Life span and pathology in offspring following nicotine and methamphetamine exposure

Martin, Joan C.; Martin, D.; Radow, Barbara; Day, Heather E.

doi:10.1080/03610737908257225

Cited by 19 publications

(16 citation statements)

References 8 publications

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“…This study was designed to assess the influence of nicotine on the same carcinogen during the perinatal stages of life. No influence on tumour development was exerted by nicotine alone (groups III and V versus group IV); this finding is in accordance with previously published data (Martin et al, 1979). In comparison to a study by Alexandrov (1976) (Habs & Schmahl, 1976;Ivankovic & Druckrey, 1968).…”

Section: Discussionsupporting

confidence: 82%

“…The latter assumption could be relevant, since a remarkable number of women do not change their smoking habits during pregnancy and subsequent lactation period. This is the case, even though the influence of nicotine on the progeny has been established in terms of underweight births in animals as well as man (Becker et al, 1968;Becker & Martin, 1971;Martin et al, 1979 Heidelberg, FRG). Both compounds were dissolved in water at 0.4% and 1 %, respectively; fresh solutions were prepared before each administration.…”

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confidence: 99%

“…The majority of these studies revealed that neither nicotine nor its primary metabolites were carcinogenic (LaVoie et al, 1985;Martin et al, 1979;Schmahl & Osswald, 1968;Toth, 1982), although two studies indicated a weak tumorigenic action (Boyland, 1968; Truhaut et al, 1984). Furthermore, a limited number of studies were concerned with a possible modulation of carcinogenesis by nicotine (Bock, 1980;Gurkalo & Volfson, 1982;Habs & Schmahl, 1976Ito et al, 1984; LaVoie et al, 1985).…”

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confidence: 99%

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Influence of perinatal nicotine administration on transplacental carcinogenesis in Sprague Dawley rats by N-methylnitrosourea

Berger¹,

Petru²,

Schmähl³

1987

Br J Cancer

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Summary The administration of nicotine during the perinatal stages of life resulted in a significant decrease in tumours occurring after transplacental induction by N-methylnitrosourea (MNU). The overall tumour incidence following p.o. application of MNU to dams was 85% in rats of the F,-generation, the main occurrence being related to the neurogenic system (62% of the animals). Regular injections of nicotine before or after birth resulted in a reduction of malignancies by 17% and 22% (P=0.08 and 0.0015), respectively. The difference in the incidence of neurogenic tumours proved to be highly significant (P<0.002) in rats of either sex, when nicotine was applied over 26 weeks following birth. There was a gender-specific imbalance in rats which received the carcinogen only, in favour of a lower tumour yield in females (P<0.04), which became less apparent when nicotine was given additionally. These findings suggest that nicotine is capable of modulating the expression of chemically induced tumours of the neurogenic system in a favourable way. Antonomov, 1976). The importance of the respective single agents in tobacco smoke in the mechanisms of tumour development is the field of current research. To avoid a multitude of concurrent mechanisms that are active in tobacco smoke, it seems necessary to investigate at first the effects of purified compounds in order to identify their inherent risk precisely.Since nicotine is the main attraction when consuming cigarettes, this constituent was primarily tested for a possible carcinogenic action. The majority of these studies revealed that neither nicotine nor its primary metabolites were carcinogenic (LaVoie et al., 1985;Martin et al., 1979;Schmahl & Osswald, 1968;Toth, 1982), although two studies indicated a weak tumorigenic action (Boyland, 1968; Truhaut et al., 1984). Furthermore, a limited number of studies were concerned with a possible modulation of carcinogenesis by nicotine (Bock, 1980;Gurkalo & Volfson, 1982;Habs & Schmahl, 1976Ito et al., 1984; LaVoie et al., 1985). These authors used well-established chemicallyinduced models for the detection of nicotine-related changes in tumour expression. Since no uniform answer was obtained from these studies, the question remains whether certain types of cancer can be influenced specifically by nicotine (Bock, 1980;Gurkalo & Volfson, 1982; LaVoie et al., 1985) and whether especially sensitive periods of life exist such as the perinatal period, in which even a very low dose of this agent can lead to tumour development. The latter assumption could be relevant, since a remarkable number of women do not change their smoking habits during pregnancy and subsequent lactation period. This is the case, even though the influence of nicotine on the progeny has been established in terms of underweight births in animals as well as man (Becker et al., 1968;Becker & Martin, 1971;Martin et al., 1979 Heidelberg, FRG). Both compounds were dissolved in water at 0.4% and 1 %, respectively; fresh solutions were prepared before each administ...

