Induction of mitochondrial chaperonin, hsp60, by cadmium in human hepatoma cells

Biochem Biophys Res Commun. 1993 Jul 15;194(1):531-6. doi: 10.1006/bbrc.1993.1852.

Abstract

Mitochondrial dysfunction is readily induced by a low level of cadmium both in vivo and in vitro. The gene expression of mitochondrial hsp60 was induced in a dose- and time-dependent manner and also in parallel with the accumulation of cadmium in mitochondria. The levels of hsp60 mRNA increased with time until 18 h, while the induction of heat shock 70 (hsp70) gene peaked at 6 h and then declined. On the other hand, the levels of metallothionein mRNA reached to a plateau at 6 h and were maintained at this level continuously. These results suggest that the regulatory mechanism and/or the signals for hsp60 induction by cadmium are independent from those of hsp70 and metallothionein.

MeSH terms

  • Biological Transport
  • Blotting, Northern
  • Cadmium / metabolism
  • Cadmium / pharmacology*
  • Cadmium Chloride
  • Carcinoma, Hepatocellular
  • Chaperonin 60
  • Chlorides / pharmacology*
  • Heat-Shock Proteins / biosynthesis*
  • Humans
  • Kinetics
  • Liver Neoplasms
  • Metallothionein / biosynthesis
  • Mitochondria / drug effects
  • Mitochondria / metabolism*
  • RNA, Messenger / metabolism
  • Tumor Cells, Cultured

Substances

  • Chaperonin 60
  • Chlorides
  • Heat-Shock Proteins
  • RNA, Messenger
  • Cadmium
  • Metallothionein
  • Cadmium Chloride