Acquired tolerance in cadmium-adapted lung epithelial cells: roles of the c-Jun N-terminal kinase signaling pathway and basal level of metallothionein

Toxicology and Applied Pharmacology
Andy T Y LauJen-Fu Chiu

Abstract

Cadmium-resistant cells were developed in our laboratory with rat lung epithelial cells (LECs) by stepwise exposure of LECs to cadmium chloride from 1 microM to 20 microM after 20 passages. To investigate the Cd-resistant phenotype in a long-term perspective, cadmium-resistant cells adapted to 20 microM cadmium (Cd(R)) were then cultured in the absence of cadmium for various passages [Cd(R)(-n)]. All these adapted cells were significantly protected from cadmium toxicity as compared to parental cadmium-sensitive LECs (Cd(S)). The cadmium-resistant phenotype of adapted cells was relatively stable in the absence of cadmium for as long as 40 passages. Basal mRNA level of metallothionein-1 (MT-1) was dramatically higher in Cd(R) than in Cd(R)(-), which may account for the higher Cd-resistance of Cd(R) than Cd(R)(-). MT-1 mRNA level decreased drastically in Cd(R) after cadmium removal, suggesting that the high basal level of MT-1 in Cd(R) may be only partially responsible for cadmium-resistance. Treatment of cells with high levels of cadmium resulted in decreased phosphorylation of c-Jun N-terminal kinase (JNK1/2) in adapted cells than in sensitive cells and this cadmium-induced JNK activity was blocked by JNK inhibitor II, SP600125....Continue Reading

Citations

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Dec 5, 2019·International Journal of Molecular Sciences·Jacopo Junio Valerio BrancaAlessandra Pacini

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