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posted by janrinok on Sunday August 09 2015, @06:28AM   Printer-friendly
from the here,-try-this dept.

El Reg reports

An enzyme from the Pseudomonas putida bacterium--originally isolated from soil in a tobacco field--consumes nicotine as its sole source of carbon and nitrogen. Research from not-for-profit The Scripps Research Institute (TSRI) shows that this NicA2 enzyme can be recreated in the lab while retaining its potency, thus making it a potential candidate for drug development.

The enzyme therapy would be used to seek out and destroy nicotine before it reaches the brain, depriving a smoker of the buzz from nicotine that can trigger a relapse into smoking.

"Our research is in the early phase of the drug development process, but the study tells us the enzyme has the right properties to eventually become a successful therapeutic," said Kim Janda, a professor of chemistry and member of the Skaggs Institute for Chemical Biology at TSRI, in a statement.

Current smoking cessation aids fail in 80-90 per cent of cases.

[...] The researchers first combined blood serum from mice with a dose of nicotine equivalent to one cigarette. When they added the enzyme, the nicotine's half-life dropped from two to three hours to just 9 to 15 minutes. A higher dose of the enzyme--and a few chemical modifications--could reduce the half-life of nicotine even further and keep it from ever reaching the brain, according to Janda and his team.

The enzyme stayed stable in the lab for more than three weeks at 98 degrees Fahrenheit. Even more importantly, the researchers detected no toxic metabolites produced when the enzyme degraded nicotine.

Related: Financial Rewards Effective in Smoking Cessation


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  • (Score: 0) by Anonymous Coward on Sunday August 09 2015, @02:58PM

    by Anonymous Coward on Sunday August 09 2015, @02:58PM (#220258)

    It isn't sloppy research it is basic research in the "early phase of the drug development process".
    The hype is for PR which is irritating but scientists are told to communicate the importance of their work and potential real-world applications to the public. TSRI also don't have the job security of academics since their labs depend entirly on "soft money" that is derived from grants with barley any institutional support. I remember someone complaining that they even have to pay for their own paper towels with their grant money.

  • (Score: 0) by Anonymous Coward on Sunday August 09 2015, @06:56PM

    by Anonymous Coward on Sunday August 09 2015, @06:56PM (#220354)

    It is sloppy. As I said, and you can easily go verify for yourself, the high from nicotine occurs nearly immediately. Addiction is strongest when the rewarding sensation occurs very soon after the behavior. The half life of a compound measured in terms of hours or minutes will have nothing to do with the addiction. In fact, this treatment sounds like something I would try adding to cigarettes to get people to smoke *more*. They will still get the reward (which causes the addiction) just as quickly but the cravings will return sooner (assuming that cravings are due to nicotine metabolism/excretion).

    Plus, I'm not sure these results make much sense. Here is the journal article: http://pubs.acs.org/doi/abs/10.1021/jacs.5b06605 [acs.org] . First, the velocity of this enzyme is reported for various temperatures in figures 2B and 3A. The data reported for the same temperatures is different by ~3 fold in the two figures.

    Second, look at figure 3D. After 30 minutes there had been 0 nicotine metabolism in the control (no enzyme) condition and ~100% when the enzyme was added to the mouse serum. It seems strange to me that nicotine is completely stable in mouse serum and the fact they report only such extreme values makes me think something went wrong during the experiment. Of course, no sample sizes or error estimates are reported for anything done during this study.