Smoke, promotion

Felmatti et al have shown that a compound in smoke promotes seed germination. 

Nalini S., Sanchezb, R., Hendlerb, S., Sampath P. Aqueous extracts of cigarette smoke promote the oxidation of low density lipoprotein by peroxidases. FEBSJ ff 1997 414(3) 549-51. 

Gremmel T, Steiner S, Seidinger D, Koppensteiner R, Panzer S, Kopp CW. Smoking promotes clopidogrel-mediated platelet inhibition in patients receiving dual antiplatelet therapy. Thromb Res 2009 124(5) 588-91. 

Ohtsuka Y, Munakata M, Tanimura K, et al. Smoking promotes insidious and chronic fanner s lung disease, deteriorates the clinical outcome. Intern Med 1995 34(10) 966 71. 

Molybdenum is also a smoke suppressant for poly(vinyl chloride). It promotes the formation of cis- rather than the trans-polymeric decomposition products which ate the precursors for smoke. The sources for molybdates ate Climax Performance Material Cotp. and Sherwin WiUiams. 

This work was supported in part by Grants-in-Aid for Cancer Research from the Ministry of Education, Science and Culture, a grant for the Program for a Comprehensive 10-Year Strategy for Cancer Control from the Ministry of Health and Welfare of Japan, grants from the Foundation for Promotion of Cancer Research, the Princess Takamatsu Cancer Research Foundation, and the Smoking Research Foundation., and by Grant CA 12623 from the National Institutes of Health. 

The interaction of carotenoids with cigarette smoke has become a subject of interest since the results of the Alpha-Tocopherol Beta-Carotene Cancer Prevention Study Group 1994 (ATBC) and CARET (Omenn et al. 1996) studies were released. P-Carotene has been hypothesized to promote lung carcinogenesis by acting as a prooxidant in the smoke-exposed lung. Thus, the autoxidation of P-carotene in the presence of cigarette smoke was studied in model systems (toluene) (Baker et al. 1999). The major product was identified as 4-nitro-P-carotene, but apocarotenals and P-carotene epoxides were also encountered. 

A somewhat related situation can be used to explain the well-publicized lung-cancer inducing effects of P-carotene in heavy smokers. This subpopulation will have low vitamin C levels and hence damage due to smoke components, such as N02 can produce P-CAR which will reach the lung and initiate damage. In nonsmokers, the vitamin C (or other water-soluble antioxidant) is likely to be present in sufficient concentration to preclude this damaging process. Indeed, this speculation has been promoted by the American Chemical Society as the subject of a press release in 1997 (Bohm et al. 1997). 

However, nicotine also has been shown to stimulate the hypothalamic-pituitary-adrenal axis in rodents, leading to elevated plasma levels of adrenocorticotropic hormone and corticosterone (Andersson et al. 1983 Cam et al. 1979), which are known to exert a wake-promoting effect. However, studies in humans have shown that only intense smoking is able to activate the hypothalamic-pituitary-adrenal axis (Gilbert et al. 1992 Kirschbaum et al. 1992). Nicotine patches, in addition to their use in nicotine suppression and craving, have been used to explore the relationship between sleep and nicotine in human... 

Several other clinically available pharmacological agents have been tested for their potential to facilitate smoking cessation, although they are not approved by the FDA for this purpose. For example, tricyclic antidepressants, which inhibit reuptake of noradrenaline and 5-HT, promote smoking cessation in conjunction with behavioral treatment in some individuals.107 However, these medications are limited because of their significant side effects. 5-HT-selective reuptake inhibitors (SSRIs) are believed to be a safer class of antidepressants but have not demonstrated effectiveness in smoking cessation.108... 

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