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Section: Discussionsupporting

confidence: 82%

mentioning

confidence: 99%

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confidence: 99%

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Influence of perinatal nicotine administration on transplacental carcinogenesis in Sprague Dawley rats by N-methylnitrosourea

Berger¹,

Petru²,

Schmähl³

1987

Br J Cancer

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“…In addition to its addictive properties, some evidences support the hypothesis that nicotine may contribute directly to carcinogenesis through stimulation of nicotinic acetylcholine receptors (nAchR) in non-neuronal cells (Carlisle et al 2004;Minna 2003), thereby affecting cell proliferation and apoptosis (Chu et al 2005;Mai et al 2003), and promoting angiogenesis (Heeschen et al 2001). Nicotine is, however, not itself tumorigenic in experimental animal studies (Martin et al 1979), but there have been limited studies of the role of nicotine in CSC (Gullihorn et al 2005). The availability of the nicotine-free Quest® cigarette offers a novel opportunity for toxicological evaluation of the role of nicotine in cigarette smoke and allows the direct assessment of the tar fraction of cigarette smoke independent of nicotine effects.…”

Section: Introductionmentioning

confidence: 99%

Toxicological analysis of low-nicotine and nicotine-free cigarettes

et al. 2008

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“…Other nicotine exposure studies in experimental animals also do not indicate that nicotine alone is tumorigenic (39)(40)(41). As a tumor promoter, however, nicotine has been reported to increase the frequency of tumors induced by agents other than NNK such as 7,12-dimethylbenz(a) anthracene (42), N-methyl-N 0 -nitro-N-nitrosoguanidine (43), and N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide (44).…”

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confidence: 99%

Long-term Nicotine Replacement Therapy: Cancer Risk in Context

Shields

2011

Cancer Prevention Research

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Nicotine replacement therapy (NRT) for up to 12 weeks is well established, safe and efficacious for fostering smoking cessation. Some smokers at a high risk of relapse may benefit from long-term use, and so long-term NRT safety and efficacy have become a paramount question for the FDA and others. Laboratory studies have indicated a carcinogenic potential of nicotine. Animal model studies reported in this issue of the journal by Maier and colleagues (beginning on page 1743) and Murphy and colleagues (beginning on page 1752), however, provide additional reassurance that NRT does not promote lung cancer. Very long-term studies of NRT effects do not yet exist and would be needed to definitively answer the question about NRT efficacy and cancer risk and some decision making will need to be made based on limited human data and experimental studies. The overall NRT safety question is complex and requires consideration of three contexts and comparator groups (long-term NRT/abstinence vs. smoking, long-term intermittent NRT/ reduced smoking vs. smoking, and long-term NRT/abstinence vs. abstinence without long-term NRT). Although the data on these issues are insufficient, the first comparison seems intuitive and may be compelling enough to allow the FDA to approve a long-term indication for NRT. An important public health goal is to help smokers and their health care providers understand the implications of potential long-term NRT risks in the context of its potential benefits and the far greater risks of continued smoking. Cancer Prev Res; 4(11); 1719-23. Ó2011 AACR.The efficacy and safety of short-term nicotine replacement therapy (NRT) for fostering long-term smoking cessation is well established, and up to 12 weeks of therapy is approved by the U.S. Food and Drug Administration (FDA; refs. 1-4). A meta-analysis indicates that there are measurable benefits in studies of 12 to 18 months of continued NRT use for relapse prevention (5), and other studies also indicate that this use is cost effective (6). An important question of considerable interest that remains today, however, is whether NRT can be recommended for long-term use, even years, to continue to promote smoking abstinence. The answer to this question requires both an efficacy and safety assessment. In this context, NRT conceptually has substantial benefits compared with long-term smoking but also, as explained later and addressed in this issue of the journal, laboratory studies suggest a potential for nicotine to foster the development of cancer.The premise of long-term NRT use is that it would prevent smoking relapse, and the risks would be limited to maintaining nicotine addiction, but without the adverse consequences of continued smoking, such as increased lung cancer risk. Like the consideration of other long-term medications, on face value it is a simple risk-benefits equation. In actuality, however, this question is not simple to answer because the risk can be considered in 3 different contexts and comparator groups namely: (i) what is the risk o...

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Life span and pathology in offspring following nicotine and methamphetamine exposure

Cited by 19 publications

References 8 publications

Influence of perinatal nicotine administration on transplacental carcinogenesis in Sprague Dawley rats by N-methylnitrosourea

Influence of perinatal nicotine administration on transplacental carcinogenesis in Sprague Dawley rats by N-methylnitrosourea

Toxicological analysis of low-nicotine and nicotine-free cigarettes

Long-term Nicotine Replacement Therapy: Cancer Risk in Context

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