Effect of Nicotine on Proliferation of Normal, Malignant, and Human Papillomavirus-Transformed Human Cervical Cells

Waggoner, Steven; Wang, Xu

doi:10.1006/gyno.1994.1254

Cited by 46 publications

(24 citation statements)

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“…Epithelial cell DNA synthesis and cell proliferation was stimulated at nicotine concentrations lower than those obtained in blood after smoking (9). Nicotine also stimulated the proliferation of a proportion of human cervical cells in vitro (10). In the present study nuclear expression of p16 was seen in smokers in 20% of clinically oral normal epithelial suggesting that smoking may lead to an increase of this cell cycle control protein.…”

Section: Discussionsupporting

confidence: 55%

An immunohistochemical study of the distribution of p 16 protein in oral mucosa in smokers, non-smokers and in frictional keratosis

Tarakji

Kujan²,

Nassani³

2010

Med Oral

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Objective: Our study aimed to characterize alteration in the immunohistochemical p16 expression in normal oral mucosa and non-neoplastic hyperproliferative disorders (i.e. frictional keratosis and mucosa from smokers). Study design: 43 specimen of oral mucosa were examined using immunohistochemistry. Results: In normal mucosa, there was strong positive nuclear staining in a proportion of fibroblasts and endothelial cells in the lamina propria, with variable expression in nuclei of the epithelial layer. However, when the patient's tobacco smoking was examined, p16 nuclear staining in oral epithelium was seen in 4/20 (20%) of smokers and 0/23 (0%) of non-smokers. In every case of frictional keratosis (n=11), there was strong nuclear staining of some basal and supra-basal cells. In addition, there was strong nuclear staining of parakeratinizing squamous in a band above the spinous layer. In clinically normal oral epithelium of smokers and in frictional keratosis, basal and supra-basal cells expressed strong p16 nuclear staining which was absent in the control tissue examined. Conclusion: Our data suggest that p16 expression may be involved in the long-term loss of proliferation in cell senescence of oral mucosa.

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Section: Discussionsupporting

confidence: 55%

An immunohistochemical study of the distribution of p 16 protein in oral mucosa in smokers, non-smokers and in frictional keratosis

Tarakji

Kujan²,

Nassani³

2010

Med Oral

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“…Alteration of heat shock protein production Hahn et al 1991), inhibition of cell metabolism and proliferation (Konno et al 1991;Waggoner and Wang 1994), and induction of nuclear aberrations (Livingstone et al 1990;Doolittle et al 1995) are some of the common results of smokeless tobacco extract and nicotine administration. In addition, it has been demonstrated that both nicotine and smokeless tobacco administration result in generation of reactive oxygen species in in vitro experimental systems Wetscher et al 1995a).…”

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confidence: 99%

Comparison of Pure Nicotine- and Smokeless Tobacco Extract-Induced Toxicities and Oxidative Stress

Yıldız

Liu

Erçal

et al. 1999

Archives of Environmental Contamination and Toxicology

110

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Abstract. The toxicities and oxidative stress-inducing actions of (Ϫ)-nicotine and smokeless tobacco extract (STE), containing equivalent amounts of nicotine, were studied. Toxicities were determined by colony formation assays using Chinese hamster ovary (CHO) cells. Results indicated that nicotine is less toxic than smokeless tobacco extract that contained the same amount of nicotine. The generation of reactive oxygen species, following treatment with smokeless tobacco extract and nicotine, was assessed by measurement of changes in glutathione (GSH) and malondialdehyde (MDA) levels. CHO cells (5 ϫ 10 5 cells/5 ml media) were incubated with 4, 0.8, and 0.08 mg of nicotine and STE containing the same amounts of nicotine. All preparations of smokeless tobacco extract significantly decreased GSH levels and increased MDA generation. However, 0.08 mg of nicotine treatment did not result in a significant change in GSH level, and only 4 mg of nicotine were sufficient to increase MDA generation. Addition of free radical scavenging enzymes, superoxide dismutase (SOD) and catalase (CAT), and an intracellular GSH precursor, N-acetyl-L-cysteine (NAC), replenished the GSH levels in nicotine-treated cells. GSH levels in cells exposed to smokeless tobacco extract containing 4 and 0.8 mg nicotine remained significantly lower than the control with the addition of SOD and CAT. However, co-addition of NAC with smokeless tobacco extract preparations returned the GSH levels to the control level. Lactate dehydrogenase (LDH) activities were measured in the media to establish the membrane damage following exposure to smokeless tobacco extract and nicotine. Treatment of cells with 4 mg nicotine caused a significant increase in LDH activity, which was returned to control level in the presence of the antioxidant enzymes and NAC. Smokeless tobacco extract did not change the LDH activity.

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“…In cell lines derived from human normal, HPV transfected cells nicotine was added to tissue culture plates at concentrations we found in cervical mucus and in higher concentrations. Nicotine enhanced cell proliferation in all three lines 48 .…”

Section: Experimental Studiesmentioning

confidence: 90%

Cervical Intraepithelial Neoplasia – Clinical and Etiological Aspects

Samir¹,

Hellberg²

2012

Intraepithelial Neoplasia

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Effect of Nicotine on Proliferation of Normal, Malignant, and Human Papillomavirus-Transformed Human Cervical Cells

Cited by 46 publications

References 0 publications

An immunohistochemical study of the distribution of p 16 protein in oral mucosa in smokers, non-smokers and in frictional keratosis

An immunohistochemical study of the distribution of p 16 protein in oral mucosa in smokers, non-smokers and in frictional keratosis

Comparison of Pure Nicotine- and Smokeless Tobacco Extract-Induced Toxicities and Oxidative Stress

Cervical Intraepithelial Neoplasia – Clinical and Etiological Aspects

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