Related Experiment Video

Updated: Jun 16, 2026

Viability Assays for Cells in Culture
12:03

Viability Assays for Cells in Culture

Published on: January 20, 2014

Snake venom toxin inhibits cell growth through induction of apoptosis in neuroblastoma cells

Mi Hee Park1, Dong Ju Son, Dong Hoon Kwak

  • 1College of Pharmacy and CBITRC, Chungbuk National University, Cheongju 361-763, Korea.

Archives of Pharmacal Research
|January 22, 2010
PubMed

Insights

Snake venom toxin from Vipera lebetina turanica induces apoptosis in human neuroblastoma cells by increasing reactive oxygen species (ROS) and disrupting mitochondrial membrane potential (MMP). This toxin shows potential as an anti-cancer agent for neuroblastoma.

Area of Science:

  • Toxicology
  • Cancer Biology
  • Neuroscience

Background:

  • Snake venom toxins exhibit anti-cancer properties.
  • The apoptotic effects of Vipera lebetina turanica toxin on neuroblastoma cells remain unstudied.

Purpose of the Study:

  • To investigate the apoptotic effect of Vipera lebetina turanica snake venom toxin on human neuroblastoma cell lines (SK-N-MC and SK-N-SH).

Main Methods:

  • Treatment of neuroblastoma cells with varying concentrations of snake venom toxin.
  • Assessment of cell detachment, apoptotic cell death, reactive oxygen species (ROS) levels, and mitochondrial membrane potential (MMP).
  • Evaluation of the role of glutathione and changes in pro-apoptotic (Bax) and anti-apoptotic (Bcl-2) protein expression.

Main Results:

  • Snake venom toxin induced cell detachment and apoptosis in neuroblastoma cells, sparing normal neuronal cells.
  • Treatment increased ROS levels and disrupted MMP, effects mitigated by glutathione.
  • The toxin upregulated Bax and downregulated Bcl-2 expression.

Conclusions:

  • Vipera lebetina turanica snake venom toxin induces apoptosis in neuroblastoma cells via ROS-dependent MMP disruption.
  • The findings suggest potential application of this snake venom toxin as an anti-cancer agent for neuroblastoma.

More Related Videos

Three-Dimensional In Vitro Biomimetic Model of Neuroblastoma Using Collagen-Based Scaffolds07:48

Three-Dimensional In Vitro Biomimetic Model of Neuroblastoma Using Collagen-Based Scaffolds

Published on: July 9, 2021

Related Concept Videos

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...
Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists01:28

Chemotherapy-Induced Nausea and Vomiting: Neurokinin-1 Receptor Antagonists

Neurokinin 1 (NK1) receptors are distributed across the GI tract, vagal afferents, and key CNS regions including the central vomiting center and chemoreceptor trigger zone (CTZ) Chemotherapy agents stimulate enterochromaffin cells in the gastrointestinal (GI) tract to release large amounts of substance P (SP). SP is a neuropeptide released by specific sensory nerves in response to many different stressors, including those in the GI mucosa affected by chemotherapy.  SP binds and activates these...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...