Potential role of autophagy in smokeless tobacco extract-induced cytotoxicity and in morin-induced protection in oral epithelial cells

Toxic components of STE induced serious, adverse human oral health outcomes. In the present study, we observed that STE was involved in oral toxicity by reducing the viability of human squamous epithelial cells, SCC-25, along with the simultaneous induction of both apoptosis and autophagic signaling...

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Bibliographic Details
Published in:Food and chemical toxicology 2016-04, Vol.90, p.160-170
Main Authors: Ganguli, Arnab, Das, Amlan, Nag, Debasish, Bhattacharya, Surela, Chakrabarti, Gopal
Format: Article
Language:English
Subjects:
Autophagy
Carcinoma
Cell Line, Tumor
Epithelial Cells - drug effects
Flavonoids - chemistry
Flavonoids - pharmacology
Humans
Molecular Structure
Morin
Mouth Neoplasms
Reactive oxygen species
Smokeless tobacco
Tobacco, Smokeless - toxicity
Vitaceae
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Summary:Toxic components of STE induced serious, adverse human oral health outcomes. In the present study, we observed that STE was involved in oral toxicity by reducing the viability of human squamous epithelial cells, SCC-25, along with the simultaneous induction of both apoptosis and autophagic signaling. STE was also found to induce significant amount ROS generation in SCC-25 cells. The dietary flavonoid morin, found abundantly in a variety of herbs, fruits and wine, has been reported to attenuate ROS-induced pathogenesis including autophagy. In this study we designed three different treatment regimes of morin treatment, such as pre, co, and post – treatment of STE challenged SCC-25 cells. In all cases morin provided cytoprotection to STE challenged SCC-25 cells by augmenting STE induced ROS-dependent cytotoxic autophagy. Hence, morin is a potential option for antioxidant therapy in treatment of STE induced toxicity. [Display omitted] •STE induced ROS dependent autophagy in oral SCC25 cell line.•Autophagy and apoptosis both act as cell death mechanism in STE treated SCC25 cell line.•Antioxidant morin reduced ROS level, and inhibited apoptosis and autophagy, hence protects STE induced oral cytotoxicity.
ISSN:0278-6915
1873-6351
DOI:10.1016/j.fct.2016.02.011