeostasis as a Potential Risk Factor for Neurodevelopmental Disorders and Neurodegenerative Diseases

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