Krumschnabel 2004 Aquat Toxicol

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Krumschnabel G, Nawaz M (2004) Acute toxicity of hexavalent chromium in isolated teleost hepatocytes. Aquat Toxicol 70:159-167.

» PMID:15522432

Krumschnabel G, Nawaz M (2004) Aquat Toxicol

Abstract: Acute toxic effects of hexavalent chromium [Cr(VI)], a widely recognised carcinogenic, mutagenic and redox active metal, were investigated in isolated hepatocytes of goldfish (Carassius auratus). Exposure to 250 microM Cr(VI) induced a significant decrease of cell viability from 94% in controls to 88% and 84% after 30 min and 4 h of exposure, respectively. Cr-toxicity was associated with a concentration-dependent stimulation of the formation of reactive oxygen species (ROS). As one potential source of ROS formation we identified the lysosomal Fe(2+) pool, since the ferric ion chelator deferoxamin inhibited ROS formation by approximately 15%. Lysosomal membranes remained nevertheless intact during Cr-exposure, as determined from neutral red retention in this compartment. Another significant source of ROS appear to be the mitochondria, where a presumably uncoupled increase of respiration by 20-30% was triggered by the metal. Inhibition of mitochondrial respiration by cyanide caused an approximately 40% decrease of Cr-induced ROS-formation, whereas the uncoupling agent carbonyl cyanide m-chlorophenyl hydrazine was without effect. Cellular Ca(2+) homeostasis was not disturbed by Cr(VI) and thus played no role in this scenario. Overall, our data show that Cr(VI) is acutely toxic to goldfish hepatocytes, and its toxicity is associated with the induction of radical stress, presumably involving lysosomes and mitochondria as important sources of ROS formation.

Keywords: chromium (VI), goldfish, hepatocyte, reactive oxygen species, calcium, lysosomes, primary hepatocytes

O2k-Network Lab: AT Innsbruck Oroboros


Labels: MiParea: Respiration, Pharmacology;toxicology 


Organism: Fishes  Tissue;cell: Liver  Preparation: Intact cells 


Coupling state: ROUTINE 

HRR: Oxygraph-2k