ArticleInternational journal of environmental research and public health2011
Toxicity of neurons treated with herbicides and neuroprotection by mitochondria-targeted antioxidant SS31.
Article in International journal of environmental research and public health, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 38 citations in OpenAlex.
- Toxic interactions between dopamine, α-synuclein, monoamine oxidase, and genes in mitochondria of Parkinson's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2024Review
- Targeting Mitochondrial Oxidative Stress as a Strategy to Treat Aging and Age-Related Diseases.Antioxidants (Basel, Switzerland) · 2023Review
- Aberrant cyclin C nuclear release induces mitochondrial fragmentation and dysfunction iniScience · 2022Article
- Epigenome-Wide DNA Methylation and Pesticide Use in the Agricultural Lung Health Study.Environmental health perspectives · 2021Article
- Endocrine disruptors also function as nervous disruptors and can be renamed endocrine and nervous disruptors (ENDs).Toxicology reports · 2021Review
- Targeted Antioxidants in Exercise-Induced Mitochondrial Oxidative Stress: Emphasis on DNA Damage.Antioxidants (Basel, Switzerland) · 2020Review
- Status Epilepticus Caused by an Herbicide Poisoning.Case reports in emergency medicine · 2019Article
- Traumatic Stress and Accelerated Cellular Aging: From Epigenetics to Cardiometabolic Disease.Current psychiatry reports · 2017Review
- Mitochondrial therapy improves limb perfusion and myopathy following hindlimb ischemia.Journal of molecular and cellular cardiology · 2016Article
- Mitochondria-targeted molecules MitoQ and SS31 reduce mutant huntingtin-induced mitochondrial toxicity and synaptic damage in Huntington's disease.Human molecular genetics · 2016Article
- Serendipity and the discovery of novel compounds that restore mitochondrial plasticity.Clinical pharmacology and therapeutics · 2014Review
- Traumatic stress, oxidative stress and post-traumatic stress disorder: neurodegeneration and the accelerated-aging hypothesis.Molecular psychiatry · 2014Review
- Mitochondria-targeted antioxidants for treatment of Parkinson's disease: preclinical and clinical outcomes.Biochimica et biophysica acta · 2014Review
- RNA silencing of genes involved in Alzheimer's disease enhances mitochondrial function and synaptic activity.Biochimica et biophysica acta · 2013Article
- MitoQ, a mitochondria-targeted antioxidant, delays disease progression and alleviates pathogenesis in an experimental autoimmune encephalomyelitis mouse model of multiple sclerosis.Biochimica et biophysica acta · 2013Article
- Reduced VDAC1 protects against Alzheimer's disease, mitochondria, and synaptic deficiencies.Journal of Alzheimer's disease : JAD · 2013Article
- Effects of xenobiotics on total antioxidant capacity.Interdisciplinary toxicology · 2012Article
- Mitochondria-targeted antioxidant attenuates high glucose-induced P38 MAPK pathway activation in human neuroblastoma cells.Molecular medicine reports · 2012Article
- Impaired mitochondrial dynamics and abnormal interaction of amyloid beta with mitochondrial protein Drp1 in neurons from patients with Alzheimer's disease: implications for neuronal damage.Human molecular genetics · 2011Article
- Mitochondrial Dysfunction and Oxidative Stress in Asthma: Implications for Mitochondria-Targeted Antioxidant Therapeutics.Pharmaceuticals (Basel, Switzerland) · 2011Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
The purpose of this study was to determine the neurotoxicity of two commonly used herbicides: picloram and triclopyr and the neuroprotective effects of the mitochondria-targeted antioxidant, SS31. Using mouse neuroblastoma (N2a) cells and primary neurons from C57BL/6 mice, we investigated the toxicity of these herbicides, and protective effects of SS1 peptide against picloram and triclopyr toxicity. We measured total RNA content, cell viability and mRNA expression of peroxiredoxins, neuroprotective genes, mitochondrial-encoded electron transport chain (ETC) genes in N2a cells treated with herbicides and SS31. Using primary neurons from C57BL/6 mice, neuronal survival was studied in neurons treated with herbicides, in neurons pretreated with SS31 plus treated with herbicides, neurons treated with SS31 alone, and untreated neurons. Significantly decreased total RNA content, and cell viability in N2a cells treated with picloram and triclopyr were found compared to untreated N2a cells. Decreased mRNA expression of neuroprotective genes, and ETC genes in cells treated with herbicides was found compared to untreated cells. Decreased mRNA expression of peroxiredoxins 1-6 in N2a cells treated with picloram was found, suggesting that picloram affects the antioxidant enzymes in N2a cells. Immunofluorescence analysis of primary neurons revealed that decreased neuronal branching and degenerating neurons in neurons treated with picloram and triclopyr. However, neurons pretreated with SS31 prevented degenerative process caused by herbicides. Based on these results, we propose that herbicides--picloram and triclopyr appear to damage neurons, and the SS31 peptide appears to protect neurons from herbicide toxicity.
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