Subacute exposure to cadmium chloride induces HSP-72 in rat liver.
Two groups of rats (n = 5) weighing 175-185 g were implanted (sc) with osmotic minipumps to deliver (0.5 microliter/hr) deionized water or cadmium chloride (CdCl2; 0.2 M) for 14 days. On completion of subacute treatment, liver and kidneys were collected from control and CdCl2 treated groups for analysis. We report that, subacute exposure to CdCl2 results in significant Cd accumulation in liver and kidneys, and heat-shock-protein 72 (HSP-72) induction in the liver. Results affirm a role for liver HSP-72 in Cd-toxicity.
Curtis
S L
SL
Florida A&M University, College of Pharmacy and Pharmaceutical Sciences, Tallahassee 32307, USA.
Nonavinakere
V K
VK
Potmis
R A
RA
Rasekh
H R
HR
Reams
R
R
Early
J L
JL
D000818:Animals; D019256:Cadmium Chloride / Q000494:pharmacology*; D004305:Dose-Response Relationship, Drug; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000096:biosynthesis*; D008099:Liver / Q000187:drug effects* / Q000378:metabolism; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley
D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D019256:Cadmium Chloride