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Study on the browning mechanism of betel nut (Betel catechu L.) kernel.

ABSTRACT: Taking betel nut (Betel catechu L.) kernel as raw materials, to analyze the browning mechanism of betel nut kernel. First, we extract and separate the phenolic substances and polyphenol oxidase (PPO) from the betel nut kernel and then find out how O2 penetrates into the kernel, study the above 3 key factors of enzymatic browning so as to prove the possibility of enzymatic browning, and further study the browning products to clarify the mechanism of browning of betel nut kernel during storage process. The results showed that 11 kinds of phenolic compounds were isolated and identified from the betel nut kernel by liquid chromatography-mass spectrometry, among which chlorogenic acid was the highest, followed by dopamine and L-epicatechin, and other contents were relatively low. Meanwhile, PPO was also separated from the betel nut kernel by DEAE-Sepharose Fast Flow and Phenyl-Sepharose 6 Fast Flow column chromatography. On this basis, scanning electron microscopy showed that the damage of the betel nut tissue was aggravated with the prolonged storage time, the wax was gradually decomposed, and the stratum corneum of the peel is destroyed in a honeycomb-shaped; the lignification of the flesh was aggravated, and the interstitial space was increased; and the crack of the kernel membrane was also enlarged. These changes of structure contribute to increase gas exchange within and outside the organization, including the entry of O2. Finally, the oxidation products generated from simulated reaction of chlorogenic acid, dopamine, and epicatechin with purified PPO under aerobic conditions in vitro were compared with the products extracted from naturally brown betel nut, and the same absorption spectra were found. Therefore, it indicates that the browning of betel nut kernel is an enzymatic browning caused by the reaction of phenolic substrates were oxidized by PPO.

SUBMITTER: Guo Y

PROVIDER: S-EPMC7174209 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature

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Study on the browning mechanism of betel nut (Betel catechu L.) kernel.

Guo Yuting Y Pan Yonggui Y Zhang Zhengke Z Zhang Weimin W

Food science & nutrition 20200310 4

Taking betel nut (Betel catechu L.) kernel as raw materials, to analyze the browning mechanism of betel nut kernel. First, we extract and separate the phenolic substances and polyphenol oxidase (PPO) from the betel nut kernel and then find out how O2 penetrates into the kernel, study the above 3 key factors of enzymatic browning so as to prove the possibility of enzymatic browning, and further study the browning products to clarify the mechanism of browning of betel nut kernel ...[more]

PMID: 32328247

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Project description:Oral cancers are attributed to a number of causal agents including tobacco, alcohol, human papillomavirus (HPV), and areca (betel) nut. Although betel nut chewing has been established as an independent cause of oral cancer, the mechanisms of carcinogenesis are poorly understood. An investigation was undertaken to evaluate the influence of betel nut chewing on the oral microbiome and oral premalignant lesions. Study participants were recruited from a dental clinic in Guam. Structured interviews and oral examinations were performed. Oral swabbing and saliva samples were evaluated by 454 pyrosequencing of the V3- V5 region of the 16S rRNA bacterial gene and genotyped for HPV. One hundred twenty-two adults were enrolled including 64 current betel nut chewers, 37 former chewers, and 21 with no history of betel nut use. Oral premalignant lesions, including leukoplakia and submucous fibrosis, were observed in 10 chewers. Within-sample bacterial diversity was significantly lower in long-term (?10 years) chewers vs. never chewers and in current chewers with oral lesions vs. individuals without lesions. Between-sample bacterial diversity based on Unifrac distances significantly differed by chewing status and oral lesion status. Current chewers had significantly elevated levels of Streptococcus infantis and higher and lower levels of distinct taxa of the Actinomyces and Streptococcus genera. Long-term chewers had reduced levels of Parascardovia and Streptococcus. Chewers with oral lesions had significantly elevated levels of Oribacterium, Actinomyces, and Streptococcus, including Streptococcus anginosus. In multivariate analyses, controlling for smoking, oral HPV, S.anginosus, and S. infantis levels, current betel nut chewing remained the only predictor of oral premalignant lesions. Our study provides evidence that betel nut chewing alters the oral bacterial microbiome including that of chewers who develop oral premalignant lesions. Nonetheless, whether microbial changes are involved in betel nut-induced oral carcinogenesis is only speculative. Further research is needed to discern the clinical significance of an altered oral microbiome and the mechanisms of oral cancer development in betel nut chewers.

Project description:INTRODUCTION:The use of betel quid is the most understudied major addiction in the world. The neuropsychological activity of betel quid has been attributed to alkaloids of Areca catechu. With the goal of developing novel addiction treatments, we evaluate the muscarinic and nicotinic activity of the four major Areca alkaloids: arecoline, arecaidine, guvacoline, and guvacine and four structurally related compounds. METHODS:Acetylcholine receptors were expressed in Xenopus oocytes and studied with two-electrode voltage clamp. RESULTS:Both arecoline- and guvacoline-activated muscarinic acetylcholine receptors (mAChR), while only arecoline produced significant activation of nicotinic AChR (nAChR). We characterized four additional arecoline-related compounds, seeking an analog that would retain selective activity for a α4* nAChR, with diminished effects on mAChR and not be a desensitizer of α7 nAChR. We show that this profile is largely met by isoarecolone. Three additional arecoline analogs were characterized. While the quaternary dimethyl analog had a broad range of activities, including activation of mAChR and muscle-type nAChR, the methyl analog only activated a range of α4* nAChR, albeit with low potency. The ethyl analog had no detectable cholinergic activity. CONCLUSIONS:Evidence indicates that α4* nAChR are at the root of nicotine addiction, and this may also be the case for betel addiction. Our characterization of isoarecolone and 1-(4-methylpiperazin-1-yl) ethanone as truly selective α4*nAChR selective partial agonists with low muscarinic activity may point toward a promising new direction for the development of drugs to treat both nicotine and betel addiction. IMPLICATIONS:Nearly 600 million people use Areca nut, often with tobacco. Two of the Areca alkaloids are muscarinic acetylcholine receptor agonists, and one, arecoline, is a partial agonist for the α4* nicotinic acetylcholine receptors (nAChR) associated with tobacco addiction. The profile of arecoline activity suggested its potential to be used as a scaffold for developing new tobacco cessation drugs if analogs can be identified that retain the same nicotinic receptor selectivity without muscarinic activity. We report that isoarecolone is a selective partial agonist for α4* nAChR with minimal muscarinic activity and 1-(4-methylpiperazin-1-yl) ethanone has similar nAChR selectivity and no detectable muscarinic action.

Dataset Information

Study on the browning mechanism of betel nut (Betel catechu L.) kernel.

Publications

Study on the browning mechanism of betel nut (<i>Betel catechu</i> L.) kernel.

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