ArticleCellular and molecular neurobiology2009
Impaired mitochondrial functions in organophosphate induced delayed neuropathy in rats.
Article in Cellular and molecular neurobiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 61 citations in OpenAlex.
- Adverse effect propensity: A new feature of Gulf War illness predicted by environmental exposures.iScience · 2023Article
- Succinate prodrugs in combination with atropine and pralidoxime protect cerebral mitochondrial function in a rodent model of acute organophosphate poisoning.Scientific reports · 2022Article
- A cellular approach to understanding and treating Gulf War Illness.Cellular and molecular life sciences : CMLS · 2021Article
- The Effect of Organophosphate Exposure on Neuronal Cell Coenzyme QNeurochemical research · 2021Article
- Oxidative stress and mitochondrial dysfunction in organophosphate pesticide-induced neurotoxicity and its amelioration: a review.Environmental science and pollution research international · 2020Review
- Article
- Impact of chronic low dose exposure of monocrotophos in rat brain: Oxidative/ nitrosative stress, neuronal changes and cholinesterase activity.Toxicology reports · 2019Article
- C. elegans as a model in developmental neurotoxicology.Toxicology and applied pharmacology · 2018Review
- Protective effect of amlodipine on diazinon-induced changes on oxidative/antioxidant balance in rat hippocampus.Research in pharmaceutical sciences · 2018Article
- Pharmacologically increasing microtubule acetylation corrects stress-exacerbated effects of organophosphates on neurons.Traffic (Copenhagen, Denmark) · 2017Article
- Monocrotophos Induces the Expression of Xenobiotic Metabolizing Cytochrome P450s (CYP2C8 and CYP3A4) and Neurotoxicity in Human Brain Cells.Molecular neurobiology · 2017Article
- Apelin-13 Prevents the Delayed Neuropathy Induced by Tri-ortho-cresyl Phosphate Through Regulation the Autophagy Flux in Hens.Neurochemical research · 2015Article
- Mitochondrial Redox Dysfunction and Environmental Exposures.Antioxidants & redox signaling · 2015Review
- Mitochondrial complex I inhibition as a possible mechanism of chlorpyrifos induced neurotoxicity.Annals of neurosciences · 2014Article
- Mitochondrial dysfunction in aging rat brain regions upon chlorpyrifos toxicity and cold stress: an interactive study.Cellular and molecular neurobiology · 2014Article
- Monocrotophos induces the expression and activity of xenobiotic metabolizing enzymes in pre-sensitized cultured human brain cells.PloS one · 2014Article
- Alterations in gene expression in Caenorhabditis elegans associated with organophosphate pesticide intoxication and recovery.BMC genomics · 2013Article
- Analysis of the cytotoxicity of differentially sized titanium dioxide nanoparticles in murine MC3T3-E1 preosteoblasts.Journal of materials science. Materials in medicine · 2011Article
- Monocrotophos induced apoptosis in PC12 cells: role of xenobiotic metabolizing cytochrome P450s.PloS one · 2011Article
- Neurodevelopmental manifestations of mitochondrial disease.Journal of developmental and behavioral pediatrics : JDBP · 2010Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute exposure to organophosphates induces a delayed neurodegenerative condition known as organophosphate-induced delayed neuropathy (OPIDN). The mechanism of OPIDN has not been fully understood as it does not involve cholinergic crisis. The present study has been designed to evaluate the role of mitochondrial dysfunctions in the development of OPIDN. OPIDN was induced in rats by administering acute dose of monocrotophos (MCP, 20 mg/kg body weight, orally) or dichlorvos (DDVP, 200 mg/kg body weight, subcutaneously), 15-20 min after treatment with antidotes [atropine (20 mg/kg body weight) and 2-PAM (100 mg/kg body weight) intraperitoneally]. MDA levels were observed to be higher and thiol content was lower in mitochondria from brain regions of OP exposed animals. This was accompanied by decreased activities of the mitochondrial enzymes; NADH dehydrogenase, succinate dehydrogenase, and cytochrome oxidase. In addition, mitochondrial functions assessed by MTT reduction also confirmed mitochondrial dysfunctions following development of OPIDN. The spatial long-term memory evaluated using elevated plus-maze test was observed to be deficit in OPIDN. The results suggest impaired mitochondrial functions as a mechanism involved in the development of organophosphate induced delayed neuropathy.
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