Arsenic-induced gene expression changes in the neural tube of folate transport defective mouse embryos

Wlodarczyk, Bogdan J.; Cabrera, Robert M.; Hill, Denise S.; Bozinov, Daniel; Zhu, Huiping; Finnell, Richard H.

doi:10.1016/j.neuro.2006.02.005

Cited by 43 publications

(23 citation statements)

References 69 publications

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“…Ground water samples from wells showed excess arsenic levels in the Jinzhong basins in which Heshun is located (Yu et al 2007). Of note, Wlodarczyk et al (2006) analyzed gene expression in the neural tubes of arsenic exposed mouse embryos and found that there was a significant dysregulation in a group of genes directly involved in the mitochondrial process of energy production. The local government has been developing environmental requirements and accompanying enforcement mechanisms for larger mines, but this case study shows that more needs to be done.…”

Section: Discussionmentioning

confidence: 99%

Spatial analysis of neural tube defects in a rural coal mining area

Liao

Wang

et al. 2010

International Journal of Environmental Health Research

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Shanxi province in northern China has one of the highest reported prevalence rates of neural tube defects (NTDs) in the world. The current study selected Heshun, the county with the highest rate of NTDs in Shanxi, as a study area and tested whether residence in a coal mining area was a contributing factor. A NTD cluster was detected in an area within 6 km of the coal mines for almost every year during 1998-2005. Poisson regression analysis revealed that there may be an association between production in coal mines and prevalence of NTDs in coal mine areas. Future work identifying factors independently correlated with NTDs in coal mining regions may provide further insights into the health effects of coal mines on NTDs.

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Section: Discussionmentioning

confidence: 99%

Spatial analysis of neural tube defects in a rural coal mining area

Liao

Wang

et al. 2010

International Journal of Environmental Health Research

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“…The types of skin cancer associated with arsenic include intraepidermal carcinomas (Bowen disease) [2], squamous cell carcinomas (SCC), basal cell carcinomas (BCC) [3], Merkel cell carcinoma (MCC) [4] and head and neck cancers [5]. Microarrays gene expression has revealed that arsenicals impact the function of diverse tissue types including the skin, [6,7], bladder and kidney [8], liver [9], prostate and lung [10], peripheral lymphocytes [11], neural tube [12], and urogenital cells [13]. Arsenic also is useful for the treatment of relapsed or refractory acute promyelocytic leukemia as well as solid tumors [14–17].…”

Section: Introductionmentioning

confidence: 99%

Proteomics-Based Identification of Differentially Abundant Proteins from Human Keratinocytes Exposed to Arsenic Trioxide

Udensi

Tackett

Byrum

et al. 2014

J Proteomics Bioinform

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IntroductionArsenic is a widely distributed environmental toxicant that can cause multi-tissue pathologies. Proteomic assays allow for the identification of biological processes modulated by arsenic in diverse tissue types.MethodThe altered abundance of proteins from HaCaT human keratinocyte cell line exposed to arsenic was quantified using a label-free LC-MS/MS mass spectrometry workflow. Selected proteomics results were validated using western blot and RT-PCR. A functional annotation analytics strategy that included visual analytical integration of heterogeneous data sets was developed to elucidate functional categories. The annotations integrated were mainly tissue localization, biological process and gene family.ResultThe abundance of 173 proteins was altered in keratinocytes exposed to arsenic; in which 96 proteins had increased abundance while 77 proteins had decreased abundance. These proteins were also classified into 69 Gene Ontology biological process terms. The increased abundance of transferrin receptor protein (TFRC) was validated and also annotated to participate in response to hypoxia. A total of 33 proteins (11 increased abundance and 22 decreased abundance) were associated with 18 metabolic process terms. The Glutamate--cysteine ligase catalytic subunit (GCLC), the only protein annotated with the term sulfur amino acid metabolism process, had increased abundance while succinate dehydrogenase [ubiquinone] iron-sulfur subunit, mitochondrial precursor (SDHB), a tumor suppressor, had decreased abundance.ConclusionA list of 173 differentially abundant proteins in response to arsenic trioxide was grouped using three major functional annotations covering tissue localization, biological process and protein families. A possible explanation for hyperpigmentation pathologies observed in arsenic toxicity is that arsenic exposure leads to increased iron uptake in the normally hypoxic human skin. The proteins mapped to metabolic process terms and differentially abundant are candidates for evaluating metabolic pathways perturbed by arsenicals.

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“…While the results demonstrated that arsenic induced mitochondrial disruption and oxidative stress, this study also revealed many genes whose altered pattern of expression has previously been shown to induce birth defects in mouse models. These genes included engrailed 1 (En-1), platelet-derived growth factor receptor alpha (Pdgfra) and ephrinA7 (EphA7) (Wlodarczyk et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Reproductive consequences of oral arsenate exposure during pregnancy in a mouse model

Hill

Wlodarczyk

Finnell

2008

Birth Defects Research Pt B

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BACKGROUND:The second most common of all structural birth defects, neural tube defects (NTDs), affect approximately 2.6/1,000 births worldwide, and 1/1,000 births in the United States. Of the many environmental agents suspected of being teratogenic, arsenic (As) is capable of inducing NTDs in laboratory animals. METHODS: We evaluated the teratogenicity of oral exposure on embryonic day (E) 7.5 and E:8.5 to As 4.8, 9.6, or 14.4 mg/kg (as sodium arsenate) in an inbred mouse strain, LM/Bc/Fnn, that does not exhibit spontaneous neural tube malformations. Control and arsenic-treated dams (20 per treatment group) were weighed daily, and evaluated for signs of maternal toxicity. Fetuses were evaluated for soft tissue and skeletal malformations. RESULTS: There was no maternal toxicity as evidenced by losses in maternal body weight following As treatment. However, liver weights were lower in all As-treated groups, suggesting hepatotoxicity due to As exposure. The number of litters affected with an NTD (exencephaly) in each treatment group was: 0, 1, 5, and 9 for control, As 4.8, 9.6, or 14.4, respectively, which exhibited a positive linear trend. There was evidence for trends between As dose and the number of litters displaying vertebral (po0.001) and calvarial (po0.01) abnormalities, components of the axial skeleton. Mean fetal weight of all As-treated groups was significantly less than in control. DISCUSSION: In our model, maternal oral treatment with As induced NTDs. It also significantly increased the frequency of axial skeletal anomalies in the offspring exposed in utero, and reduced mean fetal weight, without evidence of maternal toxicity. Birth Defects Res (Part B) 83: 40-47, 2008.

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Arsenic-induced gene expression changes in the neural tube of folate transport defective mouse embryos

Cited by 43 publications

References 69 publications

Spatial analysis of neural tube defects in a rural coal mining area

Spatial analysis of neural tube defects in a rural coal mining area

Proteomics-Based Identification of Differentially Abundant Proteins from Human Keratinocytes Exposed to Arsenic Trioxide

Reproductive consequences of oral arsenate exposure during pregnancy in a mouse model

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