ArticleJournal of toxicology2016
Neurotoxic Effect of Benzo[a]pyrene and Its Possible Association with 6-Hydroxydopamine Induced Neurobehavioral Changes during Early Adolescence Period in Rats.
Article in Journal of toxicology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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
8 citing papers in PubMed, 43 citations in OpenAlex.
- The zebrafish gut microbiome influences benzo[a]pyrene developmental neurobehavioral toxicity.Scientific reports · 2024Article
- Protective Effect ofNutrients · 2023Article
- Ambient particulate matter (PMEnvironmental toxicology and pharmacology · 2023Article
- Short-Term Exposure to Benzo(a)Pyrene Causes Disruption of GnRH Network in Zebrafish Embryos.International journal of molecular sciences · 2023Article
- The use of tocofersolan as a rescue agent in larval zebrafish exposed to benzo[a]pyrene in early development.Neurotoxicology · 2021Article
- Modulation of Benzo[a]Pyrene Induced Anxiolytic-Like Behavior by Retinoic Acid in Zebrafish: Involvement of Oxidative Stress and Antioxidant Defense System.Neurotoxicity research · 2017Article
- Botulinum Neurotoxin A Injected Ipsilaterally or Contralaterally into the Striatum in the Rat 6-OHDA Model of Unilateral Parkinson's Disease Differently Affects Behavior.Frontiers in behavioral neuroscience · 2017Article
- Protective Effects of 17β-Estradiol on Benzo(e) pyrene[B(e)P]-induced Toxicity in ARPE-19 cells.Journal of ophthalmic & vision researchArticle
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Exposure to persistent genotoxicants like benzo[a]pyrene (B[a]P) during postnatal days causes neurobehavioral changes in animal models. However, neurotoxic potential of B[a]P and its association with 6-hydroxydopamine (6-OHDA) induced neurobehavioral changes are yet to be explored. The growth of rat brain peaks at the first week of birth and continues up to one month with the attainment of adolescence. Hence, the present study was conducted on male Wistar rats at postnatal day 5 (PND 5) following single intracisternal administration of B[a]P to compare with neurobehavioral and neurotransmitter changes induced by 6-OHDA at PND 30. Spontaneous motor activity was significantly increased by 6-OHDA showing similar trend following B[a]P administration. Total distance travelled in novel open field arena and elevated plus maze was significantly increased following B[a]P and 6-OHDA administration. Neurotransmitter estimation showed significant alleviation of dopamine in striatum following B[a]P and 6-OHDA administration. Histopathological studies of striatum by hematoxylin and eosin (H&E) staining revealed the neurodegenerative potential of B[a]P and 6-OHDA. Our results indicate that B[a]P-induced spontaneous motor hyperactivity in rats showed symptomatic similarities with 6-OHDA. In conclusion, early postnatal exposure to B[a]P in rats causing neurobehavioral changes may lead to serious neurodegenerative consequences during adolescence.
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Registered trials
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