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丙烯酰胺诱导的毒性以及植物化学物质的改善倾向:综述

Acrylamide Induced Toxicity and the Propensity of Phytochemicals in Amelioration: A Review.

作者信息

Kunnel Shinomol George, Subramanya Sunitha, Satapathy Pankaj, Sahoo Ishtapran, Zameer Farhan

机构信息

Department of Biotechnology, Dayananda Sagar College of Engineering (An Autonomous Institute Affiliated to VTU, Belagavi), Shavige Malleshwara Hills, Kumaraswamy Layout, Bengaluru - 560 078, Karnataka, India.

Department of Biological Sciences, School of Basic and Applied Sciences, Dayananda Sagar University, Shavige Malleshwara Hills, Kumaraswamy Layout, Bengaluru-560 078, Karnataka, India.

出版信息

Cent Nerv Syst Agents Med Chem. 2019;19(2):100-113. doi: 10.2174/1871524919666190207160236.

DOI:10.2174/1871524919666190207160236
PMID:30734688
Abstract

Acrylamide is widely found in baked and fried foods, produced in large amount in industries and is a prime component in toxicity. This review highlights various toxicities that are induced due to acrylamide, its proposed mode of action including oxidative stress cascades and ameliorative mechanisms using phytochemicals. Acrylamide formation, the mechanism of toxicity and the studies on the role of oxidative stress and mitochondrial dysfunctions are elaborated in this paper. The various types of toxicities caused by Acrylamide and the modulation studies using phytochemicals that are carried out on various type of toxicity like neurotoxicity, hepatotoxicity, cardiotoxicity, immune system, and skeletal system, as well as embryos have been explored. Lacunae of studies include the need to explore methods for reducing the formation of acrylamide in food while cooking and also better modulators for alleviating the toxicity and associated dysfunctions along with identifying its molecular mechanisms.

摘要

丙烯酰胺广泛存在于烘焙和油炸食品中,在工业中大量生产,是毒性的主要成分。本综述重点介绍了丙烯酰胺引起的各种毒性、其推测的作用模式(包括氧化应激级联反应)以及使用植物化学物质的改善机制。本文阐述了丙烯酰胺的形成、毒性机制以及关于氧化应激和线粒体功能障碍作用的研究。已经探讨了丙烯酰胺引起的各种类型的毒性以及使用植物化学物质对各种类型毒性(如神经毒性、肝毒性、心脏毒性、免疫系统、骨骼系统以及胚胎毒性)进行的调节研究。研究的空白包括需要探索在烹饪时减少食品中丙烯酰胺形成的方法,以及更好的调节剂以减轻毒性和相关功能障碍,并确定其分子机制。

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