Evidence map›Paper›PMID 28342135›Full record

ArticleNeurotoxicity research2017

PACAP Protects Against Ethanol and Nicotine Toxicity in SH-SY5Y Cells: Implications for Drinking-Smoking Co-morbidity.

Sridharan Manavalan, Bruk Getachew, Kebreten F Manaye, Syed J Khundmiri, Antonei B Csoka, Raechel McKinley, Andrea Tamas, Dora Reglodi, Yousef Tizabi

Abstract read
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Article in Neurotoxicity research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

11 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Effects of Pituitary Adenylate Cyclase Activating Polypeptide on Cell Death.International journal of molecular sciences · 2022
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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

9 authors at 2 institutions in 2 countries.

Sridharan ManavalanDepartment of Basic Sciences, National University of Health Sciences, Pinellas Park, FL, USA.
Bruk GetachewDepartment of Pharmacology, Howard University College of Medicine, 520 W Street, NW, Washington, DC, 20059, USA.
Kebreten F ManayeDepartment of Physiology and Biophysics, Howard University College of Medicine, Washington, DC, USA.
Syed J KhundmiriDepartment of Physiology and Biophysics, Howard University College of Medicine, Washington, DC, USA.
Antonei B CsokaDepartment of Anatomy, Howard University College of Medicine, Washington, DC, USA.
Raechel McKinleyDepartment of Anatomy, Howard University College of Medicine, Washington, DC, USA.
Andrea TamasDepartment of Anatomy, University of Pecs, Pécs, Hungary.
Dora ReglodiDepartment of Anatomy, University of Pecs, Pécs, Hungary.
Yousef TizabiDepartment of Pharmacology, Howard University College of Medicine, 520 W Street, NW, Washington, DC, 20059, USA. ytizabi@howard.edu.
Howard University · USUniversity of Pecs · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The detrimental effects of heavy drinking and smoking are multiplied when the two are combined. Treatment modalities for each and especially for the combination are very limited. Although in low concentration, alcohol and nicotine, each may have beneficial effects including neuroprotection, their combination, instead of providing additive protection, may actually lead to toxicity in cell cultures. Pituitary adenylate cyclase-activating polypeptide (PACAP) is an endogenous 38 amino-acid peptide with demonstrated protection against neuronal injury, trauma as well as various endogenous and exogenous toxic agents. The aim of this study was to investigate whether PACAP may also protect against toxicity induced by high alcohol, high nicotine, or the combination of low alcohol and nicotine concentrations, and if so, whether this effect was mediated via PAC1 receptor. We used the neuroblastoma-derived SH-SY5Y cells and applied various colorimetric assays for determination of cell viability or toxicity. Results indicate that PACAP blocks toxicity induced by high alcohol and high nicotine as well as their combination at low concentrations. The effects of PACAP in turn were blocked by the PACAP antagonist (PACAP 6-38), indicating involvement of the PACAP receptor PAC1 and possibly vasoactive intestinal peptide (VIP) receptors in PACAP's protection. Moreover, no combined toxicity of low alcohol and low nicotine could be detected in calcium-free medium. These findings suggest possible beneficial effects of PACAP in preventing alcohol and nicotine toxicity and that calcium contributes to the damage induced by combination of low alcohol and nicotine in SH-SY5Y cells.

Indexed as

CalciumCell Line, TumorCell SurvivalCentral Nervous System DepressantsDose-Response Relationship, DrugDrug CombinationsEthanolFluoresceinsHumansNeuroblastomaNeurotransmitter AgentsNicotineNicotinic AgonistsPituitary Adenylate Cyclase-Activating PolypeptideCalciumCentral Nervous System DepressantsDrug CombinationsEthanolFluoresceinsfluorexonNeurotransmitter AgentsNicotineNicotinic AgonistsPituitary Adenylate Cyclase-Activating PolypeptideAlcoholCalciumNeuroprotectionNeurotoxicityNicotinePACAPSH-SY5Y cell line

Identifiers

PMID28342135
OpenAlexW2603226068

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.