Induction of hemolysis and eryptosis by occupational pollutant nickel chloride is mediated through calcium influx and p38 MAP kinase signaling.
calcium
eryptosis
hemolysis
nickel
oxidative stress
p38 MAPK
Journal
International journal of occupational medicine and environmental health
ISSN: 1896-494X
Titre abrégé: Int J Occup Med Environ Health
Pays: Poland
ID NLM: 9437093
Informations de publication
Date de publication:
15 Feb 2022
15 Feb 2022
Historique:
pubmed:
16
9
2021
medline:
19
2
2022
entrez:
15
9
2021
Statut:
ppublish
Résumé
Nickel (Ni) is an abundant environmental hazard and an occupational pollutant. Exposure to Ni compounds is prevalent in electroplating workers and in the printing industry, among others. The toxicity of Ni manifests as dermatological, gastrointestinal, respiratory, allergic, and cardiovascular symptoms. In particular, hyperbilirubinemia and reticulocytosis have been detected in intoxicated subjects; an observation possibly implicating selective red blood cell (RBC) toxicity. Herein, the interaction of nickel chloride (NiCl Cells from healthy donors were incubated for 24 h at 37°C in the presence or absence of 0.5‒10 mM of NiCl It was found that NiCl2 at 10 mM caused profound intracellular calcium overload and significant calcium-dependent hemolysis. Also, NiCl It is concluded that NiCl
Identifiants
pubmed: 34524276
pii: 135747
doi: 10.13075/ijomeh.1896.01814
pmc: PMC10464773
pii:
doi:
Substances chimiques
Environmental Pollutants
0
Reactive Oxygen Species
0
nickel chloride
696BNE976J
Nickel
7OV03QG267
p38 Mitogen-Activated Protein Kinases
EC 2.7.11.24
Calcium
SY7Q814VUP
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1-11Informations de copyright
This work is available in Open Access model and licensed under a CC BY-NC 3.0 PL license.
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