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Usage

Uses

Used in Pharmaceutical Research:
NICOTINE-N-B-GLUCURONIDE is used as a biomarker for nicotine in the rat brain, which aids in understanding the distribution, metabolism, and effects of nicotine on the central nervous system. This information can be crucial for the development of new treatments and therapies related to nicotine addiction and smoking cessation.
Used in Toxicology Studies:
As a biomarker, NICOTINE-N-B-GLUCURONIDE can be employed in toxicology studies to assess the potential harmful effects of nicotine and its metabolites on the brain and other organs. This can help in evaluating the safety and risk associated with nicotine exposure, as well as in the development of strategies to mitigate these risks.
Used in Analytical Chemistry:
The identification and quantification of NICOTINE-N-B-GLUCURONIDE in biological samples can be utilized in analytical chemistry for the development of new methods and techniques for detecting and measuring nicotine and its metabolites. This can be particularly useful in forensic science, drug testing, and environmental monitoring.
Used in Neuroscience:
NICOTINE-N-B-GLUCURONIDE can be employed as a research tool in neuroscience to study the effects of nicotine on brain function and behavior. Understanding the role of this metabolite in the brain can provide insights into the mechanisms underlying nicotine addiction and the potential for developing new therapeutic approaches to treat nicotine dependence.

Upstream product

• 2624-48-8 nicotine ditartrate 
• 2616-64-0 UDP-glucuronic acid 

Relevant academic research and scientific papers

Nicotine glucuronidation and the human UDP-glucuronosyltransferase UGT2B10

Nicotine biotransformation affects the smoking habits of addicted individuals and therefore their health risk. Using an improved analytical method, we have discovered that the human UDP-glucuronosyltransferase (UGT) 2B10, a liver enzyme previously unknown to conjugate nicotine or exhibit considerable activity toward any compound, plays a major role in nicotine inactivation by direct conjugation with glucuronic acid at the aromatic nitrogen atom. The Km value of recombinant UGT2B10 for nicotine (0.29 mM) was similar to that determined for human liver microsomes (0.33 mM), whereas the Km value of UGT1A4 for nicotine was almost 10-fold greater (2.4 mM). UGT2B10 was also more active than UGT1A4 in N-glucuronidation of cotinine (oxidative nicotine metabolite), whereas UGT2B7 exhibited only low nicotine glucuronidation activity and was essentially inactive toward cotinine. UGT1A9 did not glucuronidate nicotine or cotinine. Quantitative reverse transcription-polymerase chain reaction showed that UGT2B10 mRNA was exclusively expressed in human liver, whereas UGTs 1A4 and 2B7 were expressed at comparable, although somewhat lower, levels in liver and several other extrahepatic tissues, including kidney and intestine. These findings for UGT2B10 (but not for UGT1A4 and UGT2B7) were mirrored by human tissue activities because nicotine and cotinine glucuronidation rates in intestine microsomes were less than 0.1% that of human liver microsomes. These novel findings solve two seemingly separate questions: which UGT is primarily responsible for nicotine glucuronidation in human liver, and what conjugation reactions are catalyzed by UGT2B10. Copyright