Metallothionein cadmium uptake

Leung, K.M.Y., J. Svavarsson, M. Crane, and D. Morritt. 2002. Influence of static and fluctuating salinity on cadmium uptake and metallothionein expression by the dogwhelk Nucella lapillus (L.). J. Exp. Biol. Ecol. 274 175-189. 

The lethal effects of cadmium are thought to be caused by free cadmium ions, that is, cadmium not bound to metallothioneins or other proteins. Free cadmium ions may inactivate various metal-dependent enzymes however, cadmium not bound to metallothionein may have the capacity to directly damage renal tubular membranes during uptake (USPHS 1993). 

After uptake, cadmium is tightly bound to a certain depot protein called metallothionein, which is rich in sulfhydryl (SH) groups and stored in depots in kidney and liver tissues, resulting in very high levels of the metal in these organs. 

In vivo mercury exposure does induce the synthesis of metallo-thionein in the kidney. The absolute amount of thionein bound mercury, however, usually is small for example, less than 2% of the total renal content at 24 hr after the injection of 0.5 mg Hg2+/kg body weight into the male rat (Webb and Magos, 1976). In contrast, at low-level cadmium exposure, most of the metal accumulated in the kidney is bound to metallothionein. The synthesis of this metalloprotein under these conditions parallels the renal uptake of cadmium until, at least, old age (Cain et al., unpublished). The critical renal concentration at which kidney dysfunction occurs at chronic exposure is high - about 200 yg Cd /g wet weight (Friberg et al., 1974), since only about 20% of this cadmium will be in the toxic non-thionein bound form. 

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