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From this article I heard about a study (search "Tewksbury") which concluded that chilies make capsaicin to discourage mammals from eating their seeds, since grinding by mammals' molars render the seeds unable to germinate. Birds, on the other hand, don't break open the seeds and spread the plants far and wide.

But, they also reference a different theory: capsaicin evolved to defend against a certain kind of fungi that infected pepper plants.

My question is: why does the same chemical do these two things? It seems like quite a coincidence, unless capsaicin has some general destructive properties. But Wikipedia's explanation talks about how capsaicin artificially stimulates a certain receptor in our mouths -- which sounds totally unrelated to fungi.

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Recent study has shown that capsaicin indeed has antimicrobial properties. For example, see this article:

Two pungent compounds found in Capsicum species (capsaicin and dihydrocapsaicin) were also tested for their anti-microbial effects. The plain and heated extracts were found to exhibit varying degrees of inhibition against Bacillus cereus, Bacillus subtilis, Clostridium sporogenes, Clostridium tetani, and Streptococcus pyogenes.

In one of the attempts to study its mechanism, a study on yeasts suggested that it works in following ways:

  1. Detoxification of capsaicin by a PDR-type ABC superfamily of multi-drug resistance transporters

  2. Osmotic stress response and damages in membrane structure caused by the capsaicin treatment

  3. Genotoxicity of capsaicin to yeast cells

  4. The effects of the deletions of the genes those were induced by the capsaicin treatment

  5. Mechanism of capsaicin in the growth inhbition to yeast cells:

    The DNA microarray analysis of antimicrobial mechanism of capsaicin shows that capsaicin induced an osmotic stress element, the key genes for membrane biosynthesis, and the PDR network and repressed the genes for ribosomal components and cellular growth. The growth characteristics of deletion strains suggest that PDR5 is important for the resistance to capsaicin. These observations that the PDR network may pump out capsaicin from cells are the first findings. The contribution of the PDR network also suggests that capsaicin enters to the cells and capsaicin functions as a toxic substance to the yeast cells. This toxicity is possibly to the mebrane structure and/or as osmotic stress.

    Full article (PDF) here.

Though in mammals, its mechanism of action is quite different; it acts on ion channels to give a burning sensation. See this article:

The burning and painful sensations associated with capsaicin result from its chemical interaction with sensory neurons. Capsaicin, as a member of the vanilloid family, binds to a receptor called the vanilloid receptor subtype 1 (TRPV1). TRPV1, which can also be stimulated with heat, protons and physical abrasion, permits cations to pass through the cell membrane when activated. The resulting depolarization of the neuron stimulates it to signal the brain. By binding to the TRPV1 receptor, the capsaicin molecule produces similar sensations to those of excessive heat or abrasive damage, explaining why the spiciness of capsaicin is described as a burning sensation.

However, it is toxic for mammals too. Capsaicin is a highly irritant material requiring proper protective goggles, respirators, and proper hazardous material-handling procedures. Capsaicin takes effect upon skin contact (irritant, sensitizer), eye contact (irritant), ingestion, and inhalation (lung irritant, lung sensitizer). The LD50 in mice is 47.2 mg/kg.

Though its mechanisms are different, it performs quite similar functions: protecting the plant from predators and infections i.e. a defense system.

It seems like quite a coincidence, unless capsaicin has some general destructive properties.

It is neither a coincidence nor capsaicin has general destructive properties. In fact, capsaicin is being used as an analgesic too. See this article:

Capsaicin is a chili pepper extract with analgesic properties. Capsaicin is a neuropeptide releasing agent selective for primary sensory peripheral neurons. Used topically, capsaicin aids in controlling peripheral nerve pain. This agent has been used experimentally to manipulate substance P and other tachykinins. In addition, capsaicin may be useful in controlling chemotherapy- and radiotherapy-induced mucositis.

Its mode of action is, seemingly, somewhat similar. See this:

The mechanism of action of topical capsaicin has been ascribed to depletion of substance P. However, experimental and clinical studies show that depletion of substance P from nociceptors is only a correlate of capsaicin treatment and has little, if any, causative role in pain relief. Rather, topical capsaicin acts in the skin to attenuate cutaneous hypersensitivity and reduce pain by a process best described as ‘defunctionalization’ of nociceptor fibres. Defunctionalization is due to a number of effects that include temporary loss of membrane potential, inability to transport neurotrophic factors leading to altered phenotype, and reversible retraction of epidermal and dermal nerve fibre terminals. Peripheral neuropathic hypersensitivity is mediated by diverse mechanisms, including altered expression of the capsaicin receptor TRPV1 or other key ion channels in affected or intact adjacent peripheral nociceptive nerve fibres, aberrant re-innervation, and collateral sprouting, all of which are defunctionalized by topical capsaicin. Evidence suggests that the utility of topical capsaicin may extend beyond painful peripheral neuropathies.

mechanisms of capsaicin in nociceptors

(P.S. substance P is a neuropeptide, a potent vasodilator & iniates expression of almost all known cytokines.)

Pay attention to the last line 'utility of topical capsaicin may extendbeyond painful peripheral neuropathies.' i.e. capsaicin may have more effects on body than known!

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  • $\begingroup$ So why does the same substance have these different mechanisms of action in different organisms? Is this common in biology? $\endgroup$
    – Eli Rose
    Jan 28, 2017 at 4:45
  • $\begingroup$ It is so because of structural complexity of compounds. Many compounds out there and in here are similar in structure; this is the cause of side-effects of drugs, it is the cause of competitive inhibition of enzymes, and so on. It is not very common, but no surprise if we keep finding more such cases. $\endgroup$ Jan 28, 2017 at 15:21
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Capsaicin binds to an ion channel that is fairly well-conserved across metazoa and fungi. Influencing the activity of an ion channel can have a seemingly small impact on us (e.g. spicy food 'taste') but for a colony of fungus, such activity can cause the individual cells to stop dividing or migrating in a certain direction (fundamentally changing their behavior). In other words, capsaicin can be lethal or at least make living difficult! For more information about these channels and the specific mode of action of capsaicin in mammals, see David Julius' lab website.

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  • $\begingroup$ Interesting, and thanks for the link. Since I don't have a biology background, what is an ion channel and what functions does it perform? Would it be correct or approximately correct to say "Yes, capsaicin does have 'general destructive properties', the property being that it binds to this ion channel which is important in a lot of life forms" ? $\endgroup$
    – Eli Rose
    Jan 11, 2017 at 2:13
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    $\begingroup$ see metroplex's tome-like response below. 'destructive' is inaccurate; it's not destructive to birds apparently, and it's not destructive to the plants that produce the compound. $\endgroup$
    – dblyons
    Jan 12, 2017 at 3:10

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