Cadmium (Cd) exposure in mice induces transcription of metallothionein (MT) mRNA and protein accumulation in both liver and kidney. Resistance to hepatotoxicity through chronic exposure to heavy metals is the result of this induction. However, the same chronic exposure results in damage to kidney. W
Metallothionein induction in the liver, kidney, heart and aorta of cadmium and isoproterenol treated rats
β Scribed by Sylvie Bobillier-Chaumont; Veronique Maupoil; Alain Berthelot
- Publisher
- John Wiley and Sons
- Year
- 2005
- Tongue
- English
- Weight
- 397 KB
- Volume
- 26
- Category
- Article
- ISSN
- 0260-437X
- DOI
- 10.1002/jat.1104
No coin nor oath required. For personal study only.
β¦ Synopsis
Metallothionein (MT), induced in different organs in response to heavy metals and oxidative conditions, exerts antioxidant properties and thus could be implicated in cardiovascular physiopathology. The aim of this study was to investigate the capacity of cadmium (Cd) and isoproterenol to induce in vivo MT not only in rat liver and kidneys but also in heart and aorta. Tissue MT levels, catalase (CAT) and glutathione peroxidase (GPX) activities were assayed at different times after Cd or isoproterenol injection. Cd induced a dose-dependent induction of MT with a higher response in the liver than in the kidney, aorta and heart. The hepatic increase was early (12 h) and maintained (72 h), whereas the elevation was maximal around 48 h for the other organs. Isoproterenol induced a transient (12 h) hepatic and a biphasic (12 and 36 h) renal and cardiac increase. CAT activity was decreased in the liver and increased in the heart with the higher Cd doses. Isoproterenol increased the cardiac GPX activity. In conclusion, the results demonstrate that MT can be induced in rat liver and kidneys but also in heart after a Cd or isoproterenol injection. This enhancement of cardiac and vascular MT levels could be used to study the potential protective effect of MT in cardiovascular diseases.
π SIMILAR VOLUMES
KY 405364236. USA Cigarette smoking constitutes a major source of cadmium exposure via inhalation in man. To determine how smoke exposure affects the organ distribution and accumulation of cadmium, male C57B1 mice and Sprague-Dawley rats were exposed daily for 52-60 consecutive weeks to mainstream s