Venkatesh Deepak, Puranik R S, Vanaki S S, Puranik Surekha R
Department of Dentistry, ESIC Medical College and Hospital, Bengaluru, Karnataka, India.
Department of Oral and Maxillofacial Pathology, PMNM Dental College and Hospital, Bagalkot, Karnataka, India.
J Oral Maxillofac Pathol. 2018 Sep-Dec;22(3):446. doi: 10.4103/jomfp.JOMFP_143_18.
Arecoline, a predominant alkaloid present in arecanut, has been implicated in the pathogenesis of several oral diseases because of its mutagenic and carcinogenic potential. The response of cultured cells to arecoline is highly dependent on its concentration; arecoline stimulates cultured cells above 0.1 μg/ml and is cytotoxic above 10 μg/ ml. Although this alkaloid seems important for areca nut induced oral diseases and carcinogenesis, little is known of the levels achieved before, during and after chewing. Also, it is prudent to understand its effects in arecanut chewers for a comprehensive understanding of its pathogenesis. Accordingly, the present study quantified the salivary arecoline levels in arecanut chewers.
The study participants were divided into Study Group A & B and Control Group C; unstimulated whole saliva was collected by spitting method for a period of 5 min. Then, participants in Group A and C chewed 0.5 g of areca nut without any other additives while in Group B were asked to chew 0.5 g of inert rubber base impression material. Stimulated whole saliva from all three groups was collected into graduated tubes during chewing at time intervals of 1, 3, 5, 10, 15, 20 and 25 min. Then, all participants were asked to remove nut particles or inert rubber base material from the mouth, and saliva samples were collected further up to 20 min, changing tubes at 5 min interval. Salivary arecoline was quantitated by HPLC-MS. The tabulation and descriptive statistics of the study were carried out.
In the present study, baseline levels of arecoline were zero in all three groups, whereas mean salivary arecoline levels during chewing were 76.93 ng/ml, 129.83 ng/ml and 64.83 ng/ml and after chewing were 196.17 ng/ml, 321.12 ng/ml and 43.75 ng/ml in Groups A, B and Control respectively, which were significantly higher than reported threshold levels.
The data from this study reveals that a significant amount of arecoline would be trapped in oral cavity, or being re-circulated between blood and saliva might have resulted in surprisingly high levels of arecoline even 10 mins after chewing in both groups after which the levels started declining. The higher levels of salivary arecoline achieved during and after chewing are enough to cause cytotoxic and genotoxic effects on oral tissues over a period of time in chronic chewers. The great differences in salivary arecoline levels achieved during chewing, may contribute to the variable response to areca nut seen in communities where this habit is widespread. Areca nut users have persistent background salivary arecoline levels long after chewing, whereas concentrations achieved are highly variable and consistent with a role in oral pre-malignancy and malignancy..
槟榔碱是槟榔中的主要生物碱，因其具有致突变和致癌潜力，与多种口腔疾病的发病机制有关。培养细胞对槟榔碱的反应高度依赖于其浓度；槟榔碱在浓度高于0.1μg/ml时刺激培养细胞，在浓度高于10μg/ml时具有细胞毒性。尽管这种生物碱似乎对槟榔诱导的口腔疾病和致癌作用很重要，但对于咀嚼前、咀嚼期间和咀嚼后所达到的水平知之甚少。此外，了解其在嚼槟榔者中的作用对于全面理解其发病机制是谨慎的做法。因此，本研究对嚼槟榔者唾液中槟榔碱水平进行了定量。
研究参与者分为研究A组和B组以及对照组C；通过吐唾法收集5分钟的非刺激性全唾液。然后，A组和C组的参与者咀嚼0.5克无任何其他添加剂的槟榔，而B组的参与者被要求咀嚼0.5克惰性橡胶基印模材料。在咀嚼期间，于1、3、5、10、15、20和25分钟的时间间隔，将三组的刺激性全唾液收集到刻度管中。然后，要求所有参与者从口中取出槟榔颗粒或惰性橡胶基材料，并在接下来的20分钟内进一步收集唾液样本，每隔5分钟更换一次试管。通过高效液相色谱-质谱法定量唾液中的槟榔碱。对研究进行列表和描述性统计。
在本研究中，三组的槟榔碱基线水平均为零，而咀嚼期间A组、B组和对照组的唾液槟榔碱平均水平分别为76.93 ng/ml、129.83 ng/ml和64.83 ng/ml，咀嚼后分别为196.17 ng/ml、321.12 ng/ml和43.75 ng/ml，均显著高于报告的阈值水平。
本研究数据表明，大量槟榔碱会滞留在口腔中，或者在血液和唾液之间再循环，可能导致两组在咀嚼后甚至10分钟时槟榔碱水平高得出奇，之后水平开始下降。咀嚼期间和咀嚼后唾液中较高的槟榔碱水平足以在一段时间内对慢性咀嚼者的口腔组织造成细胞毒性和基因毒性作用。咀嚼期间唾液槟榔碱水平的巨大差异，可能导致在这种习惯普遍存在的社区中对槟榔的反应存在差异。槟榔使用者在咀嚼后很长时间唾液中槟榔碱水平持续存在，而所达到的浓度高度可变，与口腔癌前病变和恶性肿瘤中的作用一致。
