Evidence map›Paper›PMID 27908784›Full record

ArticleFree radical biology & medicine2017

Cisplatin-induced mitochondrial dysfunction is associated with impaired cognitive function in rats.

Naomi Lomeli, Kaijun Di, Jennifer Czerniawski, John F Guzowski, Daniela A Bota

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed, 1 pooled it
9.2field-weighted citation impact, top 2% 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

88 citing papers in PubMed, 1 synthesis or guideline pooled it, 160 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. The effect of 12 sessions of lymphatic massage and Pilates exercise on the executive functions of breast cancer survivors.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2026
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  15. Cognitive dysfunction in chemobrain: Molecular mechanisms and therapeutic implications.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025
    Review
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28 more citing papers are in PubMed but not listed here.

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

5 authors at 2 institutions in 1 country.

Naomi LomeliDepartment of Pathology & Laboratory Medicine, University of California Irvine, Irvine, CA, USA. Electronic address: nrlomeli@uci.edu.
Kaijun DiDepartment of Neurological Surgery, University of California Irvine, Irvine, CA, USA; Chao Family Comprehensive Cancer Center, University of California Irvine, Irvine, CA, USA. Electronic address: kdi@uci.edu.
Jennifer CzerniawskiDepartment of Neurobiology & Behavior, University of California Irvine, Irvine, CA, USA; Center for the Neurobiology of Learning & Memory, University of California Irvine, Irvine, CA, USA. Electronic address: jczernia@uci.edu.
John F GuzowskiDepartment of Neurobiology & Behavior, University of California Irvine, Irvine, CA, USA; Center for the Neurobiology of Learning & Memory, University of California Irvine, Irvine, CA, USA. Electronic address: john.g@uci.edu.
Daniela A BotaDepartment of Pathology & Laboratory Medicine, University of California Irvine, Irvine, CA, USA; Department of Neurological Surgery, University of California Irvine, Irvine, CA, USA; Chao Family Comprehensive Cancer Center, University of California Irvine, Irvine, CA, USA; Department of Neurology, University of California Irvine, Irvine, CA, USA. Electronic address: dbota@uci.edu.
University of California, Irvine · USNeurological Surgery · US

Funding

Univ.of Calif., Irvine Cancer Center Support GrantP30CA062203 · NCI · UNIVERSITY OF CALIFORNIA-IRVINE · PI Joel E Milam · 1994 to 2026
$57.9M
University of California Health Participation in the National COVID Cohort Collaborative (N3C)UL1TR001414 · NCATS · UNIVERSITY OF CALIFORNIA-IRVINE · PI COOPER, DAN M, VILAIN, ERIC J. · 2015 to 2023
$35.1M
MINORITY BIOMEDICAL RESEARCHERS PROGRAMR25GM055246 · NIGMS · UNIVERSITY OF CALIFORNIA-IRVINE · PI MOTA-BRAVO, LUIS M · 1996 to 2022
$15.3M
Training Program in Stem Cell Translational Medicine for Neurological DisordersT32NS082174 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI PETER John DONOVAN, Leslie Michels Thompson · 2013 to 2026
$3.3M
Mechanisms of Chemotherapy Induced Cognitive DefectsK08NS072234 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI BOTA, DANIELA ANNENELIE · 2011 to 2015
$866k
NCATS NIH HHS UL1 TR001414NCI NIH HHS P30 CA062203NIGMS NIH HHS R25 GM055246NINDS NIH HHS K08 NS072234NINDS NIH HHS T32 NS082174
6 · The paper itself

Abstract

purposeChemotherapy-related cognitive impairment (CRCI) is commonly reported following the administration of chemotherapeutic agents and comprises a wide variety of neurological problems. No effective treatments for CRCI are currently available. Here we examined the mechanisms involving cisplatin-induced hippocampal damage following cisplatin administration in a rat model and in cultured rat hippocampal neurons and neural stem/progenitor cells (NSCs). We also assessed the protective effects of the antioxidant, N-acetylcysteine in mitigating these damages. EXPERIMENTAL

designAdult male rats received 6mg/kg cisplatin in the acute studies. In chronic studies, rats received 5mg/kg cisplatin or saline injections once per week for 4 weeks. N-acetylcysteine (250mg/kg/day) or saline was administered for five consecutive days during cisplatin treatment. Cognitive testing was performed 5 weeks after treatment cessation. Cisplatin-treated cultured hippocampal neurons and NSCs were examined for changes in mitochondrial function, oxidative stress production, caspase-9 activation, and neuronal dendritic spine density.

resultsAcute cisplatin treatment reduced dendritic branching and spine density, and induced mitochondrial degradation. Rats receiving the chronic cisplatin regimen showed impaired performance in contextual fear conditioning, context object discrimination, and novel object recognition tasks compared to controls. Cisplatin induced mitochondrial DNA damage, impaired respiratory activity, increased oxidative stress, and activated caspase-9 in cultured hippocampal neurons and NSCs. N-acetylcysteine treatment prevented free radical production, ameliorated apoptotic cellular death and dendritic spine loss, and partially reversed the cisplatin-induced cognitive impairments.

conclusionsOur results suggest that mitochondrial dysfunction and increased oxidative stress are involved in cisplatin-induced cognitive impairments. Therapeutic agents, such as N-acetylcysteine, may be effective in mitigating the deleterious effects of cisplatin.

Indexed as

AnimalsAntineoplastic AgentsAntioxidantsApoptosisCisplatinCognitionCognitive DysfunctionHumansMitochondriaNeoplasmsNeuronsOxidative StressRatsAntineoplastic AgentsAntioxidantsCisplatinChemotherapyChemotherapy-related cognitive impairment (CRCI)Cisplatin (CDDP)DNA damageHippocampal neuronsMitochondriaN-acetylcysteine (NAC)Neural stem/precursor cells (NSCs)Oxidative stress

Identifiers

PMID27908784
PMCPMC5308450
OpenAlexW2558267228

What OpenQuestion holds

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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.