- also known to those who hate the letter 'y' (I know you're listening, Britain!) as valaciclovir
- trade name is Valtrex (see: Paris Hilton)
- is a prodrug, meaning that it is converted into acyclovir, the drug that actually does drug stuff, once it is absorbed into the body
- is active against both types of the herpes simplex virus (both can cause blistering of the mouth and/or genitals) and the varicella zoster virus (VZV, causes chickenpox when you first get infected with it, then it goes into hiding and is reactivated in some people in later life to produce herpes zoster, or shingles)
- doesn't curve these viral infections (there is no cure...mwahahahaha) but can reduce duration of symptoms and promote healing
- is a nucleoside analog, meaning that it mimics the basic components of DNA and RNA in order to mess with the replication and spread of the aforementioned viruses
I use Google Analytics to track the people (including you, welcome reader!) who visit my blog. In addition to telling me how many people visit each day and where they are from and exactly what web browsing software they are utilizing (Firefox rules!), I get to see what keywords bring people to my blog. In other words, what they are typing into Google (or Yahoo or MSN Search or whatever) that gets them here. Occasionally these queries are stated as questions, some of which are inadvertently answered by the contents of this blog, others of which are not. Therefore, in the interest of keeping things mildly interesting (which is the only sort of interesting that I do) I am going to attempt to answer some of the more unique questions that have been posed. Please note that I've edited for spelling or grammar where necessary.
Does catnip cause hangovers in cats ?
Hmm. Well, catnip contains a psychedelic drug, and most psychedelic drugs that I have heard of will cause a mild hangover in some people, so it's possible that some cats do experience negative effects after going nuts on catnip. I realize that is a weak answer, but I can't really ask my cat and it doesn't appear that anyone in the scientific community has studied this particular aspect of catnip use. What I want to know is if they get flashbacks. Because that would explain so very much.
Why does Pepto Bismol make poo black ?
The manufactures of said fine product have answered this question here.
Can Benadryl make you fat ?
Diphenhydramine (Benadryl) is an antihistamine (opposes the action of histamine, which is responsible for many of the symptoms of an allergic reaction) and sedative. It is also used as an antiemetic. I've looked through three pharmacology textbooks (I swear), and none of them mentioned weight gain as a side effect of this drug. Given that two known side effects of this drug are loss of appetite and nausea, I'm going to say that no, Benadryl does not make you fat.
How does Clostridium difficile toxin kill you ?
I totally sort of answered this one already! The toxins produced by C. difficile can cause pseudomembranous colitis (a particular type of infection of the colon) and toxic megacolon, which can lead to the development of sepsis, shock, and/or perforation of the colon with generalization of the infection. In such cases, death usually occurs from septic shock.
Can an overdose on amitriptyline kill you ?
Is a tylenol overdose a good way to die ?
My, aren't we a morbid bunch. An overdose of either of these drugs can kill you, and in both cases, it is a terrible way to die. While I'm at it, aspirin is a really bad idea too.
Types: Questions + Answers
- colourless gas with a faint garlic odour that is produced when metals containing arsenic react with acid
- primarily used in the microelectronics industry - the processing of semiconductors used in computer chips involves the etching of gallium arsenide with acids
- is the most toxic form of arsenic (and that is saying something, since elemental arsenic is a badass carcinogenic and highly toxic metal that'll mess you up something awful)
- Lewisite is an arsine derivative that was developed prior to World War II for use in chemical warfare as a blistering agent like mustard gas
- is a pancytotoxin, meaning that it can mess up every organ in your body
- inhalation of this gas produces, among other things, a fulminant (massive) hemolytic anemia (a substantial loss of red blood cells because a bunch of 'em all go and burst open), likely by inducing oxidative damage such that the membrane integrity of the blood cells is compromised
- the hemolysis in turn leads to nephrotoxicity (hemoglobin in red blood cells is released and precipitates as arsenic-hemoglobin complexes in nephrons, disrupting kidney function) and cardiac affects (red blood cells contain lots of potassium, so when they break open you get lots of potassium released in your blood, which causes conduction disturbances that can lead to heart failure)
- more affectionately (and chemically) known as beta-ketoamphetamine
- an amphetamine-like stimulant that is the primary psychoactive (does things to your brain) compound found in khat (Catha edulis), a flowering evergreen shrub that is native to East Africa
