Cadmium endocytosis

One of the mechanisms of active reabsorption is endocytosis. Fluid phase endocytosis consists of the incorporation of fluid and solutes in vesicles formed at the base of the brush border membrane of the proximal tubular cells (Figure 1). A more efficient absorptive endocytosis involves first binding of a drug, such as the cationic aminoglycoside and/or may be cadmium [30, 31], to a carrier (phosphatidyhnositol) located in the luminal membrane of the wall of the pinocytotic vesicle occurs followed by endocytosis and lysosomal fusion [32, 33]. 

The sequestration of cadmium by MT is a double-edged sword, i.e., although Cd-MT is relatively inert when stored as an intracellular complex, it becomes a potent nephrotoxicant after reaching the systemic circulation (Cherian et al. 1976 Squibb et al. 1984). Human cadmium nephrotoxicity may be related to Cd-MT exposure, because this may be a major form of cadmium in diet (Maitani et al. 1984). Cadmium salts absorbed from the GI tract or lungs are initially transported to liver, where synthesis of MT is induced. Continual exposure to cadmium results in liver injury with leakage of Cd-MT into the systemic circulation (Dudley et al. 1985). The complex is transported to kidney, filtered, and reabsorbed by the proximal tubule, possibly via a mechanism involving receptor mediated endocytosis (Foulkes... 

MT scavenges cadmium in most cells and also contributes to carrying it in the circulation. Proximal tubules internalize Cd-MT by receptor-mediated endocytosis... 

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