ArticleBMC neuroscience2024
Diethyl nitrosamine-induces neurobehavioral deficit, oxido-nitrosative stress in rats' brain: a neuroprotective role of diphenyl diselenide.
Article in BMC neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Mediation of sphingolipid metabolism on the relationship between human nitrosamines exposure and esophageal cancer risk.Scientific reports · 2026Article
- Diphenyl diselenide promotes antioxidant activity and reduces apoptosis, offering hepatorenal protection in Wistar rats exposed to diethyl nitrosamine.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
Corrections and comments
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Authors and funding
5 authors.
Funding
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Abstract
Diethylnitrosamine (DEN), a common dietary carcinogen, is associated with neurotoxicity in humans and animals. This study investigated the neuroprotective effects of diphenyl diselenide (DPDS) against DEN-induced neurotoxicity in male Albino Wistar rats (n = 40). Rats were randomly distributed into cohorts and treated as follows: vehicle control (corn oil 2 mL/kg; gavage), DPDS-only (5 mg/kg; gavage) and DEN-only (200 mg/kg; single dose i.p.). Also, two other rat cohorts were pre-treated with DPDS (3 or 5 mg/kg) for 15 days (day: 0-15), subsequently administered with DEN (200 mg/kg) and continuously treated with DPDS for another 7 days, (days:15-21). Behavioural tests (OFT- using the open field test; NORT- novel object recognition test; FST- forced swimming test and Y-maze) were conducted from days 19-21, followed by biochemical analysis of the hippocampus and prefrontal cortex for oxidative stress, inflammation, neurotransmitter metabolic enzyme, and histopathology. DEN-treated rats exhibited decreased locomotor activity, spatial memory function and antioxidant activity, increased oxidative and nitration stress, anxiety, and depressive-like behaviour, causing histoarchitectural damage in prefrontal and hippocampal cortices. DPDS treatment (pre- and post-DEN exposure) significantly alleviated these neurotoxic, oxidative, and nitration effects, reversed DEN-induced histopathological alterations, and improved locomotive and cognitive functions. In conclusion, DPDS demonstrates potent neuroprotective effects against DEN-induced toxicity, likely through enhanced endogenous antioxidant capacity that mitigates oxido-nitrative damage. These findings suggest that the organo-selenium -DPDS- is a promising chemotherapeutic agent potent in alleviating DEN-mediated neurotoxicity and maintaining brain health.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.