Heat, bacteria, and evolution


in Daily updates, Geek stuff, Science

Rusty metal

For those who are unfamiliar, capsaicin is one of the most interesting molecules out there. This is the chemical that makes chili peppers spicy; it is also the active ingredient in pepper spray. Pure capsaicin is rated at about 15 million Scoville heat units: a scale where Tabasco sauce is scored at about 2,500.

Capsaicin is quite an amazing adaptation, actually. Plants developed it to deter animals from eating them. Eventually, animals realized that capsaicin was painful to them, but not actually harmful. By contrast, it is very harmful to some of the species of bacteria that spoil food. As such, spicy foods emerged in hot climates as a defence against nasty prokaryotes. A direct descendent of that realization are the veggie vindaloos I enjoy so much.

Spices have been mentioned here before.

{ 4 comments… read them below or add one }

Neal October 9, 2007 at 9:44 pm

Capsaicin peppers actually evolved because capsaicin deters mammals only. Birds are unaffected. After all, capsaicin is concentrated in the fruit.

. October 10, 2007 at 1:14 am

Why are chillies pungent?

The sensations of heat and pain in the mouth are the result of the stimulation of local heat receptors in the skin and mucous membranes by capsaicin. The capsaicin (vanilloid) receptor VR1 is a sensory neuron-specific ion channel that serves as a polymodal detector of pain-producing chemical and physical stimuli. Capsaicin is a trigeminal stimulant that is important in gustatory physiology (Liu and Simon 2000). Interestingly, capsaicin can also help in the mediation of pain: prolonged application of capsaicin is thought to cause the desensitization of sensory neurons responsible for pain. This might occur via the depletion of substance P, a peptide neurotransmitter in sensory “pain” fibres (Goettl et al 1997), the final outcome being the release ofB-endoprhins which are endogenous opioids. Capsaicin can induce sweating, which is why chillies are popular in hot dry climates. Further, it stimulates the actions of the muscles of the stomach and intestine; this improves digestion and makes chili peppers an attractive condiment for a food that might upset the stomach (Andrews 1984). Most importantly, it appears that capsaicin was developed by plants as a way of preventing animals with digestive systems that can destroy chili pepper seeds from eating them, while allowing animals who will pass the seeds to eat them with no ill effects (Robbins 1992; Tewksbury and Nabhan, 2001). That may be the evolutionary explanation of why chillies are so pungent.

Surprisingly, most of the work on pain-induced by capsaicin had concentrated on mammals, with very little work on gustatory responses in birds. Recently Bryant et al (2000) cultured trigeminal nociceptors (pain receptors) from the Norway rat (Rattus norvegicus, laboratory strain), white leghorn chicken (Gallus gallus), coyote (Canis latrans), white-tailed deer (Odocoileus virginianus) and Canada goose (Branta canadensis) and then applied digital fluorescence microscopy to measure changes in intracellular calcium (an index of cellular activation) in response to applications of known and effective repellents. They found that capsaicin was a more effective stimulus for rat, coyote, and deer neurons than cells from chicken. Does this mean that birds do not have capsaicin-stimulated or vanilloid-receptors in their oral linings, or do they have potent antagonists? The limited effect of capsaicin on birds appears to be why capsaicin is now believed to cause directed toxicity or directed deterrence of potential mammalian seed predators in the chiltepine chilli plant (Capsicum annuum var. glabriusculum) in southern Arizona, while having no effect on seed-dispersing birds, the curve-billed thrashers (Toxostoma curvisrostre) (Tewksbury and Nabhan 2001). To find out whether small fruit-consuming mammals such as cactus mice (Peromyscus eremicus) and packrats (Neotoma lepida) avoid chillies because of their capsaicin content, the authors presented these mammals as well as desert thrasher birds with the pungent chilli fruit (C. annuum), fruit of a non-pungent mutant variety of C. chacoense which is similar is all other aspects to the fruit of C. annuum except in lacking pungency, as well as desert hackberry fruit (Celtis pallida) as a control.

They found that while the birds consumed all three types of fruits equally, the mammals consumed no pungent chilli fruit, an intermediate amount of the non-pungent chilli fruit and all the hackberry fruit. It appears that the capsaicin in the chiltepine chilli fruit deters consumption by mammals. Furthermore, germination trials of C. chacoense fruit (non-pungent chilli) showed that there was zero germination following gut passage through the mammals, while germination levels following gut passage of chiltepine seeds and non-pungent chilli seeds through the birds were excellent and comparable with that of control seeds taken directly from the fruit and planted. If seeds can germinate just as well with and without passage through bird guts, what is the advantage to being consumed by the birds? Tewksbury and Nabhan (2001) found that birds that consumed chilli fruit are more likely to deposit these seeds in shaded sites suitable for germination. This fact coupled with the zero germination on passage through mammalian guts can explain why the chiltepine chilli plant “wants to encourage consumption” by the thrasher birds and to deter consumption by mammals.

Kerrie October 14, 2007 at 2:42 am

Hahahah! They were trying to deter me from eating them but it only made them tastier!

Milan October 31, 2007 at 10:27 am

Hot spice used to cool pain
Chemical from chili peppers is being tested on surgical wounds

“Bite a hot pepper, and after the burn your tongue goes numb. The Baltimore Sun reports that Capsaicin, the chemical that gives chili peppers their fire, is being dripped directly into open wounds during highly painful operations, bathing surgically exposed nerves in a high enough dose to numb them for weeks. As a result patients suffer less pain and require fewer narcotic painkillers as they heal. ‘We wanted to exploit this numbness,’ says Dr. Eske Aasvang, a pain specialist who is testing the substance. Capsaicin works by binding to C fibers called TRPV1, the nerve endings responsible for long-lasting aching and throbbing pain. Experiments are under way involving several hundred patients undergoing various surgeries, including knee and hip replacements using an ultra-purified version of Capsaicin to avoid infection. Volunteers are under anesthesia so they don’t feel the initial burn.”

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