A single pain receptor is solely responsible for the kick delivered by mustard oil and garlic, according to research in the Cell. Mustard oil is the active ingredient in mustard and in the pungent green sushi condiment known as wasabi.
The sensory receptor also underlies the response to a variety of environmental irritants, such as acrolein, the researchers report. Acrolein accounts for the toxic and inflammatory actions of tear gas, vehicle exhaust, tobacco smoke, and the byproducts of some chemotherapy drugs widely used in the treatment of cancer, severe arthritis, multiple sclerosis, and lupus. The insights therefore suggest potential new avenues for the development of anti-inflammatory and pain medications, according to the researchers.
The research team, led by David Julius at the University of California San Francisco, report cellular and behavioral evidence in mice linking the sensory ion channel TRPA1 to the pain response evoked by mustard oil, garlic, and acrolein. Mice deficient for TRPA1 also show pronounced deficits in their reaction to a natural agent produced in response to injury, inflammation, or oxygen shortage, they found.
"By understanding what triggers TRP channel receptors, we can learn something new about how pain is sensed," Julius said. The TRP family of channels includes receptors for a variety of natural plant products that elicit pain and inflammation by stimulating a subset of neurons, collectively known as nociceptors.
Earlier studies identified a heat-activated TRP channel as the receptor for capsaicin, the pungent ingredient in chili peppers. Similarly, a cold-activated channel underlies the response to menthol and other cooling agents, previous research showed.
While earlier evidence had shown mustard oil and garlic extract to stimulate TRPA1, it had not been determined whether the channel was their exclusive target, Julius said.
In the current study, the researchers examined whether neurons taken from mice lacking the TRPA1 receptor responded normally to the pungent compounds found in mustard oil and garlic. Neurons from the TRPA1-deficient mice were completely insensitive to either ingredient, they reported.
Furthermore, animals lacking the sensory gene did not flinch or try to lick when mustard oil was applied to their paws, as normal animals do. Their paws also swelled less and became less sensitive to pain in response to mustard oil exposure.
Chemical similarities between the wasabi and garlic ingredients and acrolein led the team to examine that environmental pollutant's ability to stimulate TRPA1 receptors. Cells made to express TRPA1 became responsive to acrolein and a structurally related irritant, they reported.
The team also found that TRPA1 is an important target of bradykinin, one of the body's natural inflammatory agents that stimulates pain-sensing neurons and leads to hypersensitivity to heat or touch.