- is present mostly in the shoots and leaves (insert dry literary panda joke here) of the plant, which are often chewed or brewed into tea
- methcathinone, a synthetic designer amphetamine that became popular in Russia in the 1960s, is a methyl derivative of cathinone
- is converted into cathine and norephedrine, two less active amphetamine-like compounds, as the plant matures and when it is dried - hence fresh young plants contain the highest concentrations of cathinone, and so will produce the greatest stimulant effects
Snakes and spiders are obvious examples of animals that are capable of producing venom, which they employ to capture prey and/or defend against predators. However, one does not generally associate mammals with being venomous (unless of course, one is a mammalogist or is exceptionally good with trivia). Truly I say to you, several mammals are indeed venomous, possessing the biochemical means to produce toxins solely for the purpose of using them against other animals. They include the platypus, solenodons, the slow loris, and several species of shrew. Here's the breakdown:
The venomous saliva of northern short-tailed shrew (Blarina brevicauda), which is native to North America and is roughly the size of a house mouse, is known to contain at least one toxic compound, blarina toxin (BLTX). This shrew is an insatiable little bugger, eating almost constantly due to its incredibly high metabolic rate. It is thought that it uses its venomous saliva to paralyze and catch prey larger than itself, such as rodents and frogs, in order to satisfy its extreme hunger. The shrew produces BLTX in its salivary glands, such that it is secreted along with, and so present in, its saliva.
BLTX is a tissue kallikrein-like protease, an enzyme capable of cleaving kinins, such as bradykinin, from precursor proteins known as kininogens. Bradykinin produces vasodilatation (widening of the blood vessels), contraction of smooth muscle, increased vascular permeability, and pain. In mice, BLTX causes rapid and irregular respiration, hypotension (decreased blood pressure), hind limb paralysis, and convulsions, with death generally occurring 3-5 hr after exposure. I'm guessing that the respiratory difficulties and hypotension are at least partly the result of systemic vasodilatation and bronchial constriction mediated by the bradykinin that is released by the toxin. The actual mechanism by which the venom causes death is still unknown. Since humans are much larger than rodents and frogs, if we are bitten by B. brevicauda the quantity of venom is presumably insufficient to produce a systemic reaction, such that only a local inflammation (burning sensation, redness, swelling), likely due to BLTX-mediated bradykinin release, is typically observed at the site of the bite.
Not only is the Australian duck-bill platypus (Ornithorhynchus anatinus) one of only five species of mammals that lay eggs, it is also one of the few mammals that produce venom. Male platypuses possess spurs on their hind limbs which they use to deliver a venom produced in pelvic venom glands as an offensive and defensive weapon. Envenomation (getting the venom injected into you) causes a severe localized response featuring intense pain, hyperalgesia (increased sensitivity to pain), and plasma extravasation (swelling due to fluid entering the tissue from blood vessels). When administered systemically to lab animals, the venom causes hypotension and peripheral vasodilatation (increased blood flow to the skin and other body surfaces). The mechanisms by which these effects are produced is unknown.
What is known is that platypus venom contains at least 19 different peptide/protein components, including two C-type natriuretic peptides (OvCNPa and OvCNPb) and four defensin-like peptides (DLPs). C-type natriuretic peptides are naturally produced by endothelial cells (form the innermost layer of blood vessels) in mammals and have been found in brain, intestine, and kidney. Their primary function is thought to be to regulate blood flow by causing vasodilatation. These peptides have been found in the venom of the South American pit viper (Bothrops neuwiedi), suggesting that they are capable of producing toxic effects as well. Defensins are small peptides found in a wide variety of invertebrates and vertebrates that are capable of killing bacteria, fungi, and viruses. Interestingly, the DLPs in platypus venom have not been shown to possess antimicrobial activity, suggesting they may have a role in mediating the toxic effects of the venom instead.
OvCNPa and OvCNPb have been shown to cause the release of histamine from mast cells, an important process in the development of inflammation. This would explain the swelling and increased sensitivity to pain. Additionally, platypus venom is capable of causing the formation of voltage-dependent ion channels in artificial cell membranes, with OvCNPa and OvCNPb having been shown to have a role in this phenomenon. It has been suggested that these channels, by altering membrane potentials and/or the movement of calcium ion across cell membranes, can modulate signal transduction pathways in cells so as to adversely affect cellular functions.
