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Related Concept Videos

Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...

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Updated: Jun 2, 2026

Visualization and Quantitative Analysis of Genotoxin-Induced PARP1/PARP2 Activation in Cells Using a Fluorescent Fusion Protein-Based Reporter
07:53

Visualization and Quantitative Analysis of Genotoxin-Induced PARP1/PARP2 Activation in Cells Using a Fluorescent Fusion Protein-Based Reporter

Published on: April 17, 2026

Oxidative stress and PARP activation mediate the NADH-induced decrease in glioma cell survival.

Yingxin Ma, Heyu Chen, Weiliang Xia

    International Journal of Physiology, Pathophysiology and Pharmacology
    |April 12, 2011
    PubMed
    Summary
    This summary is machine-generated.

    Reduced nicotinamide adenine dinucleotide (NADH) significantly decreases glioma cell survival by increasing oxidative stress and activating poly(ADP-ribose) polymerase (PARP). These findings suggest NADH may be a potential therapeutic for glioma treatment.

    Keywords:
    NADHcell deathglioma cellsoxidative stresspoly(ADP-ribose) polymerase

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    Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage
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    Visualization and Quantitative Analysis of Genotoxin-Induced PARP1/PARP2 Activation in Cells Using a Fluorescent Fusion Protein-Based Reporter
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    Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage
    10:44

    Laser Microirradiation to Study In Vivo Cellular Responses to Simple and Complex DNA Damage

    Published on: January 31, 2018

    Area of Science:

    • Biochemistry
    • Cell Biology
    • Neuro-oncology

    Background:

    • Reduced nicotinamide adenine dinucleotide (NADH) is crucial for cellular energy metabolism and mitochondrial function.
    • Limited research exists on the specific impact of NADH on cancer cell survival, particularly in gliomas.

    Purpose of the Study:

    • To investigate the effect of NADH treatment on the survival of C6 glioma cells.
    • To elucidate the mechanisms underlying NADH's impact on glioma cell viability.

    Main Methods:

    • Treatment of C6 glioma cells with varying concentrations of NADH.
    • Measurement of intracellular reactive oxygen species (ROS) levels.
    • Assessment of poly(ADP-ribose) polymerase (PARP) activity and inhibition.
    • Evaluation of cell survival rates post-treatment with NADH, antioxidants, and PARP inhibitors.

    Main Results:

    • NADH treatment significantly reduced C6 glioma cell survival in a dose- and time-dependent manner.
    • NADH induced increased intracellular ROS, indicating oxidative stress mediation.
    • Antioxidants (N-acetyl cysteine, Trolox) attenuated NADH's cytotoxic effect.
    • NADH increased PARP activity, and PARP inhibitors lessened NADH's impact on cell survival.

    Conclusions:

    • NADH exhibits a novel cytotoxic effect on glioma cells, mediated by oxidative stress and PARP activation.
    • NADH demonstrates potential as a therapeutic agent for glioma treatment due to its ability to reduce cancer cell survival.