ArticleJournal of molecular neuroscience : MN2011
Inhibition of axonal transport caused by tert-butyl hydroperoxide in cultured mouse dorsal root ganglion neurons.
Article in Journal of molecular neuroscience : MN, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed, 6 citations in OpenAlex.
- Preventing Axonal Sodium Overload or Mitochondrial Calcium Uptake Protects Axonal Mitochondria from Oxidative Stress-Induced Alterations.Oxidative medicine and cellular longevity · 2022Article
- Design, Synthesis, and In Vitro Evaluation of a Novel Probucol Derivative: Protective Activity in Neuronal Cells Through GPx Upregulation.Molecular neurobiology · 2018Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
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Abstract
Reactive oxygen species (ROS) are capable of affecting neuronal cell function and structure. Here, we investigated the direct effects of hydrogen peroxide (H(2)O(2)), one of the ROS, on axonal transport in cultured mouse dorsal root ganglion neurons using video-enhanced microscopy. Treatment of neurons with the H(2)O(2) donor tert-butyl hydroperoxide (TBHP; 10 nM-1 mM) inhibited anterograde and retrograde movement of organelles in a time- and concentration-dependent manner. Mitochondria and lysosomes were clearly swollen by TBHP at 100 μM and 1 mM in association with complete and irreversible cessation of axonal transport. In contrast, cytoskeletal structures were apparently unchanged even at the highest TBHP concentration (1 mM). Lipid peroxides, detected by swallow-tailed perylene derivative fluorescence, were produced by TBHP in plasma membranes and more highly in organelle membranes. The TBHP-induced inhibition of axonal transport, lipid peroxide production, and organelle swelling were blocked by pretreatment with α-tocopherol (vitamin E, 1 mM). These results suggest that H(2)O(2) inhibited axonal transport via lipid peroxidation along with degenerative changes in organelles.
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