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嚼食槟榔所产生的碱性环境协力增加香菸所含丙烯醛与NNK之毒性(英文)

刘宗荣  
【摘要】:Betel quid(BQ) chewing has been demonstrated to synergistically potentiate Cigarette smoking(CS) associated oral squamous cell carcinoma(OSCC) in Taiwan.However,the underlying mechanisms remain elusive.This study tests the hypothesis that BQ generated alkalinity facilitates cigarette smoke contained acrolein and NNK absorption and consequently toxicity.In a group of OSCC patients(97) and healthy subjects(230) we have demonstrated that CS and BQ chewing generated significantly higher(P0.05) 3-HPMA,a specific metabolite of acrolein in urine,than that in smokers or BQ chewers indicating tat CS and BQ chewing promotes acrolein absorption.However,3-HPMA levels in patients with OSCC weresignificantly lower than those in healthy subjects,indicatingimpaired acrolein metabolism.Our results showed that the level of Acr-dG adductsin buccal cells was 1.4-fold higher in patients with OSCC thanin healthy subjects with CS and/or BQ chewing histories(P0.001).By using hamster as a animal moedl,we have demonstrated that safrole(1 mg/kg/d) induced CYP2A6 activity,reducedurinary NNAL,specific metabolite of NNK,levels,and increased NNK-induced DNAdamage,including N7-methylguanine,8-OH-deoxyguanosine and DNA strand breaks.Furthermore,altered NNK metabolism and increased NNK-induced DNA damage werealso observed in healthy subjects with CS and BQ chewing histories compared to healthy subjects with CS habit.This suggests that BQ containing safrole induced tobacco-specific NNK metabolic activation,resulting in higher NNK-induced genotoxicity.In conclusion,we provided evidence to show that BQ chewing increased acrolein and NNK uptake and impaired GSH metabolism and NNK activation by safrole may contribute to the synergistic potential of BQ-and CS-induced OSCC.

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