ArticleNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2011
Low doses of 3-nitropropionic acid in vivo induce damage in mouse skeletal muscle.
Article in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 12 citations in OpenAlex.
- 3-Nitropropionic Acid-Induced Huntington's Disease in Preclinical Models: Mechanisms, Peripheral Toxicities, Model Gaps, and Future Directions.Molecular neurobiology · 2026Review
- Systemic Neuroprotection by Chlorogenic Acid: Antioxidant and Anti-inflammatory Evaluation in Early Neurodegeneration Induced by 3-Nitropropionic Acid in Mice.Neurochemical research · 2025Article
- Converging evidence in support of omega-3 polyunsaturated fatty acids as a potential therapy for Huntington's disease symptoms.Reviews in the neurosciences · 2021Review
- Mice deficient in L-12/15 lipoxygenase show increased vulnerability to 3-nitropropionic acid neurotoxicity.Neuroscience letters · 2017Article
- 3-Nitropropionic acid modifies neurotrophin mRNA expression in the mouse striatum: 18S-rRNA is a reliable control gene for studies of the striatum.Neuroscience bulletin · 2012Article
- Effect of pesticides on the aggregation of mutant huntingtin protein.Molecular neurobiology · 2012Article
- Oxidative stress in neurodegenerative diseases: mechanisms and therapeutic perspectives.Oxidative medicine and cellular longevity · 2011Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial alterations are believed to play a critical role in the pathophysiology of neurodegenerative diseases and in some well-described myopathies. In the present study, we evaluated muscle changes in vivo after blocking the mitochondrial complex II of the respiratory chain by using 3-nitropropionic acid (3-NP). This neurotoxin has been used as a pharmacological tool in animal models to address some of the metabolic modifications that might underlie central neurodegeneration; however, changes in peripheral musculature have not been documented. We believe that skeletal muscles must be affected because their integrity highly depends on oxidative metabolism. Therefore, histochemical, ultrastructural, and biochemical changes were studied in the muscles of mice treated with low doses of 3-NP (15 mg/kg, i.p., for 5 days). 3-NP-treated mice displayed changes in alkaline phosphatase (APase), succinic dehydrogenase (SDH), and cytochrome c oxidase (COX) levels in the gracilis and gastrocnemius muscles. These changes were statistically significant for APase and SDH in both muscles and for COX only in the gastrocnemius. No significant alterations in acetylcholinesterase (AChE) expression were observed in either muscle. Analysis of the muscle ultrastructure revealed mitochondrial atrophy as well as sarcomere and nuclei disorganization. At the biochemical level, nitric oxide (NO) and lipid peroxidation (LPO) changed in the muscles of 3-NP-treated mice, suggesting metabolic alterations due to oxidative stress. Early damage in the striatal tissue and behavioral modifications are also documented.
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