A neurotransmitter called acetylcholine (or ACh) helps your muscles contract, as well as regulating functions as diverse as sweating, heart function, and pupil dilation. When everything is working correctly, ACh is a transient thing. It sends a message – for example, contract this muscle – and it is then broken down by an enzyme. It is important that, once it’s done its job, ACh get broken down so the muscle quits contracting. If it doesn’t get broken down, the muscle will be paralyzed.

VX throws a wrench into the body’s mechanism for breaking down ACh, wreaking havoc on the broad array of ACh-mediated functions found in the body. As such, it’s a potent poison.

The US has destroyed much of its stocks of VX. Today, chemical treatment and incineration are the preferred methods of destroying VX, but some of the earliest VX stock disposal was performed in the colorfully named Operation CHASE (Cut holes and sink ‘em), wherein ships were filled with unwanted weapons and sunk into the ocean.

Interestingly, some molecules much like VX have high enough toxicity to insects and low enough toxicity to humans that they’ve found use as insecticides. Malathion is one such example.

The bromine atoms are very heavy – about 80 times as heavy as a hydrogen atom, or 7 times as heavy as a carbon atom. Bromination usually gives you a molecule that has higher density than the parent molecule.

Vegetable oil – which has a density of about 0.9 grams per milliliter – can be made as dense as water (i.e., 1 gram per milliliter) by adding the right amount of bromine.

Brominated vegetable oil can give an emulsion in water that is opaque and visually pleasing – it turns up in all kinds of opaque sodas and sugar/sport drinks. Is it OK to ingest bromine? Just about everyone gets away with the small amount he takes in from the occasional soda, but it’s definitely possible to ingest too much – awhile back, there was a case of a person who drank as much as a gallon a day of BVO-containing soda. Turns out, he got bromine poisoning!

If you take or are close to someone who takes antidepressant medication, you’re probably aware that one class, the SSRIs, is particularly prone to causing sexual side effects. These effects can run the gamut from inhibition of libido, to erectile dysfunction, to a diminished or complete inability to achieve orgasm. It’s that last one that we take a look at today – a SSRI went on sale in Britain this week that is touted as inhibiting orgasm – on purpose!

This SSRI, dapoxetine, is marketed to treat premature ejaculation. Previously sold in a few European countries, it has just gone on the market in the UK as a product called Priligy.

This compound is a rather short-acting SSRI, with a half-life (that is, the time it takes your body to eliminate it) of just under two hours. Contrast that with, say, Prozac, which has a half-life of several days. Additionally, one of the compounds your body metabolizes Prozac is also an antidepressant, with a half-life of up to about two weeks. Half-lives are an important part of designing and prescribing a drug – if you have something you want around constantly (like an antidepressant), it can be nice to have something that sticks around quite awhile. That way, if you miss a dose, your brain chemistry won’t return to the bad old days before you started taking the drug – the effect of the missed dose is blunted by the fact that you’re still carrying a fair amount around in your body. That said, if your long-half-life pill isn’t working for you, and you want to switch to a new antidepressant, it can take awhile to get it all eliminated from your system. For a pill intended to be used for something episodic (like having sex), a short half-life isn’t a liability at all – in fact, it can be a desirable feature.

Back after a long hiatus – thanks for reading!

Just like people obesity drugs, they’re intended for short-term use, coupled with a diet and exercise plan.

I really don’t understand. It’s not hard to put your dog on a diet. See here if you are interested in reading some dog forum chatter (including a first-person owner account) about the drug.

A few months ago, a tyrosine kinase inhibitor anticancer drug for people, this month, one for dogs.

It is made to treat cutaneous mast cell tumors, which apparently account for about a quarter of dog cancers.

I know a lot of people drugs end up in pets, but do pet drugs ever end up crossing over into human medicine? Anyone know anything about how the decision to go after a dog-specific drug works? Just cheaper to go after?

Skip to ca. 3 mins for the magic. Using the dance idiom.

There are a number of tobacco-associated compounds that are formed by reactions of nicotine. Cotinine is a metabolite formed from nicotine in the body – it hangs around a relatively long time, so it is a good marker for recent nicotine exposure.

Additionally, a number of nitrosamines, formed during tobacco processing, are present – many formed from nicotine. Nitrosamines are pretty nasty – just about any compound of this class is regarded as a suspect carcinogen. Nitrosamines are responsible for a lot of the bad rap cured meat gets for its role in colon cancer risk. These nicotine-derived nitrosamines have attracted similar attention for their potential causative role in tobacco-associated cancers.

NNAL is a metabolite of one of these tobacco-processing associated nitrosamines. This week, Jian-Min Yuan and colleagues presented some results demonstrating a positive correlation between NNAL and cotinine levels in urine and the later occurence of cancer.

Interestingly, it looks like brand makes a difference:

Our results reveal that urinary total NNAL levels were more than 4-fold higher among smokers in Singapore than in Shanghai. One might wonder if the lower levels of total NNAL in Shanghai versus Singapore smokers were the result of degradation of NNAL in urine during storage. Shanghai samples were collected during 1986-1989 while the Singapore samples were collected during 1994-2005. We believe this is an unlikely scenario. Our experimental data have shown that total NNAL is stable for at least 4 years in urine samples stored at -20 °C. Further, mean total NNAL (0.74 pmol/mg Cr) based on samples collected during the early phase of the Singapore Study (1994-1999) was comparable to that (0.65 pmol/mg Cr) based on samples collected later (2000-2005) (P = 0.70). We speculate that the varying levels of urinary total NNAL between smokers in Shanghai versus Singapore may stem from the considerably lower concentrations of NNK in local Chinese brands (western, imported brands were unavailable in Shanghai during 1986-1989 when subjects were recruited into the cohort) relative to the western brands used by most smokers in Singapore.

There are companies out there developing low-nitrosamine tobacco curing methods, like Star Scientific (disclosure: no position). However, they take some flak in the press – regulators and physicians tend to dislike anything that smells like a “safe cigarette” claim. Studies like the present one are a pretty good argument for harm reduction strategies like nitrosamine reduction, though. Good article on them here.

Going through emails, I came across a request from ASPEX to link to a scholarship they’re offering. $1,000 and “an opportunity to co-author a poster with ASPEX at Pittcon 2010.” If you are an undergrad thinking of applying for this, going to Pittcon might be worth more than the $1,000. You couldn’t ask for a better analytical chemistry meeting to attend, and this could be a great place to find a job or grad school advisor.

Also, if you have something you’d like to see SEM’d, they’ll do it for free (although you have to be OK having it out there for the world to see).

Yesterday, I mentioned naphthoresorcinol as a reagent for aldehyde testing. Did you know: at one point during the Cold War, the Soviets used to put a certain aldehyde on American operatives in the USSR as a tracer?

That aldehyde, NPPD, caused a kerfuffle in the 80′s. There was outrage that Americans were being “tagged,” and speculation as to whether it might be dangerous. Some analytical chemists leaned back, scratched their beards, and said “sounds kind of neat.” And even recently, the compound was re-examined.

Anyone have any NPPD stories?

Before the advent of modern spectrometry techniques (NMR and mass spectrometry), there was a compendium of tests to suss out what sort of things were hanging off a molecule. You took your stuff, added some eye of newt, and if black (but not white) soot rose up, you knew you had an arylamine (or at least had some evidence you did). You still see them occasionally in sophomore Organic chemistry labs, but they’re going by the wayside, too.

One such reagent was naphthoresorcinol:

This one will give you a red adduct with an aldehyde in acidic solution. Anyone know the pathway or care to guess??