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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

Toxicological information

Additional toxicological data

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Administrative data

Endpoint:
additional toxicological information
Type of information:
experimental study
Adequacy of study:
supporting study
Reliability:
2 (reliable with restrictions)
Rationale for reliability incl. deficiencies:
study well documented, meets generally accepted scientific principles, acceptable for assessment

Data source

Reference
Reference Type:
publication
Title:
Nickel exposure induces persistent mesenchymal phenotype in human lung epithelial cells through epigenetic activation of ZEB1
Author:
Jose CC, Jagnnathan L, Tanwar VS, Zhang X, Zang C, Cuddapah S
Year:
2018
Bibliographic source:
Molecular Carcinogenesis 57:794-806

Materials and methods

Type of study / information:
In vitro study
Test guideline
Qualifier:
no guideline followed
Principles of method if other than guideline:
- Principle of test:
Human lung epithelial cells were exposed to Nickel Chloride at concentrations of 0, 10, 50 and 100 µM and gene expression analyses and gene enrichment analyses were performed.
GLP compliance:
not specified

Test material

Constituent 1
Chemical structure
Reference substance name:
Nickel chloride
EC Number:
253-399-0
EC Name:
Nickel chloride
Cas Number:
37211-05-5
Molecular formula:
NiCl2
IUPAC Name:
nickel(2+) dichloride
Specific details on test material used for the study:
SOURCE OF TEST MATERIAL
- Source / batch No.of test material: Sigma, St Louis, MO / N6136
- Purity: Not stated

Results and discussion

Any other information on results incl. tables

A number of genes were identified as persistently differentially expressed in the presence of Ni.

Epithelial Mesenchymal Transition (EMT) was identified as the most enriched pathway in the differentially expressed genes.

Epithelial markers, such as E-cadherin (CDH1) and claudin 1 (CLDN1) were downregulated in the presence of Nickel. The mesenchymal marker, fibronectin 1 (FN1) was upregulated in the presence of Ni. These effects suggest EMT in exposed cells, and the effects occurred at 10, 50 and 100 µM NiCl2.

A persistent mesenchymal phenotype was observed in cells exposed to Ni.

Gene expression within the EMT signalling pathway revealed Zinc Finger E-Box Binding Homeobox 1 (ZEB1) to be one of the most highly upregulated genes in Ni exposed cells, and persistent upregulation of ZEB1 was confirmed.

In ZEB-1 depleted cells, EMT was not induced.

Applicant's summary and conclusion

Executive summary:

STUDY RATED BY AN INDEPENDENT REVIEWER.

ROBUST SUMMARY DEVELOPED BY AN INDEPENDENT REVIEWER.