There’s an old saying, “Don’t rub salt in his wounds” (meaning: “Don’t make something bad for him even worse”) and I overheard it a couple of days ago on the streetcar down to the library.
This got me wondering, on my way to school: I know salt hurts like anything when you get it in a cut (personal experience–don’t ask), but why exactly? It doesn’t regularly corrode the skin and I figure the human body is pretty saline to begin with…
Not sure, but salt consists of sodium and chlorine in a molecule with a chemical bond that breaks in liquids and releases the elements as individual ions. Both sodium and chlorine are highly reactive elements that undoubtedly damage unprotected tissue, as in a wound.
Salt is a powerful dehydrating agent. It sucks water out of cells, including nerve cells. This causes the nerve cells to complain. While human cells do contain ~100 millmolar sodium chloride, this is nothing in comparison to the multimolar concentration of dry salt.
I have a similar question, which I was about to start a GQ for, but it looks like we have some salt experts right here.
I was recently reading an article about cage diving wherein the author mentioned that a shark’s fin had cut him. As soon as he got to the surface, he rubbed salt into the wound hoping it would scar so he could have it as sort of a memoriam of his cage dive.
“The plasma membrane of neurons, like all other cells, has an unequal distribution of ions and electrical charges between the two sides of the membrane. The outside of the membrane has a positive charge, inside has a negative charge.”
I vaguely remembered something about salts being essential for the operation of the nervous system. Hopefully someone with real knowledge of biology and chemistry will be able to explain it for us.
Oh, man, can we please not have the rampant speculating in GQ? Squink has it right, essentially. What’s going on there is osmosis – transport of water through a semipermeable membrane (your cell membrane) from a region of low solute concentration (your cells) to a region of high solute concentration (the salt). As the salt dissolves in your blood and/or serum, it produces a very highly concentrated solution, which causes water to move out of the cells, killing them. This rapid and massive cell death produces chemical triggers which, in turn, produces nerve impulses, which the brain interprets as PAIN! DEATH! OW!
It seems unlikely that nerves are directly stimulated by ions – the flow of ions across cell membranes is mediated by proteins, and rather more mediated in nerve cells than in others.
And sodium ions and chloride ions have virtually NO characteristics in common with the neutral elements.
Total hijack here, but whatever cut this diver (if anything) it wasn’t a shark’s fin, which is made of cartilage and is about as likely to cause a cut as a Nerf bat. Sharks use their dorsal fin for stability and pectoral fins for guidance NOT as any kind of defense. They do have rough protrusions on their skin–called denticales, I think–which could abrade skin, but a shark that comes into contact with anything is likely to shy away immediately (or at least, that has been my experience.) Sounds like your boyo in the article probably cut himself on the cage and wanted a better story for the dive bunnies.
I’ve had the privledge of diving with sharks on several occasions and have had the opportuntity to observe a “chumming” and the subsequent feeding fury of reef sharks a couple of times. While they certainly aren’t anything to be blase about, they aren’t terribly aggressive toward divers unless provoked. (Provocation, in the tiny brain of a shark doesn’t take much, though.) For the most part, sharks–even ones large enough to be of danger to a human–are way down on the list of things to be worried about in the ocean. From seeing the way most divers plan, move about, and handle their equipment, they should have a much greater concern about doing injury to themselves than fear of aquatic life.
Nametage one very important points you missed in your rampant speculation on this point.
The first is that the while the flow of ions is mediated by proteins the transmission of a neuronal impulse is caused by the propagation of a depolarisation event. Once a depolarisation event has occurred it spontaneously travels the length of the neuron. Yes there are proteins involved in that but they don’t have any control over he event, they simply react to it.
As such if a piece of salt were placed adjacent to neuron it sure as hell would cause a depolarisation event as the salt dissociated and the ions changed the potential of the neural membrane. There’s no way the pore proteins could pump that many ions through the membrane fast enough to prevent it.
Osmotic death in cells is far form instantaneous. It takes from several seconds to several minutes to occur. When you place salt on a wound it causes an immediate sensation of pain, not a sensation in several seconds time.
Moreover you suggest that we have enough time for salt to draw water osmotically out of the connective tissue cells and kill them. Yet you don’t explain how this change in osmotic potential isn’t also changing the membrane potential of the adjacent neurons well before the connective tissue cells are damaged. How does that happen? How can we have a fatal change in solute concentrations outside connective tissue cells without producing the millimolar change in ion concentrations needed to trigger a depolarisation event in nerve cells? And you know what we experience when neurons depolarise, right?
Your explanation doesn’t seem hold up. you seem to be suggesting that the advanced process can occur without pasisng through the intermediate stages first.
I’m putting my money on the original explanation. The initial sensation of stinging is caused by direct change of membrane potential in the neurons.
This has nothing to do with the OP, but the explanation appears in your cite:
When the membrane is depolarized, sodium ions carry positive charges into the cell, which depolarizes the cell further, and that depolarizes the cell even further, which continues until all sodium channels are open and the nerve action potential is triggered. A depolarizaton that produces an action potential must be sufficiently large to open numerous sodium channels and thereby overcome the efflux of potassium ions resulting from the depolarization.