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J Biol Chem. 2003 Jan 17;278(3):1886-91. Epub 2002 Nov 05.
A functional role for nicotine in Bcl2 phosphorylation and suppression of apoptosis.

Mai H, May WS, Gao F, Jin Z, Deng X.

Shands Cancer Center and Department of Medicine, University of Florida, Gainesville, Florida 32610-0232, USA.

Nicotine is not only a major component in tobacco but is also a survival agonist that inhibits apoptosis induced by diverse stimuli including chemotherapeutic drugs. However, the intracellular mechanism(s) involved in nicotine suppression of apoptosis is unclear. Bcl2 is a potent antiapoptotic protein and tumor promotor that is expressed in both small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC) cells. It is possible that nicotine may regulate Bcl2 to stimulate cell survival. Here we report that nicotine can induce Bcl2 phosphorylation exclusively at the serine 70 site in association with prolonged survival of SCLC H82 cells expressing wild-type but not the phosphorylation-deficient S70A mutant Bcl2 after treatment with chemotherapeutic agents (i.e. cisplatin or VP-16). Nicotine induces activation of PKC alpha and the MAPKs ERK1 and ERK2, which are physiological Bcl2 kinases. Furthermore, ET-18-OCH3, a specific phospholipase C (PLC) inhibitor, blocks nicotine-stimulated Bcl2 phosphorylation and promotes apoptosis, suggesting that PLC may be involved in nicotine activation of Bcl2 kinases. Using a genetic approach, the gain-of-function S70E mutant, which mimics Ser(70) site phosphorylation in the flexible loop domain, potently enhances chemoresistance in SCLC cells. Thus, nicotine-induced cell survival results, at least in part, from a mechanism that involves Bcl2 phosphorylation. Therefore, novel therapeutic strategies for lung cancer in which Bcl2 is expressed may be used to abrogate the anti-apoptotic activity of Bcl2 by inhibiting multiple upstream nicotine-activated pathways.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12421819&dopt=Abstract

Neuroimmunomodulation. 1999 May-Jun;6(3):168-74.
Effects of cholinergic agonists and antagonists on interleukin-2-induced corticotropin-releasing hormone release from the mediobasal hypothalamus.

Karanth S, Lyson K, McCann SM.

Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, LA 70808-4124, USA.

In previous research we found that interleukin-2 (IL-2)-induced corticotropin-releasing hormone (CRH) release in vitro is mediated by cholinergic activation of nitric oxidergic (NOergic) neurons. The NOergic neurons release nitric oxide that stimulates CRH release. To further characterize the mechanism of IL-2-induced CRH release, the possible role of nicotinic as well as muscarinic receptors in IL-2-stimulated CRH release was evaluated. Medial hypothalamic (MH) explants from adult male rats were preincubated in Krebs-Ringer (KRB) buffer for 45 min followed by incubation for an additional 30 min in fresh KRB or KRB containing various compounds. As previously reported, acetylcholine (ACH) stimulated CRH release in a dose-related fashion. IL-2 (10(-13) M) stimulation of CRH release was unaffected by the lower concentration of ACH (10(-9) M), but surprisingly was inhibited by a 100-fold higher concentration. Atropine (ATR) (10(-7) M) blocked CRH release induced by ACH (10(-7) M) and the release of CRH induced by IL-2. The cholinergic agonist carbachol (CAR) (10(-7) M) also released CRH and this action was blocked by ATR (10(-7) M). CRH release in the presence of CAR was lowered below basal when the concentration of ATR was increased to 10(-6) M. In contrast to ACH, CAR had an additive effect to release CRH when combined with IL-2 (10(-13) M). Nicotine (10(-7) M) also stimulated CRH release and this stimulation was completely blocked by 10(-6) M but not by 10(-7) M of the nicotinic receptor blocker, hexamethonium (HEX). The lower concentration of HEX blocked the stimulatory effect of ACH (10(-7) M) and IL-2 on CRH release. Combined blockade with ATR plus HEX completely blocked the action of ACH and even reduced the CRH concentration to below basal values. Furthermore, combined blockade completely blocked the release of CRH induced by IL-2. We conclude that nicotinic as well as muscarinic receptors play an important role in CRH release, and that they both act to mediate IL-2-stimulated CRH release.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10213914&dopt=Abstract

J Psychoactive Drugs. 2002 Jul-Sep;34(3):321-3.
"Mushroom madness" in the Papua New Guinea Highlands: a case of nicotine poisoning?

Thomas B.

New Guinea Entheobotany Project, Ashgrove Queensland, Australia.

"Mushroom madness" is a condition that was first reported in the Western Highlands Province of Papua New Guinea. This condition was originally blamed on the ingestion of hallucinogenic mushrooms. This was later proven to be incorrect and this condition was explained instead as a form of collective hysteria. There is, however, ethnographic, phytochemical and pharmacological evidence to suggest that "mushroom madness" was actually a state of acute nicotine poisoning produced by the ingestion of toxic quantities of tobacco.

online pharmacy ref. source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12422944&dopt=Abstract

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