IMR Press / FBE / Volume 3 / Issue 2 / DOI: 10.2741/E258

Frontiers in Bioscience-Elite (FBE) is published by IMR Press from Volume 13 Issue 2 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Open Access Article

NAD+ treatment decreases tumor cell survival by inducing oxidative stress

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1 Med-X Research Institute, Shanghai Jiao Tong University, Shanghai 200030, P.R. China
2 Institute of Neurology, Rui Jin Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200030, P.R. China

*Author to whom correspondence should be addressed,

Academic Editor: Weihai Ying

Front. Biosci. (Elite Ed) 2011, 3(2), 434–441;
Published: 1 January 2011
(This article belongs to the Special Issue Mechanisms of neuronal Injury in neurological diseases)

NAD+ plays important roles in various biological processes. It has been shown that NAD+ treatment can decrease genotoxic agent-induced death of primary neuronal and astrocyte cultures, and NAD+ administration can reduce ischemic brain damage. However, the effects of NAD+ treatment on tumor cell survival are unknown. In this study we found that treatment of NAD+ at concentrations from 10 microMole to 1 mMole can significantly decrease the survival of various types of tumor cells such as C6 glioma cells. In contrast, NAD+ treatment did not impair the survival of primary astrocyte cultures. Our study has also indicated that oxidative stress mediates the effects of NAD+ on the survival of tumor cells, and P2X7 receptors and altered calcium homeostasis are involved in the effects of NAD+ on the cell survival. Collectively, our study has provided the first evidence that NAD+ treatment can decrease the survival of tumor cells by such mechanisms as inducing oxidative stress. Because NAD+ treatment can selectively decrease the survival of tumor cells, NAD+ may become a novel agent for treating cancer.

Tumor Cell Death
Oxidative Stress
P2X7 receptors
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