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Posted

Hi, I've read a bunch of papers on transmembrane transporters (citrate, lactate, etc) and many papers use a LiCl stop buffer to "stop" transport but do not say why LiCl stops transfer. What is the mechanism of action? Thanks.

  • 3 months later...
Posted

In physiological conditions, the concentration of sodium (Na+) is higher in the exterior of the cells than in the inner. Because of that and because the potential of the cell is negative regarding the exterior, the transport of Na+ into the cell is favoured and produces energy.

Many of the membrane transporters use this energy for transporting other substance which transport is not favoured by gradient. Usually, the transport of one or several Na+ (and/or other ions) in favour of gradient prompts a molecular change in the transporter that allows the transport of the target molecule.

 

The lithium (Li+) doesn’t adjust itself to the transporter to produce the conformational change that would allow the transport of the molecule which it works for. So, when we replace the NaCl for LiCl, these transporters don’t work.

Posted

I'm not sure about this but it sounds like it alters the partial pressures by adding -Cl but not the positive ion. Hence the use of the word "buffer". Or it may be that +Li and/or -Cl crosses the membrane but the other ions do not. This is more of a poisoning than a buffering though.

Posted

Physiologically, in the exterior of the cell, there are moderate amounts of Na+ and Cl-. But Li+ is almost inexistent. So the “stop buffer” doesn’t add Cl-. It only replaces Na+ for Li+.

 

I suppose that Li+ will be used because is the ion more similar to Na+. So, most of the extracellular medium properties are going to remain the same. But Li+ can’t join to the sites of the transporter that the Na+ does because of the size. So, it can’t provide the energy necessary for the molecule (citrate, lactate, aa..) be transported through the cellular membrane. So, the transporter doesn’t work in a medium of LiCl-

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