Evidence map›Paper›PMID 30446882›Full record

ArticleMetabolic brain disease2019

Neurochemical alterations following the exposure to di-n-butyl phthalate in rats.

Rami B Kassab, Maha S Lokman, Ehab A Essawy

Abstract read
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In one paragraph

Article in Metabolic brain disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 20% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed, 43 citations in OpenAlex.

  1. Phthalates Induced Neurotoxicity: A Mechanistic Approach.Central nervous system agents in medicinal chemistry · 2026
    Review
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  20. Nephroprotective Role ofEvidence-based complementary and alternative medicine : eCAM · 2019
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Rami B KassabZoology and Entomology Department, Faculty of Science, Helwan University, Cairo, 11795, Egypt. ramikassab@mail.muni.cz.ORCID http://orcid.org/0000-0002-1520-1601
Maha S LokmanZoology and Entomology Department, Faculty of Science, Helwan University, Cairo, 11795, Egypt.
Ehab A EssawyChemistry Department, Faculty of Science, Helwan University, Cairo, 11795, Egypt.
Helwan University · EG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Due to its ability to cross blood brain barrier and placenta, dibutyl phthalate (di-n-butyl phthalate, DBP) is expected to cause severe side effects to the central nervous system of animals and humans. A little data is available about the potential DBP neurotoxicity; therefore, this work was designed to investigate the brain tissue injury induced by DBP exposure. Forty Wister albino rats were allocated randomly into 4 groups (10 rats each). Group 1 served as control and the rats administered with physiological saline (0.9% NaCl) orally for 12 weeks. Groups 2, 3 and 4 were orally treated with DPB (100, 250 and 500 mg/kg) respectively for 12 weeks. DBP-intoxicated rats showed a disturbance in the oxidative status in cerebral cortex, striatum and brainstem, as represented by the elevated oxidants [malondialdehyde (MDA), nitric oxide (NO), 8-hydroxy-2-deoxyguanosine (8-OHdG)] and the decreased antioxidant molecules [reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione reductase (GR)]. DBP also enhanced a pro-inflammatory state through increasing the release of tumor necrosis factor- α (TNF-α) and interleukin-1β (IL-1β). The increase of these cytokines was associated with the increase of pro-apoptotic proteins [Bcl-2 associated X protein (Bax) and caspase-3] and the decrease of the anti-apoptotic protein, B cell lymphoma 2 (Bcl-2). In addition, the levels of norepinephrine (NE), dopamine (DA) and acetylcholine esterase (AChE) activity were decreased. This was accompanied by the alterations in the major excitatory and inhibitory amino acids neurotransmitters levels. The present findings indicated that DBP could exert its neuronal damage through oxidative stress, DNA oxidation, neuroinflammation, activation of apoptotic proteins and altering the monoaminergic, cholinergic and amino acids transmission.

Indexed as

AnimalsApoptosisBrainCatalaseDibutyl PhthalateGlutathione PeroxidaseInflammationInterleukin-1betaMalondialdehydeOxidative StressRatsRats, WistarSuperoxide DismutaseSynaptic TransmissionTumor Necrosis Factor-alphaCatalaseDibutyl PhthalateGlutathione PeroxidaseInterleukin-1betaMalondialdehydeSuperoxide DismutaseTumor Necrosis Factor-alphaApoptosisDibutyl phthalateInflammationNeurotoxicityOxidative stressRats

Identifiers

PMID30446882
OpenAlexW2900620228

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.