Evaluation of carcinogenic/co-carcinogenic activity of a common chewing product, pan masala, in mouse skin, stomach and esophagus
Reads0
Chats0
TLDR
In ICRC mice, EPME was inactive as a complete carcinogen, but effectively promoted the development of forestomach and esophageal papilloma and carcinoma in a concentration‐dependent manner.Abstract:
Pan masala, a dry powdered mixture of areca nut, catechu, lime, unspecified spices and flavoring agents, has gained widespread popularity as a chewing substitute in India. In this study, the carcinogenic and tumor-promoting potential of an ethanolic pan masala extract (EPME) was determined using skin of S/RVCri-ba mice and forestomach and esophagus of ICRC mice as the target tissues. Carcinogenic activity of pan masala was tested by painting the mouse skin for 40 weeks with EPME or by gavage feeding for 6 months. Following initiation with 9,10-dimethylbenz(a)anthracene (DMBA), carcinogenesis of mouse skin was promoted with different doses of EPME, while gastric- and esophageal-tumor-promoting activity was determined by administering EPME by gavage to animals initiated with diethylnitrosamine (DEN). The ability of EPME to effect progression of skin papilloma to carcinoma and cutaneous alterations after a single or multiple EPME treatment were also evaluated. EPME at 25 mg per dose promoted skin-papilloma formation between 30 and 40 weeks of treatment and enhanced the rate of conversion of papilloma to carcinoma. Induction of mild epidermal hyperplasia, dermal edema, increase in epidermal mitotic activity and the rate of epidermal and dermal DNA synthesis by EPME correlated well with its skin-tumor-promoting potential. In ICRC mice, EPME was inactive as a complete carcinogen, but effectively promoted the development of forestomach and esophageal papilloma and carcinoma in a concentration-dependent manner. The tumor incidence at 25 mg EPME per dose was comparable with that obtained in the 12-0-tetradecanoylphorbol-13 acetate(TPA)-treated group. The findings indicate that habitual pan-masala use may exert carcinogenic and co-carcinogenic influence.read more
Citations
More filters
Journal ArticleDOI
Alert for an epidemic of oral cancer due to use of the betel quid substitutes gutkha and pan masala: a review of agents and causative mechanisms
TL;DR: Evidence that strongly supports causative mechanisms for genotoxicity and carcinogenicity of these substitute products, including gutkha and pan masala, are strongly implicated in the recent increase in the incidence of oral submucous fibrosis is reviewed.
Journal ArticleDOI
Independent and combined effects of alcohol intake, tobacco smoking and betel quid chewing on the risk of esophageal cancer in Taiwan
Chien-Hung Lee,Jang-Ming Lee,Deng-Chyang Wu,Hon-Ki Hsu,Ein-Long Kao,Hsiao-Ling Huang,Tsu-Nai Wang,Meng-Chuan Huang,Ming-Tsang Wu +8 more
TL;DR: The results suggest that the intensity and the length of time alcohol and tobacco are used play different roles in the etiology of esophageal cancer.
Journal ArticleDOI
Association of betel nut with carcinogenesis: revisit with a clinical perspective.
TL;DR: A systematic review of the consequences of this widespread habit of BN/BQ mastication on oral cancer with a clinical perspective looks at various preventive efforts being made by governments and highlights the multifaceted intervention strategies required to mitigate and/or control the habit.
Journal ArticleDOI
Non-viral causes of hepatocellular carcinoma
TL;DR: Emerging evidence suggests that the etiology of many cases of HCC is in fact multifactorial, encompassing infectious etiologies, comorbid conditions and environmental exposures.
Journal ArticleDOI
Smokeless tobacco (paan and gutkha) consumption, prevalence, and contribution to oral cancer
Kamal Niaz,Faheem Maqbool,Fazlullah Khan,Haji Bahadar,Fatima Ismail Hassan,Mohammad Abdollahi +5 more
TL;DR: This review focuses on the consumption of smokeless tobacco and its components, such as paan and gutkha, and the role of these substances in the induction of OSMF and ultimately oral cancer.
References
More filters
Journal ArticleDOI
IARC Monographs on the Evaluation of the Carcinogenic Risk of Chemicals to Humans
Journal ArticleDOI
Malignant conversion of mouse skin tumours is increased by tumour initiators and unaffected by tumour promoters.
TL;DR: It is reported here that the tumour promoter 12-O-tetradecanoyl-phorbol-13-acetate (TPA) is ineffective in the conversion of papillomas to carcinomas whereas three initiators, urethane, MNNG and 4-nitroquinoline-N-oxide (4-NQO) are effective, which suggests that malignant conversion may result from a further genetic change in papilloma cells and that the in
Journal ArticleDOI
A case-control study of oral submucous fibrosis with special reference to the etiologic role of areca nut.
P. N. Sinor,Prakash C. Gupta,P. R. Murti,R. B. Bhonsle,D. K. Daftary,F. S. Mehta,J. J. Pindborg +6 more
TL;DR: Areca nut is confirmed as the most important etiologic factor in oral submucous fibrosis and the relative risks increased with increase in the frequency as well as the duration of chewing habits.
Journal ArticleDOI
Tobacco-specific and betel nut-specific N-nitroso compounds: occurrence in saliva and urine of betel quid chewers and formation in vitro by nitrosation of betel quid
TL;DR: The results indicate that N-nitroso compounds could easily be formed in vivo in the oral cavity during chewing or in the stomach after swallowing the quids, and the levels of N- Nitrosamines and alkaloids in betel quid extracts were determined before and after nitrosation at pH 7.1.