Heavy metals toxicity: effect of cadmium ions on amyloid beta protein 1–42. Possible implications for Alzheimer’s disease

Notarachille, Gabriella; Arnesano, Fabio; Calo, V.; Meleleo, Daniela

doi:10.1007/s10534-014-9719-6

Cited by 81 publications

(58 citation statements)

References 95 publications

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“…Almost all examined elements (12 out of 15) were considered as DCEs at one or more time points (p < 0.05, Table 1), which was also supported by repeated-measures analysis of variance (ANOVA). The majority of them appeared to be significantly enriched in the brain tissues of 3×Tg-AD mice for a relatively long period, including Fe, Zn, Cu, cadmium (Cd), mercury (Hg) and bismuth (Bi) whose levels in the brain have been reported to be elevated in AD383940414243444546. Excess Fe has been linked to the development of AD, which may combine with Aβ in the APs to accelerate neuronal Aβ production and cognitive impairment39.…”

Section: Resultsmentioning

confidence: 99%

Sodium selenate regulates the brain ionome in a transgenic mouse model of Alzheimer’s disease

Zheng

Zhu

Wang

et al. 2016

Sci Rep

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Many studies have shown that imbalance of mineral metabolism may play an important role in Alzheimer’s disease (AD) progression. It was recently reported that selenium could reverse memory deficits in AD mouse model. We carried out multi-time-point ionome analysis to investigate the interactions among 15 elements in the brain by using a triple-transgenic mouse model of AD with/without high-dose sodium selenate supplementation. Except selenium, the majority of significantly changed elements showed a reduced level after 6-month selenate supplementation, especially iron whose levels were completely reversed to normal state at almost all examined time points. We then built the elemental correlation network for each time point. Significant and specific elemental correlations and correlation changes were identified, implying a highly complex and dynamic crosstalk between selenium and other elements during long-term supplementation with selenate. Finally, we measured the activities of two important anti-oxidative selenoenzymes, glutathione peroxidase and thioredoxin reductase, and found that they were remarkably increased in the cerebrum of selenate-treated mice, suggesting that selenoenzyme-mediated protection against oxidative stress might also be involved in the therapeutic effect of selenate in AD. Overall, this study should contribute to our understanding of the mechanism related to the potential use of selenate in AD treatment.

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Section: Resultsmentioning

confidence: 99%

Sodium selenate regulates the brain ionome in a transgenic mouse model of Alzheimer’s disease

Zheng

Zhu

Wang

et al. 2016

Sci Rep

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“…Cadmium has been shown to induce apoptosis in vitro in rat cerebellum cortical neurons by affecting by affecting calcium homeostasis [154] and also has been shown to induce apoptosis in vitro in through damage of mitochondria in rat oligodendrocytes [155]. Cadmium has been demonstrated to interact with β amyloid peptides which may lead to the development of AD [156]. …”

Section: Epidemiologic and Experimental Evidence Of Brain Health Dmentioning

confidence: 99%

Estrogenic Endocrine Disrupting Chemicals Influencing NRF1 Regulated Gene Networks in the Development of Complex Human Brain Diseases

