학술논문
Açai (Euterpe oleracea Mart.) Seed Extract Induces ROS Production and Cell Death in MCF-7 Breast Cancer Cell Line
Document Type
article
Author
Marcos Antonio Custódio Neto da Silva; Jonas Henrique Costa; Taícia Pacheco-Fill; Ana Lúcia Tasca Gois Ruiz; Flávia Castello Branco Vidal; Kátia Regina Assunção Borges; Sulayne Janaina Araújo Guimarães; Ana Paula Silva de Azevedo-Santos; Kaio Eduardo Buglio; Mary Ann Foglio; Maria do Carmo Lacerda Barbosa; Maria do Desterro Soares Brandão Nascimento; João Ernesto de Carvalho
Source
Molecules, Vol 26, Iss 12, p 3546 (2021)
Subject
Language
English
ISSN
1420-3049
Abstract
Euterpe oleracea Mart. (açai) is a native palm from the Amazon region. There are various chemical constituents of açai with bioactive properties. This study aimed to evaluate the chemical composition and cytotoxic effects of açai seed extract on breast cancer cell line (MCF-7). Global Natural Products Social Molecular Networking (GNPS) was applied to identify chemical compounds present in açai seed extract. LC-MS/MS and molecular networking were employed to detect the phenolic compounds of açai. The antioxidant activity of açai seed extract was measured by DPPH assay. MCF-7 breast cancer cell line viability was evaluated by MTT assay. Cell death was evaluated by flow cytometry and time-lapse microscopy. Autophagy was evaluated by orange acridin immunofluorescence assay. Reactive oxygen species (ROS) production was evaluated by DAF assay. From the molecular networking, fifteen compounds were identified, mainly phenolic compounds. The açai seed extract showed cytotoxic effects against MCF-7, induced morphologic changes in the cell line by autophagy and increased the ROS production pathway. The present study suggests that açai seed extract has a high cytotoxic capacity and may induce autophagy by increasing ROS production in breast cancer. Apart from its antioxidant activity, flavonoids with high radical scavenging activity present in açai also generated NO (nitric oxide), contributing to its cytotoxic effect and autophagy induction.