On pages 80 and 81, Dr. Moalem describes Jimsonweed, a member of the nightshade family that can have hallucinogenic properties when consumed. Dr. Moalem uses Jimsonweed as an example of common plants that have evolved to produce strong toxins that discourage consumption by herbivores and by omnivores. Dr. Moalem then includes a brief excerpt from Robert Beverly's The History and Present State of Virginia, which describes an incident of Jimsonweed consumption by early American settlers.
Briefly paraphrase the side-effects of Jimsonweed on humans and on non-humans (you may use Survival of the Sickest as well as any outside research you conduct). For what purposes would the Jimsonweed plant (Datura stramonium) evolve a toxin with such effects? Then, using outside information, describe the process by which the Jimsonweed toxin is metabolized and what proteins are catabolized that cause the effects you stated for the first part of the prompt. Be sure to talk about concentration gradients, and be sure to connect back to Big Idea #4, the idea that biological systems interact and that those interactions possess complex properties - at least two mammalian body systems should be mentioned in the description of the toxin's effects.
(Justin Millman, jmillma4@students.d125.org)
Jimsonweed is a plant in the family known as nightshades. Nightshades are plants containing “large portions of alkaloids” (80), or organic bases known to have significant effects on the nervous systems of many organisms (source: http://science.howstuffworks.com/alkaloid-info.htm). In humans, jimsonweed can cause wild hallucinations and make them behave as if they are “crazy” (81). Moreover, jimsonweed contains three specific chemicals (atropine, hyoscyamine, and scopolamine) that result in side effects in BOTH human and animals (including but not limited to cattle, goats, sheep, pigs, horses, and chickens) such as restlessness, tachycardia (rapid heartbeat), twitching, convulsions, dilated pupils, irregular breathing, low blood pressure, and in the most severe cases, death. More generally, the chemicals found in jimsonweed are responsible for making organisms hyperactive, sometimes even to the point of exhaustion (source: http://www.ansci.cornell.edu/plants/jimsonweed/jimsonweed.html).
ReplyDeleteLike many other plants, jimsonweed is a plant that many organisms may (whether by accident or intentionally) consume as a food source. This, obviously, is not in the best interest of the jimsonweed plant. For this reason, the plant has had to evolve mechanisms to defend itself from or deter natural predators. While the jimsonweed’s three toxins may have the effect of deterring predators, the hallucinogenic effects of the plant may also serve to make it far less likely for an animal to consume the plant again in the same sitting, and possibly never knowingly consume the plant again. In other words, the jimsonweed plant has evolved to contain these specific toxins to repel future predators.
As previously stated, jimsonweed contains three major toxins: atropine, hyoscyamine, and scopolamine. To investigate how these chemicals cause the effects stated above, we must investigate them individually. Firstly, atropine is anticholinergic, meaning it inhibits the effects of the cation acetylcholine in the body. Specifically, atropine competitively inhibits (completely disallows the binding of a substance to its specific receptor site) the binding of acetylcholine to receptor sites on muscles and exocrine glands (glands that excrete substances to locations outside itself through a duct), which affects primarily the nervous system and the muscular system. Further, it could be generalized that atropine, like most anticholinergic toxins, may function by “blocking ionic channels” (142; source: http://jp.physoc.org/content/295/1/139.full.pdf+html) in an organism. In this way, atropine does not cause any protein to be catabolized, but works its mechanism by inhibiting critical binding of acetylcholine, which, put generally, inhibits hyperactive muscle function through sodium ion control (Campbell textbook, 1060). By binding to acetylcholine receptor sites, atropine is directly responsible for the loss of the sodium cation concentration gradient that induces muscle contraction through cellular diffusion. In these ways, it becomes obvious why jimsonweed causes twitching and hyperactivity (source: http://www.rxlist.com/atropen-drug/clinical-pharmacology.htm).
Jeeho Lee (jelee4@students.d125.org)
Next, we must examine hyoscyamine. This chemical is very similar in its mechanism to atropine in that it also competitively inhibits the binding of acetylcholine; however, the difference is that hyoscyamine can bind not only to acetylcholine receptors on muscles and exocrine glands, but also the gastrointestinal tract, heart, and eyes. As a result, hyoscyamine can cause not only the symptoms of atropine poisoning, but also dilated pupils (overactive eye muscles), extremely rapid heartbeat (tachycardia), and loss of gastrointestinal function. Again, hyoscyamine does not directly result in the catabolism, or building up, of a specific protein, but functions by creating an abnormal sodium ion concentration gradient in muscles, eyes, heart, and GI tract through competitive inhibition of a critical muscle activity regulator ion, with significant effects on the muscular, nervous, and digestive body systems in mammals (source: http://www.drugbank.ca/drugs/DB00424).
ReplyDeleteThe final jimsonweed toxin to be examined is scopolamine. Scopolamine, like atropine and hyoscyamine, is a competitive inhibitor of acetylcholine binding. But unlike the other two, scopolamine seems to have a much more pronounced effect on the nervous system rather than muscular or digestive systems. According to a journal article published in early 2006 (Abstract: http://www.sciencedirect.com/science/article/pii/S1074742705000869), scopolamine may cause short-term memory loss. But this is not the only effect of scopolamine. In fact, by blocking acetylcholine in the same manner as described above, scopolamine is able to interfere with nerve signaling with the specific effect of preventing vomiting, which explains why vomiting is not a symptom of jimsonweed poisoning. While not clear why scopolamine has this effect, it could be hypothesized that this is because of scopolamine’s effects on nerve impulses that cause the vomiting reflex in muscles of the digestive system. Or, scopolamine “may work directly on the vomiting center” (source: http://www.drugbank.ca/drugs/DB00747).
Looking at the big picture, it is visible how jimsonweed poisoning relates to Big Idea 4. The three alkaloids found in jimsonweed and other nightshades work to destroy communications between at least four different body systems: nervous, muscular, cardiovascular, and digestive. These interactions are the result of interference of nerve impulses by the alkaloids, and the competitive inhibition of acetylcholine leads to a very complex set of reactions that can cause hyperactivity in multiple body systems and loss of digestive function as well.
Jeeho Lee (jelee4@students.d125.org)