Related Experiment Video

Updated: May 26, 2026

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons
10:36

Modeling Neuronal Death and Degeneration in Mouse Primary Cerebellar Granule Neurons

Published on: November 6, 2017

Apoptosis Induced by Manganese on Neuronal SK-N-MC Cell Line: Endoplasmic Reticulum (ER) Stress and Mitochondria

Hyonok Yoon1, Do-Sung Kim, Geum-Hwa Lee

  • 1Department of Pharmacology, School of Medicine, Chonbuk National University, Jeonju, Korea.

Environmental Health and Toxicology
|January 11, 2012
PubMed
Abstract

Insights

Manganese chloride (MnCl2) exposure causes cell death by increasing reactive oxygen species and damaging mitochondria. This heavy metal induces neurotoxicity through endoplasmic reticulum stress and mitochondrial dysfunction, leading to neuronal apoptosis.

Area of Science:

  • Neuroscience
  • Toxicology
  • Cell Biology

Background:

  • Heavy metals like manganese chloride (MnCl2) are known to cause neurodegenerative conditions such as Manganism.
  • Understanding the mechanisms of manganese toxicity is crucial for developing preventative and therapeutic strategies.

Purpose of the Study:

  • To investigate the acute toxicity of MnCl2 in the neuroblastoma cell line SK-N-MC.
  • To determine if MnCl2-induced neurotoxicity involves endoplasmic reticulum (ER) stress and mitochondrial dysfunction.
  • To explore the role of these organelle disorders in mediating neuronal apoptosis.

Main Methods:

  • Acute toxicity was assessed using various concentrations (200–1,000 µM) and exposure times (3–48 hours) of MnCl2.
  • Mechanisms of toxicity were examined by measuring reactive oxygen species (ROS), mitochondrial membrane potential, and caspase-3 activity.
  • Western blotting and mitochondrial complex activities were analyzed to understand cellular responses.

Main Results:

  • Increased MnCl2 concentration and exposure time led to higher cell death rates.
  • MnCl2 significantly increased intracellular ROS production and caspase-3 activation.
  • Mitochondrial membrane potential was significantly dissipated, indicating mitochondrial dysfunction.

Conclusions:

  • MnCl2 induces apoptosis in neuroblastoma cells through ER stress and mitochondrial dysfunction.
  • The toxicity primarily affects mitochondrial complex I activity.
  • These findings highlight the critical role of organelle integrity in manganese neurotoxicity.
Keywords:
ApoptosisEndoplasmic reticulum stressManganese chloride (MnCl2)Mitochondria dysfunction

More Related Videos

Quantitative Analysis of Mitochondria-Associated Endoplasmic Reticulum Membrane (MAM) Stabilization in a Neural Model of Alzheimer's Disease (AD)06:41

Quantitative Analysis of Mitochondria-Associated Endoplasmic Reticulum Membrane (MAM) Stabilization in a Neural Model of Alzheimer's Disease (AD)

Published on: January 10, 2025

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons10:50

Molecular Modulation by Lentivirus-Delivered Specific shRNAs in Endoplasmic Reticulum Stressed Neurons

Published on: April 24, 2021

Related Concept Videos

Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...
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...
Cellular Injury IV: Necrosis01:16

Cellular Injury IV: Necrosis

Necrosis is a form of irreversible cell death caused by severe injury such as ischemia, toxins, or trauma. Unlike programmed cell death, it is an uncontrolled, pathological process that typically provokes inflammation in surrounding tissues.Pathophysiologic ChangesNecrosis begins when cells sustain critical damage, leading to swelling of organelles, particularly mitochondria, and rapid ATP depletion. As energy levels decline, membrane ion pumps fail, leading to calcium influx and eventually,...
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size reduction of the tissue.
Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the 20th century...