ArticleNeurotoxicity research2018
2,4 Dinitrophenol Attenuates Mitochondrial Dysfunction and Improves Neurobehavioral Outcomes Postanoxia in Neonatal Rats.
Article in Neurotoxicity research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 9 citations in OpenAlex.
- The relationship between experimental 2,4-Dinitrophenol administration and neurological oxidative stress: in terms of dose, time and gender differences.Molecular and cellular biochemistry · 2023Article
- Mitochondrial dysfunction in perinatal asphyxia: role in pathogenesis and potential therapeutic interventions.Molecular and cellular biochemistry · 2021Review
- Mitochondrial Uncoupling: A Key Controller of Biological Processes in Physiology and Diseases.Cells · 2019Review
- Rebamipide Mitigates Impairments in Mitochondrial Function and Bioenergetics with α-Synuclein Pathology in 6-OHDA-Induced Hemiparkinson's Model in Rats.Neurotoxicity research · 2019Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Following anoxia, a rapid and marked mitochondrial-linked cell death occurs in the cerebral cortex of newborn rats which leads to insult advancement within a couple of days and causes lifelong neurobehavioral abnormalities. The present study investigated the role of 2,4 dinitrophenol (2,4 DNP) in three doses, i.e.,1, 2.5, and 5 mg/kg on anoxia-induced time-dependent mitochondrial dysfunction and associated neurobehavioral outcome using a well-established global model of anoxia. Briefly, rat pups of 30-h age (P2) were subjected to two episodes of anoxia (10 min each) at 24 h of the time interval in an enclosed chamber supplied with 100% N
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