Kita M, Nakamura Y, Okumura Y, Ohdachi SD, Oba Y, Yoshikuni M, Kido H, Uemura D. Blarina toxin, a mammalian lethal venom from the short-tailed shrew Blarina brevicauda: Isolation and characterization. Proc Natl Acad Sci USA. 2004 May 18;101(20):7542-7.
Kourie JI. Characterization of a C-type natriuretic peptide (CNP-39)-formed cation-selective channel from platypus (Ornithorhynchus anatinus) venom. J Physiol. 1999 Jul 15;518 (Pt 2):359-69.
Torres AM et al. Mammalian l-to-d-amino-acid-residue isomerase from platypus venom. FEBS Lett. 2006 Mar 6;580(6):1587-91.
- has been compared to methamphetamine (crystal meth, crank) in terms of its effects (both are stimulants that produce intense euphoria) but has a longer duration of action (typically >12 hours)
- the infinite creativity and apparent rampant dislike of pronouncing and/or spelling actual chemical names in the street drug community has resulted in this compound also being called: Euphoria, U4EA (clever!), U4Euh (!), 4MA, 4-MAR, and 4-MAX
- derivative of the appetite suppressant (anorectic) aminorex, which was popular in Europe in the 1970s (hmm...something popular in Europe in the 1970s that causes one to lose their appetite...could it be, oh i dunno, ABBA?! OH HE'S ON FIRE TODAY FOLKS!)
- both aminorex and U4Euh (it's growing on me) have been associated with pulmonary hypertension (which is pretty bad, but there are worse things)
- apparently is relatively easy to synthesize in your kitchen using old cookware and phenylpropanolamine (an OTC diet pill)
Tolevamer is a high molecular mass polyanion (i.e. a bunch of highly charged goop) that is used to treat the particularly profuse diarrhea (when you're sittin' in your Chevy / and you feel something heavy!) associated with an infection caused by the bacterium Clostridium difficile. As it's name implies, C. difficile (or C. diff, as the kids call it these days) is a pain in the ass (heh) to treat, since it generally shows up and takes over your intestines when you are already on antibiotics (which kill the normal intestinal bacterial flora that helps protect your gut from infection).
Tolevamer strongly binding to and inhibits the action of C. difficile toxins A and B, which otherwise act on the walls of the intestine in such a manner as to cause inflammation and tissue damage, resulting in your favourite and mine, liquid stool . In extreme cases, these toxins can cause pseudomembranous colitis and toxic megacolon, the latter of which is pretty much the worst thing ever. Notably, tolevamer is not an antibiotic, since it doesn't directly affect C. difficile, making it a novel means of treating infection: neutralize the toxin that is responsible for the pathogenicity instead of trying the kill the bug!
 Braunlin W, Xu Q, Hook P, Fitzpatrick R, Klinger JD, Burrier R, Kurtz CB. (2004). Toxin binding of tolevamer, a polyanionic drug that protects against antibiotic-associated diarrhea. Biophys J 87: 534-539.
- one of several structurally-related toxic compounds designated with a letter of the alphabet that are produced by moulds belonging to the common and largely-soil based genera Aspergillus and Penicillium (including its namesake Aspergillus ochraceus, itself named for its ocher-coloured colonies)
- has been demonstrated to be carcinogenic (causes cancer), teratogenic (causes birth defects), immunotoxic (buggers up and suppresses the immune system), nephrotoxic (kidney-damaging) and hepatotoxic (liver-damaging) in several animal species
- is thought to be the cause of urinary tract (kidneys->ureters->bladder->urethra) cancers and nephropathies (kidney diseases featuring chronic dysfunction and progressing to kidney failure and/or cancer) such as Balkan Endemic Nephropathy (BEN) and Chronic Interstitial Nephropathy (CIN)
- BEN has been noted only in certain rural areas of the Balkan countries (southeastern Europe) for some strange reason
- may contaminate (due to mould growth) cereal grains, pork, coffee and cocoa beans, dried fruit, and red wine (grapes)
- O'Brien E, Dietrich DR. Ochratoxin A: the continuing enigma. Crit Rev Toxicol. 2005 Jan;35(1):33-60.
Disclaimer: Yes, this post is pretty tasteless. However, it should be noted that I am in no way condoning suicide with this post. I am, in fact, merely pointing out why overdosing on the following compounds is a really bad idea.