Preciados

Yoo

Roy

2016

IJMS

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During the development of an individual from a single cell to prenatal stages to adolescence to adulthood and through the complete life span, humans are exposed to countless environmental and stochastic factors, including estrogenic endocrine disrupting chemicals. Brain cells and neural circuits are likely to be influenced by estrogenic endocrine disruptors (EEDs) because they strongly dependent on estrogens. In this review, we discuss both environmental, epidemiological, and experimental evidence on brain health with exposure to oral contraceptives, hormonal therapy, and EEDs such as bisphenol-A (BPA), polychlorinated biphenyls (PCBs), phthalates, and metalloestrogens, such as, arsenic, cadmium, and manganese. Also we discuss the brain health effects associated from exposure to EEDs including the promotion of neurodegeneration, protection against neurodegeneration, and involvement in various neurological deficits; changes in rearing behavior, locomotion, anxiety, learning difficulties, memory issues, and neuronal abnormalities. The effects of EEDs on the brain are varied during the entire life span and far-reaching with many different mechanisms. To understand endocrine disrupting chemicals mechanisms, we use bioinformatics, molecular, and epidemiologic approaches. Through those approaches, we learn how the effects of EEDs on the brain go beyond known mechanism to disrupt the circulatory and neural estrogen function and estrogen-mediated signaling. Effects on EEDs-modified estrogen and nuclear respiratory factor 1 (NRF1) signaling genes with exposure to natural estrogen, pharmacological estrogen-ethinyl estradiol, PCBs, phthalates, BPA, and metalloestrogens are presented here. Bioinformatics analysis of gene-EEDs interactions and brain disease associations identified hundreds of genes that were altered by exposure to estrogen, phthalate, PCBs, BPA or metalloestrogens. Many genes modified by EEDs are common targets of both 17 β-estradiol (E2) and NRF1. Some of these genes are involved with brain diseases, such as Alzheimer’s Disease (AD), Parkinson’s Disease, Huntington’s Disease, Amyotrophic Lateral Sclerosis, Autism Spectrum Disorder, and Brain Neoplasms. For example, the search of enriched pathways showed that top ten E2 interacting genes in AD—APOE, APP, ATP5A1, CALM1, CASP3, GSK3B, IL1B, MAPT, PSEN2 and TNF—underlie the enrichment of the Kyoto Encyclopedia of Genes and Genomes (KEGG) AD pathway. With AD, the six E2-responsive genes are NRF1 target genes: APBB2, DPYSL2, EIF2S1, ENO1, MAPT, and PAXIP1. These genes are also responsive to the following EEDs: ethinyl estradiol (APBB2, DPYSL2, EIF2S1, ENO1, MAPT, and PAXIP1), BPA (APBB2, EIF2S1, ENO1, MAPT, and PAXIP1), dibutyl phthalate (DPYSL2, EIF2S1, and ENO1), diethylhexyl phthalate (DPYSL2 and MAPT). To validate findings from Comparative Toxicogenomics Database (CTD) curated data, we used Bayesian network (BN) analysis on microarray data of AD patients. We observed that both gender and NRF1 were associated with AD. The female NRF1 gene network is completely ...

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“…Heavy metals have widespreadly consisted in soils as the results of industrialization and anthropogenic activities (Chen et al 2007;Singh et al 2004), and their toxicities to public health and environment have drawn great attention of the government and researchers (Notarachille et al 2014;Saeed et al 2014). With respect to other categories of contaminants, heavy metals are particularly dangerous because they are not biodegradable (Maslin and Maier.…”

Section: Introductionmentioning

confidence: 99%

Alleviating the toxicity of heavy metals by combined amendments in cultivated bag of Pleurotus cornucopiae

Liu

Guo

Jia

et al. 2015

Environ Sci Pollut Res

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The substrate of mushroom can be polluted with heavy metals and subsequently contaminate mushroom, which requires alternative solutions to reduce associated environmental and human health risks. The effects of amendment application on alleviating Cu and Cd toxicities to Pleurotus cornucopiae were investigated in a cultivated bag experiment conducted with the naturally contaminated substrate. Addition of combined amendments (sodium bentonite, silicon fertilizer, activated carbon, and potassium dihydrogen phosphate) increased the P. cornucopiae biomass and substrate pH. Cu and Cd concentration in P. cornucopiae as well as the available Cu and Cd in substrate reduced for the presence of amendments, and the silicon fertilizer had the biggest inhibition on metal uptake. The smallest amount of Cu and Cd in P. cornucopiae was only 30.8 and 5.51% of control, respectively. Moreover, application of amendments also decreased malondialdehyde (MDA) and hydrogen peroxide (H2O2) level in metal-stressed mushroom by 4.38-53.74 and 8.90-58.42% relative to control, respectively. The decreased oxidative stress could well contribute to the growth of P. cornucopiae, and the elevated substrate pH might lead to the lower metal availability, thus resulting in the reduction of metal accumulation in mushroom. These above results suggest that application of combined amendments in mushroom substrate could be implemented in a general scheme aiming at controlling metal content in P. cornucopiae.

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Heavy metals toxicity: effect of cadmium ions on amyloid beta protein 1–42. Possible implications for Alzheimer’s disease

Cited by 81 publications

References 95 publications

Sodium selenate regulates the brain ionome in a transgenic mouse model of Alzheimer’s disease

Sodium selenate regulates the brain ionome in a transgenic mouse model of Alzheimer’s disease

Estrogenic Endocrine Disrupting Chemicals Influencing NRF1 Regulated Gene Networks in the Development of Complex Human Brain Diseases

Alleviating the toxicity of heavy metals by combined amendments in cultivated bag of Pleurotus cornucopiae

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