Along with sweet, sour, salty, bitter, and umami, ammonium chloride has been recognized by researchers as the sixth fundamental taste sense. The research, which was published in Nature Communications, shows that the ammonium chloride present in some Scandinavian candies causes the tongue’s OTOP1 protein receptor to become active. This receptor, which senses sour tastes, reacts to the effect of ammonium chloride on hydrogen ion concentration in cells. The study clarifies taste perception systems and hypothesizes that ammonium chloride tasting may have developed as a defense against poisonous compounds.
Ammonium chloride has been identified by researchers as the sixth fundamental taste experience, joining sweet, sour, salty, bitter, and umami.
This discovery clarifies how the tongue can identify this distinctive flavor, which is primarily present in some Scandinavian confectionery.
The discovery, which was written up in the journal Nature Communications, reveals the fundamental processes that underlie this taste perception, which have baffled scientists for many years.
Scandinavian candies have a taste of ammonium chloride.
The study emphasizes the distinct flavor of ammonium chloride, a favorite component in some Scandinavian sweets.
According to neuroscientist Emily Liman, a co-author of the study from the University of Southern California, people from Scandinavian nations may already be accustomed to and enjoy this flavor.
Salmiak salt or ammonium chloride is frequently found in salt licorice, a sweet that is popular in northern European countries.
Mechanism of tongue reaction
Although prior research had suggested that ammonium chloride could cause a reaction in the tongue, finding the precise protein receptors in question had proven to be difficult.
A crucial role in detecting sour tastes is played by the protein OTOP1, which has recently come to light in studies. When exposed to sour, acidic foods like lemonade and vinegar, it acts as a route for hydrogen ions.
The effect that ammonium chloride has on the quantity of hydrogen ions in cells led researchers to hypothesize that it may also activate OTOP1.
The OTOP1 receptor was produced in lab-grown human cells when the OTOP1 receptor gene was injected into the cells.
The reactions of these cells were then carefully measured when they were exposed to acid or ammonium chloride.
The research discovered that ammonium chloride vigorously activated the OTOP1 channel, matching or exceeding acid’s levels of activation.
The cell was exposed to minute amounts of ammonia from ammonium chloride, which increased pH and reduced the number of hydrogen ions.
Through OTOP1, this pH difference caused a surge of hydrogen ions that were visible as variations in electrical conductivity across the channel.
As opposed to cells missing OTOP1, taste bud cells from normal mice showed a large increase in action potentials in response to ammonium chloride, demonstrating OTOP1’s function in ammonium chloride perception.
The OTOP1 channel showed variable sensitivity to ammonium chloride in several species, according to researchers.
Due to this divergence, it is possible that the capacity to taste ammonium chloride evolved as a defense mechanism against potentially dangerous ammonium-rich compounds.
