Cadmium is acutely toxic for murine hepatocytes: effects on intracellular free Ca2+ homeostasis

Title:

Cadmium is acutely toxic for murine hepatocytes: effects on intracellular free Ca2+ homeostasis

Creator:

Wang, S. S., Chen, L., and Xia, S. K.

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:19f71d65-5012-41b3-bc03-6204f8f33fa8
uuid:19f71d65-5012-41b3-bc03-6204f8f33fa8
issn:0862-8408

Subject:

Biochemie. Molekulární biologie. Biofyzika, biochemie, toxicita, kadmium, jaterní buňky, homeostáza, biochemistry, toxicity, cadmium, liver cells, homeostasis, kalciový iont, calcium ion, 2, and 577

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

We studied cadmium toxicity in murine hepatocytes in vitro. Cadmium effects on intracellular free Ca2+ concentration ([Ca2+]i) were assayed, using a laser scanning confocal microscope with a fluorescent probe, Fluo-3/AM. The results showed that administration of cadmium chloride (CdCl2, 5, 10, 25 μM) resulted in a dose-dependent decrease of hepatocyte viability and an elevated aspartate aminotransfe rase (AST) activity in the culture medium (p<0.05 for 25 μM CdCl2 vs. control). Significant increases of lactate dehydrogenase (LDH) activities in 10 and 25 μM CdCl2-exposed groups were observed (p<0.05 and p<0.01, respectively). A greatly decreased albumin content and a more malondialdehyde (MDA) formation also occurred after CdCl2 treatment. The Ca2+ concentrations in the culture medium of CdCl2-exposed hepatocytes were significantly decreased, while [Ca2+]i appeared to be significantly elevated (p<0.05 or p<0.01 vs. control). We found that in Ca2+-containing hydroxyethyl piperazine ethanesulfonic acid-buffered salt solution (HBSS) only, CdCl2 elicited [Ca2+]i increases, which comprised an initially slow ascent and a strong elevated phase. However, in Ca2+-containing HBSS with addition of 2-aminoethoxydiphenyl borane (2-APB), CdCl2 caused a mild [Ca 2+] i elevation in the absence of an initial rise phase. Removal of extracellular Ca2+ showed that CdCl2 induced an initially slow [Ca2+]i rise alone without being followed by a markedly elevated phase, but in a Ca2+-free HBSS with addition of 2-APB, CdCl2 failed to elicit the [Ca2+]i elevation. These results suggest that abnormal Ca2+ homeostasis due to cadmium may be an important mechanism of the development of the toxic effect in murine hepatocytes. [Ca2+]i elevation in acutely cadmium-exposed hepatocytes is closely related to the extracellular Ca2+ entry and an excessive release of Ca2+ from intracellular stores., S. S. Wang, L. Chen, S. K. Xia., and Obsahuje bibliografii a bibliografické odkazy

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2007 Volume:56 | Number:2

Harvested from:

CDK

Metadata only:

false