Also commonly known as paracetamol and Tylenol, is the most common cause of intentional self-poisoning in adults in many countries on account of it being widely available and cheap. What doesn't appear to be well known is that it is selectively toxic to the liver and kidneys, meaning that even if you take enough to destroy these organs, it can still take up to two weeks to actually die. The pain is excruciating.
A bipyridylium herbicide found in many weed control products (e.g. Gramoxone), if ingested in sufficiently large quantities it will cause multisystem organ failure with death occurring within hours to a few days. However, should you fail to drink enough of it, it will selectively accumulate and persist in your lungs and slowly eat away at them while you spend several weeks gasping for breath in terrible pain before you expire. There is currently no antidote, and even people who manage to get lung transplants find that their new lungs are eventually destroyed as well, since the poison also hangs out in the fat surrounding them.
Tricyclic Antidepressants (TCAs)
In overdose, these drugs (amitriptyline, imipramine, desipramine, etc.) make you very ill. You got your cardiac toxicity (arrhythmias are the usual cause of death), neutoxicity (seizures), and hypotension. Plus a whole lots of anticholinergic effects going on. Not a peaceful way to go.
Being strongly acidic or strongly alkaline, will corrode anything organic, including your mouth, esophagus, and stomach. Then all of your stomach acid will escape into the trunk of your body, dissolving your internal organs. That doesn't sound painful at all, does it?
As was discussed previously, a painful and terrifying way to die. You remain fully conscious and coherent as you experience repeated bouts of violent convulsions until your breathing eventually stops and you asphyxiate.
Better known to car sickness aficionados as Dramamine or Gravol, dimenhydrinate is used prevent or treat the nausea and emesis (i.e. barfing, puking, ralphing, spewing, vomiting) associated with such delightful conditions as motion sickness, radiation sickness, being under general anaesthesia, chemotherapy, and my personal favourite, Ménière's disease.
Dimenhydrinate is actually a combination preparation of two drugs. The first is diphenhydramine (also known as Benadryl), an antihistamine that produces sedation and is used to alleviate allergies, nausea and upchucking. The second drug is 8-chlorotheophylline, which is included to counteract the sedating effects of diphenhydramine (it's a derivative of theophylline, which is a chemical found in tea that is similar in both chemical structure and pharmacological effect to caffeine).
In large doses dimenhydrinate can cause seizures (young children are particularly susceptible), ataxia (i.e. loss of muscle coordination), stupor (duh what?), euphoria (feels good man), and hallucinations  . As a result of its euphoric and hallucinogenic effects, people do abuse it to trip out (honestly, just spend the money on shrooms). Abuse of dimenhydrinate among psychiatric patients has also been reported due to its anxiolytic (i.e. anti-anxiety) effects .
 Winn RE, McDonnell KP. (1993). Fatality secondary to massive overdose of dimenhydrinate. Ann Emerg Med 22: 1481-1484.
 Halpert AG, Olmstead MC, Beninger RJ. (2002). Mechanisms and abuse liability of the anti-histamine dimenhydrinate. Neurosci Biobehav Rev 26: 61-67.
Addendum: The comments section of this post has inadvertently accumulated several very interesting anecdotes regarding recreational dimenhydrinate use, and comes highly recommended.
When a drug is first isolated/synthesized and preliminarily investigated by a pharmaceutical company for possible development into a marketable drug, it is often assigned a code number for use by the company. If the drug is then found to be capable of producing a useful pharmacological effect (e.g. reducing blood pressure) without serious toxicity (e.g. liver failure) in animals, it is given a catchier name (like ibuprofen or bacitracin) and evaluated in humans in a series of clinical trials. Should these trials confirm the animal results, and the drug is more effective than currently available drugs that do the same thing (if these drugs are available), and the government is happy with the way things were carried out, a new drug can be brought to market. Hooray!
The majority of drugs that are developed by drug companies never make it to market. A good number of them don't even make it to human trials, and thus are never even granted a nifty moniker. Instead, they retain a boring old drug company code, and are filed away in a company storage room and forgotten. However, sometimes pesky scientists get their hands on these defunct drugs and discover that they possess other interesting effects, which they employ to investigate how the body works. This is the story of those drugs, and why they are so gosh darn groovy.
