Metallothionein induction in the liver, kidney, heart and aorta of cadmium and isoproterenol treated rats

Abstract

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.

Renal metallothionein responds rapidly and site specifically to zinc repletion in growing rats

“…While we did not observe MT staining in the glomerulus, others have reported upregulated MT-I mRNA levels at this site in response to oxidative stress [30]. Beyond a role in zinc excretion, zinc-containing MT at these sites may also be important for oxidative protection, as several authors have shown that MT protects against cadmium-, copper-, mercury-, iron-or isoproterenol-induced renal damage [16,29,[31][32][33][34][35][36] and more specifically against proximal convoluted tubular damage [29,35], agreeing with MT localization in the current study. Also, in a mouse model of diabetic nephropathy, those cross-bred with MT-transgenic mice had delayed progression of renal disease that included tubulointerstitial fibrosis [12], further defining a protective role of MT on tubular pathology.…”

Effect of Chlorella vulgaris intake on cadmium detoxification in rats fed cadmium

“…The other study showed that urinary Cd excretion and MT concentrations in kidney were significantly increased in rats exposed to 500 ppm Cd in drinking water for 20 weeks (Kim et al, 2003a). MT content was increased in several tissues (liver, kidney, heart and lung) in different species upon time-dependent Cd exposure (Bobillier-Chaumont et al, 2006; Bonda et al, 2004; Lange et al, 2002). …”

Zinc dyshomeostasis in rats with aldosteronism. Response to spironolactone

“…Increased cardiac MT-I expression is seen in mice in response to streptozocin-induced diabetic cardiomyopathy and in rats in response to cadmium or isoproterenol-induced cardiac injury (9,41). In the silencing of MT expression with a small interfering mRNA, this cardioprotective response is selectively abolished (51).…”