Chromosome-damaging effect of betel leaf

Sadasivan, G.; Rani, G Geetha; Kumari, C.Kusuma

doi:10.1016/0027-5107(78)90266-x

Cited by 16 publications

(3 citation statements)

References 4 publications

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“…Furthermore, PBL extract inhibits the mutagenicity of a large array of environmental mutagens and carcinogens (Nagabhushan et al ., 1987), such as two tobacco‐specific nitrosamines (Padma et al ., 1989a). On the contrary, a 24‐h exposure of human white blood cells to PBL extract leads to pronounced chromatid aberrations (Sadasivan et al ., 1978). In addition, an organic PBL extract exerts cytotoxicity in human buccal fibroblasts when given in concentrations ranging from 3 μg ml −1 to 1 mg ml −1 .…”

Section: Introductionmentioning

confidence: 99%

Inducing the cell cycle arrest and apoptosis of oral KB carcinoma cells by hydroxychavicol: roles of glutathione and reactive oxygen species

Chang

Uang

et al. 2002

British J Pharmacology

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1 Hydroxychavicol (HC; 10 ± 50 mM), a betel leaf component, was found to suppress the 2% H 2 O 2 -induced lucigenin chemiluminescence for 53 ± 75%. HC (0.02 ± 2 mM) was also able to trap superoxide radicals generated by a xanthine/xanthine oxidase system with 38 ± 94% of inhibition. Hydroxyl radicals-induced PUC18 plasmid DNA breaks was prevented by HC (1.6 ± 16 mM). 2 A 24-h exposure of KB cells to HC (0.5, 1 mM) resulted in 54 ± 74% cell death as analysed by a 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyl-tetrazolium bromide (MTT) assay. HC (10, 50 mM) further suppressed the growth of KB cells (15 and 76%, respectively). Long-term colony formation of KB cells was inhibited by 51% with 10 mM HC. 3 Pretreatment of KB cells with 100 mM HC inhibited the attachment of KB cells to type I collagen and ®bronectin by 59 and 29%, respectively. 4 Exposure of KB cells to 0.1 mM HC for 24 h resulted in cell cycle arrest at late S and G2/M phase. Increasing the HC concentration to 0.25 and 0.5 mM led to apoptosis as revealed by detection of sub-G 0 /G 1 peaks with a concomitant decrease in the number of cells residing in late S and G 2 /M phase. 5 Inducing the apoptosis of KB cells by HC was accompanied by marked depletion in reduced form of GSH (40.2 mM) and the increasing of reactive oxygen species production (40.1 mM) as analysed by CMF-and DCF-single cell¯uorescence¯ow cytometry. 6 These results indicate that HC exerts antioxidant property at low concentration. HC also inhibits the growth, adhesion and cell cycle progression of KB cells, whereas its induction of KB cell apoptosis (HC40.1 mM) was accompanied by cellular redox changes.

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Section: Introductionmentioning

confidence: 99%

Inducing the cell cycle arrest and apoptosis of oral KB carcinoma cells by hydroxychavicol: roles of glutathione and reactive oxygen species

Chang

Uang

et al. 2002

British J Pharmacology

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“…Accordingly, an epidemiological study also found that chewing BQ containing PBL but without IPB is less risky for oral cancer occurrence than chewing BQ that contains IPB [2]. However, PBL extract inhibits O 6 -methyl-guanine-DNA methyltransferase activity [16], a crucial enzyme for DNA repair, and induces chromatid aberrations on human white blood cells [17]. Possibly, different PBL ingredients have a differential effect, and thus the toxicities of each PBL component and its roles in the BQ-related oral mucosal lesions warrant further elucidation.…”

mentioning

confidence: 99%

Reactive oxygen species are crucial for hydroxychavicol toxicity toward KB epithelial cells

Jeng

Wang

Chang

et al. 2004

Cellular and Molecular Life Sciences (CMLS)

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Betel quid (BQ) chewing shows a strong correlation to the incidence of oral submucous fibrosis (OSF), leukoplakia and oral cancer. BQ contains mainly areca nut, lime, Piper betle leaf (PBL) and the inflorescence of P. betle (IPB). Hydroxychavicol (4-allyl-catechol, HC), as a major phenolic compound in PBL and IPB, is shown to induce oxidative stress, glutathione (GSH) depletion and cell cycle deregulation. Using bivariate BrdU/PI flow cytometry, KB cells in DNA synthesis (S phase) are shown to be sensitive to the toxic effect of HC and show cell cycle arrest and apoptosis following exposure to 0.1 and 0.3 mM HC. HC-induced apoptosis and cell cycle arrest are associated with mitochondrial membrane potential (delta Psim) depolarization as revealed by a decrease in rhodamine fluorescence. N-acetyl-L-cysteine (1 mM), superoxide dismutase (100 U/ml) and catalase (1000 U/ml) were effective in prevention of HC-induced GSH depletion (as indicated by chloromethylfluorescein fluorescence), reactive oxygen species (ROS) production (by dichlorofluorescein fluorescence), cell cycle arrest and apoptosis. However, dimethylthiourea (2 mM), neocuproine (1 mM), 1,10-phenanthroline (200 microM) and desferrioxamine (0.5 mM) showed little effect on HC-induced cell changes. HC elevated the cellular and mitochondrial GSH levels at moderate concentrations (0.05-0.1 mM), whereas at a concentration of 0.3 mM, inhibitory effects were noted. These results indicate that HC consumption may be associated with BQ-chewing-related oral mucosal diseases via GSH depletion, ROS production, mitochondrial dysfunction, cell cycle disturbance and the induction of apoptosis. These events are related to the production of superoxide radicals and hydrogen peroxide.

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“…The betel nut contains arecoline which is a stimulant to the central nervous system and can be nitrosated to several strong mutagens in vivo (Wenke et al 1984), the whole mixture being carcinogenic to the mouth and upper alimentary tract. The mutagenic effect of betel leaf extract has been shown, for instance, in its ability to increase chromatid exchanges in lymphocyte cultures (Sadasivan et al 1978). Betel or Areca nuts, like tobacco, are also potent sources and precursors of nitrosamines.…”

Section: Studies On Ground-up Betel ( a R E C A C A T E C H U L ) Nmentioning

confidence: 99%

Possible dietary factors in the induction of diabetes and its inheritance in man, with studies in mice

Stowers

Ewen

1991

proc nutr soc

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Chromosome-damaging effect of betel leaf

Cited by 16 publications

References 4 publications

Inducing the cell cycle arrest and apoptosis of oral KB carcinoma cells by hydroxychavicol: roles of glutathione and reactive oxygen species

Inducing the cell cycle arrest and apoptosis of oral KB carcinoma cells by hydroxychavicol: roles of glutathione and reactive oxygen species

Reactive oxygen species are crucial for hydroxychavicol toxicity toward KB epithelial cells

Possible dietary factors in the induction of diabetes and its inheritance in man, with studies in mice

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