Very rarely, a particular drug company code is so awesome, that it sticks around even after a 'catchier' name has been assigned and the drug reaches market. RU-486, also known as mifepristone (tradenames include Mifegyne and Mifeprex) is used to terminate pregnancy (within 49 days of gestation) and as an emergency contraceptive. It accomplishes these actions by promoting the breakdown and shedding of the uterine endometrium (the lining of the uterus in which the fetus is implanted early on in a pregnancy) and by preventing ovulation (and thus pregnancy). So not a big winner with the pro-lifers.
Reverses the behavioural effects of ethanol. It stops you from being drunk. It does this horrible, horrible thing by blocking the action of ethanol at GABA receptors in the brain. The worst part is that it can't even be used to treat alcohol poisoning, since it doesn't block the respiratory depression that is usually what kills you if you drink way too much. If that wasn't it enough, it also increases the risk of seizures. So not a big winner with anyone.
BRL 37344, CL 316,243, and SR 58611A
These beauties activate lipolysis (i.e. increase the breakdown of fat) in rats and hamsters, which made the drug companies practically wet themselves when they first stumbled upon them (see: the obesity epidemic in America). However, upon further investigation, they were found not to work in humans, since our fat cells don't appreciably express the particular receptor by which these drugs act.
This is a classic example of a promising new drug gone horribly wrong. It was originally developed as a sedative, but when screened for its ability to cause mutations in bacteria (using the Ames test, a quick way of testing to see if something causes cancer without actually having to expose an animal to it and wait to see what develops), it was found to cause mutations in the presence of light. It's chemical structure is such that it can inadvertently absorb light energy and use it to generate reactive oxygen species, which then cause oxidative damage to DNA, leading to mutations.
- Bousquet-Melou A, Galitzky J, Carpene C, Lafontan M, Berlan M. beta-Adrenergic control of lipolysis in primate white fat cells: a comparative study with nonprimate mammals. Am J Physiol. 1994 Jul;267(1 Pt 2):R115-23.
- Ticku MK, Kulkarni SK. Molecular interactions of ethanol with GABAergic system and potential of RO15-4513 as an ethanol antagonist. Pharmacol Biochem Behav. 1988 Jun;30(2):501-10.
- Will O et al. Oxidative DNA damage and mutations induced by a polar photosensitizer, Ro19-8022. Mutat Res. 1999 Sep 13;435(1):89-101.
Bismuth subsalicylate is the active ingredient in Pepto-Bismol (or if you're a cheapo university student like me, Life Brand Stomach Ache Settler) and Kaopectate. Incidentally, Pepto-Bismol ice cream is a thing.
Consisting of bismuth (a cool-looking metal that like water is less dense as a solid than a liquid) and salicylic acid (essentially the same drug found in aspirin), bismuth subsalicylate has arguably one of the best harmless side effect of all time: temporary darkening of the tongue and/or stool. The bismuth in the drug can react with tiny amounts of sulfur found in saliva and the gastrointestinal tract to form bismuth sulfide, which like many sulfide minerals (e.g. ferrous sulphide, lead sulphide), is black.
It is purported to be an excellent hangover cure, which makes sense given its stomach-settling properties. In addition to its painkilling effect, salicylic acid may be active against stomach-upsetting bacteria. As a sort of paradox, salicylic acid, when taken chronically, can cause peptic ulcers, while bismuth salicylate, which contains salicylic acid, can be used to prevent and treat such ulcers (by coating the lining of the stomach to help protect it from digestive juices).
- thermal breakdown product of a meperidine-like synthetic opioid called 1-methyl-4-phenyl-4-propionoxypiperidine (MPPP) that is used by drug addicts as a heroin substitute and may be accidentally produced during the synthesis of MPPP
- produces severe Parkinsonian symptoms in humans and primates (the humans are often addicts who unwillingly inject themselves with some MPTP-laced MPPP)
- hallucinations and near total immobility ('the frozen addict')
- is transformed in the brain to MPP+ (1-methyl-4-phenylpyridinium, in case you were wondering), which selectively destroys dopamine-releasing neurons in the substantia nigra, the area of the brain that is damaged in people with Parkinson's disease
- in 1982, six people in San Jose, California were exposed to MPTP and developed Parkinson's disease - one of the docs who examined them wrote a book about his experiences
- is used to generate a model for Parkinson's disease in lab animals, permitting the study of the disease and the development of ways to treat it