Oxidative damage to DNA induced by areca nut extract

Liu, Tsung‐Yun; Chen, Chiu-Lan; Chi, Chin‐Wen

doi:10.1016/s0165-1218(96)90018-x

Cited by 105 publications

(93 citation statements)

References 17 publications

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“…In this study, all HCC patients with habitual betel quid chewing also had cirrhosis (Table 6). Although cirrhosis is a late sequela of chronic HBV/HCV infection, declining liver function and reactive oxygen species induced during chronic betel quid chewing (Liu et al, 1996) may contribute, at least in part, to an additive interaction between betel quid chewing and chronic HBV/HCV infection.…”

Section: Discussionmentioning

confidence: 99%

Betel quid chewing as a risk factor for hepatocellular carcinoma: a case–control study

Tsai¹,

Chuang²,

Jeng

et al. 2001

Br J Cancer

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The role of betel quid chewing in the aetiology of hepatocellular carcinoma (HCC) was evaluated in a case–control study including 263 pairs of age- and sex-matched HCC patients and healthy controls. Serum hepatitis B surface antigen (HBsAg), and antibodies to hepatitis C virus (anti-HCV) were determined, and standardized personal interview conducted using a structured questionnaire. Multivariate analysis indicated that betel quid chewing (odds ratio (OR), 3.49; 95% confidence interval (CI), 1.74–6.96), HBsAg (OR, 16.69; 95% CI, 9.92–28.07), anti-HCV (OR, 38.57; 95% CI, 18.15–81.96), and educational duration of less than 10 years (OR, 1.71; 95% CI, 1.05–2.78) are independent risk factors of HCC. In addition, there was an additive interaction between betel quid chewing and chronic infection with either hepatitis B virus (synergy index, 5.37) or hepatitis C virus (synergy index, 1.66). Moreover, risk on HCC increased as duration of betel quid chewing increased, or amount of betel quid consumed (each P for trend < 0.0001). © 2001 Cancer Research Campaign http://www.bjcancer.com

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Section: Discussionmentioning

confidence: 99%

Betel quid chewing as a risk factor for hepatocellular carcinoma: a case–control study

Tsai¹,

Chuang²,

Jeng

et al. 2001

Br J Cancer

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“…[126][127][128][129][130][131][132][133][134][135][136][137] As such, hydrogen peroxide may be directly involved in the earliest tumor initiating events. 126,127,137,138 In accordance with this notion, addition of catalase to the extracellular tissue culture media is indeed sufficient to prevent or dramatically delay the onset of cell transformation and genomic instability, when normal cells are presented with an oncogenic stimulus.…”

Section: Metabolic-coupling and Drug Resistancementioning

confidence: 99%

Hydrogen peroxide fuels aging, inflammation, cancer metabolism and metastasis

et al. 2011

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“…The pellet was resuspended in 200 µl of TE buffer and total DNA of the tissues was extracted by proteinase K/SDS lysis followed by phenol/chloroform extraction as previously described (Liu et al 1996). After ethanol precipitation, the DNA was dissolved in 100 µl of distilled water and frozen at -30°C until use.…”

Section: Dna Extractionmentioning

confidence: 99%

Increased salivary level of 8-hydroxydeoxyguanosine is a marker of premature oxidative mitochondrial DNA damage in gingival tissue of patients with periodontitis

Çanakçı

Tatar

et al. 2009

Arch. Immunol. Ther. Exp.

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Introduction: Oxidative stress may contribute to the pathogenesis of periodontitis. However, the detailed molecular mechanism remains unclear. Both 8-hydroxydeoxyguanosine (8-OHdG) and mitochondrial DNA (mtDNA) deletion have been reported as early oxidative DNA damage markers. In this study, 8-OHdG levels in saliva and mtDNA deletions in gingival tissue of patients with chronic periodontitis (CP) were evaluated. Materials and Methods: Gingival tissue and whole saliva samples were collected from 32 patients with CP and 32 healthy control subjects. To determine the clinical condition of each subject, the plaque index, gingival index, clinical attachment level (CAL), and probing depth (PD) were measured. Using the ELISA and polymerase chain reaction methods, the salivary 8-OHdG levels and the 7.4-kbp and 5-kbp mtDNA deletions were examined. Results: The 5-kbp mtDNA deletion was detected in 20 of the 32 periodontitis patients (62.5%), but was not detected in the healthy controls. The mean value of 8-OHdG in the saliva of the periodontitis patients with deleted mtDNA was significantly higher than in the patients with non-deleted mtDNA (p<0.01). Also, significant correlation was found between the occurrence of the 5-kbp mtDNA deletion and salivary 8-OHdG levels (p<0.01). Similar correlations were detected between salivary 8-OHdG levels and age, PD, and CAL (p<0.01, p<0.05). Conclusion: Increased oxidative stress may lead to premature oxidative DNA damage in the gingival tissue of periodontitis patients and the salivary 8-OHdG level may signify premature oxidative mtDNA damage in diseased gingival tissue.

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Oxidative damage to DNA induced by areca nut extract

Cited by 105 publications

References 17 publications

Betel quid chewing as a risk factor for hepatocellular carcinoma: a case–control study

Betel quid chewing as a risk factor for hepatocellular carcinoma: a case–control study

Hydrogen peroxide fuels aging, inflammation, cancer metabolism and metastasis

Increased salivary level of 8-hydroxydeoxyguanosine is a marker of premature oxidative mitochondrial DNA damage in gingival tissue of patients with periodontitis

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