NDLI: Drug-induced reactive oxygen species (ROS) rely on cell membrane properties to exert anticancer effects

Content Provider	PubMed Central
Author	Molavian, Hamid R. Goldman, Aaron Phipps, Colin J. Mohammad, Kohandel Wouters, Bradly G. Sengupta, Shiladitya Sivaloganathan, Sivabal
Copyright Year	2016
Abstract	Pharmacological concentrations of small molecule natural products, such as ascorbic acid, have exhibited distinct cell killing outcomes between cancer and normal cells whereby cancer cells undergo apoptosis or necrosis while normal cells are not adversely affected. Here, we develop a mathematical model for ascorbic acid that can be utilized as a tool to understand the dynamics of reactive oxygen species (ROS) induced cell death. We determine that not only do endogenous antioxidants such as catalase contribute to ROS-induced cell death, but also cell membrane properties play a critical role in the efficacy of ROS as a cytotoxic mechanism against cancer cells vs. normal cells. Using in vitro assays with breast cancer cells, we have confirmed that cell membrane properties are essential for ROS, in the form of hydrogen peroxide (H2O2), to induce cell death. Interestingly, we did not observe any correlation between intracellular H2O2 and cell survival, suggesting that cell death by H2O2 is triggered by interaction with the cell membrane and not necessarily due to intracellular levels of H2O2. These findings provide a putative mechanistic explanation for the efficacy and selectivity of therapies such as ascorbic acid that rely on ROS-induced cell death for their anti-tumor properties.
Related Links	http://dx.doi.org/10.1038/srep27439
Starting Page	27439
File Format	PDF
ISSN	20452322
e-ISSN	20452322
Journal	Scientific Reports
Volume Number	6
Language	English
Publisher	Nature Publishing Group
Publisher Date	2016-06-01
Access Restriction	Open
Rights Holder	Nature Publishing Group
Subject Keyword	Science and technology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

Drug-induced reactive oxygen species (ROS) rely on cell membrane properties to exert anticancer effects

Bid-induced mitochondrial membrane permeabilization waves propagated by local reactive oxygen species (ROS) signaling

Biophysical properties and functional consequences of reactive oxygen species (ROS)-induced ROS release in intact myocardium

Responses of Solid Tumor Cells in DMEM to Reactive Oxygen Species Generated by Non-Thermal Plasma and Chemically Induced ROS Systems

Reactive Oxygen Species (Ros-Induced) Ros Release

Induction of Reactive Oxygen Species-mediated Autophagy by a Novel Microtubule-modulating Agent

Drug-induced Senescence Generates Chemoresistant Stemlike Cells with Low Reactive Oxygen Species

Reactive oxygen species exert opposite effects on Tyr23 phosphorylation of the nuclear and cortical pools of annexin A2

The quinone-based derivative, HMNQ induces apoptotic and autophagic cell death by modulating reactive oxygen species in cancer cells.

Drug-induced reactive oxygen species (ROS) rely on cell membrane properties to exert anticancer effects

Similar Documents

Drug-induced reactive oxygen species (ROS) rely on cell membrane properties to exert anticancer effects

Bid-induced mitochondrial membrane permeabilization waves propagated by local reactive oxygen species (ROS) signaling

Biophysical properties and functional consequences of reactive oxygen species (ROS)-induced ROS release in intact myocardium

Responses of Solid Tumor Cells in DMEM to Reactive Oxygen Species Generated by Non-Thermal Plasma and Chemically Induced ROS Systems

Reactive Oxygen Species (Ros-Induced) Ros Release

Induction of Reactive Oxygen Species-mediated Autophagy by a Novel Microtubule-modulating Agent

Drug-induced Senescence Generates Chemoresistant Stemlike Cells with Low Reactive Oxygen Species

Reactive oxygen species exert opposite effects on Tyr23 phosphorylation of the nuclear and cortical pools of annexin A2

The quinone-based derivative, HMNQ induces apoptotic and autophagic cell death by modulating reactive oxygen species in cancer cells.

Drug-induced reactive oxygen species (ROS) rely on cell membrane properties to exert anticancer effects