Re:How does mercury get into the cells?

March 19, 2007

check this paper out:

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstra\

ctPlus&list_uids=15845419&query_hl=1&itool=pubmed_docsum

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March 20, 2007

Thank you very much! This looks like exactly what I was looking for.

I'm now trying to get a copy of this article and will post it if I can.

Thanks!

I've included info on an earlier related article below.

Zoe

Transport of toxic metals by molecular mimicry.

Ballatori N.

Environ Health Perspect. 2002 Oct;110 Suppl 5:689-94. Review.

" Intracellular concentrations of essential metals are normally maintained within

a narrow range, whereas the nonessential metals generally lack homeostatic

controls.

" Some of the factors that contribute to metal homeostasis have recently been

identified at the molecular level and include proteins that mediate import of

essential metals from the extracellular environment, those that regulate

delivery to specific intracellular proteins or compartments, and those that

mediate metal export from the cell.

" Some of these proteins appear highly selective for a given essential metal;

however, others are less specific and interact with multiple metals, including

toxic metals. For example, DCT1 (divalent cation transporter-1; also known as

NRAMP2 or DMT1) is considered to be a major cellular uptake mechanism for Fe(2+)

and other essential divalent metals, but this protein also mediates uptake of

Cd(2+), Pb(2+), and possibly of other toxic divalent metals.

" The ability of nonessential metals to interact with binding sites for essential

metals is critical for their ability to gain access to specific cellular

compartments and for their ability to disrupt normal biochemical or

physiological functions.

" Another major mechanism by which metals traverse cell membranes and produce

cell injury is by forming complexes whose overall structures mimic those of

endogenous molecules. For example, it has long been known that arsenate and

vanadate can compete with phosphate for transport and metabolism, thereby

disrupting normal cellular functions. Similarly, cromate and molybdate can mimic

sulfate in biological systems.

" Studies in our laboratory have focused on the transport and toxicity of

methylmercury (MeHg) and inorganic mercury. Mercury has a high affinity for

reduced sulfhydryl groups, including those of cysteine and glutathione (GSH).

MeHg-l-cysteine is structurally similar to the amino acid methionine, and this

complex is a substrate for transport systems that carry methionine across cell

membranes.

" Once MeHg has entered the cell, some of it binds to GSH, and the resulting

MeHg-glutathione complex appears to be a substrate for proteins that mediate

cellular export of glutathione S-conjugates, including the apically located MRP2

(multidrug resistance-associated protein 2) transporter, a member of the

adenosine triphosphate-binding cassette protein superfamily.