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Abstract
Despite many scientific advances, human exposure to, and intoxication by, toxic metal
species continues to occur. Surprisingly, little is understood about the mechanisms
by which certain metals and metal-containing species gain entry into target cells.
Since there do not appear to be transporters designed specifically for the entry of
most toxic metal species into mammalian cells, it has been postulated that some of
these metals gain entry into target cells, through the mechanisms of ionic and/or
molecular mimicry, at the site of transporters of essential elements and/or molecules.
The primary purpose of this review is to discuss the transport of selective toxic
metals in target organs and provide evidence supporting a role of ionic and/or molecular
mimicry. In the context of this review, molecular mimicry refers to the ability of
a metal ion to bond to an endogenous organic molecule to form an organic metal species
that acts as a functional or structural mimic of essential molecules at the sites
of transporters of those molecules. Ionic mimicry refers to the ability of a cationic
form of a toxic metal to mimic an essential element or cationic species of an element
at the site of a transporter of that element. Molecular and ionic mimics can also
be sub-classified as structural or functional mimics. This review will present the
established and putative roles of molecular and ionic mimicry in the transport of
mercury, cadmium, lead, arsenic, selenium, and selected oxyanions in target organs
and tissues.