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NADPH treatment decreases C6 glioma cell survival by increasing oxidative stress
Yingxin Ma1, Heyu Chen, Cuiping Zhao
1Med-X Research Institute, Shanghai Jiao Tong University, Shanghai, PR China.
Abstract:
NADPH (nicotinamide adenine dinucleotide phosphate, reduced form) plays pivotal roles in antioxidation and reductive biosynthesis. However, the effect of NADPH treatment on cell survival is unknown. In this study, we determined the effect of NADPH treatment on the survival of glioma cells. Treatment of C6 glioma cells with as low as 1 μM NADPH for 24 hrs induced a significant decrease in the survival of the glioma cells, while NADPH treatment had no effect on the survival of primary astrocyte cultures. We also found that NADPH treatment increased intracellular oxidative stress. Three antioxidants and the NADPH oxidase inhibitor, apocynin, attenuated the effect of NADPH. Poly(ADP-ribose) polymerase (PARP) activation appears to be a downstream effector of the oxidative stress, since PARP inhibitors reduced the effect of NADPH. Calcium chelator, BAPTA-AM, also attenuated the effect of NADPH. Collectively, these data indicate a novel property of NADPH: NADPH decreases glioma cell survival by inducing the NADPH oxidase-dependent increase in oxidative stress and by PARP activation. These results also suggest a potential therapeutic effect of NADPH on gliomas.
Insights
Nicotinamide adenine dinucleotide phosphate (NADPH) treatment significantly reduces glioma cell survival by increasing oxidative stress and activating PARP. This suggests a potential therapeutic role for NADPH in glioma treatment.
Area of Science:
- Biochemistry
- Cell Biology
- Neuro-oncology
Background:
- Nicotinamide adenine dinucleotide phosphate (NADPH) is crucial for antioxidation and reductive biosynthesis.
- The impact of NADPH on glioma cell survival remains largely uncharacterized.
Purpose of the Study:
- To investigate the effect of NADPH treatment on the survival of glioma cells.
- To elucidate the underlying mechanisms of NADPH-induced cell death in gliomas.
Main Methods:
- Treatment of C6 glioma cells and primary astrocyte cultures with NADPH.
- Assessment of cell survival, intracellular oxidative stress, and activation of signaling pathways (NADPH oxidase, PARP, calcium).
- Utilized antioxidants, NADPH oxidase inhibitor (apocynin), PARP inhibitors, and calcium chelator (BAPTA-AM).
Main Results:
- NADPH treatment significantly decreased C6 glioma cell survival but not primary astrocytes.
- NADPH increased intracellular oxidative stress, an effect attenuated by antioxidants and apocynin.
- PARP activation and calcium signaling were identified as downstream effectors, as their inhibition reduced NADPH's effect.
Conclusions:
- NADPH exhibits a novel inhibitory effect on glioma cell survival.
- This effect is mediated by NADPH oxidase-dependent oxidative stress and subsequent PARP activation.
- NADPH presents a potential therapeutic strategy for glioma treatment.
