Evidence map›Paper›PMID 38311193›Full record

ArticleToxicology letters2024

Evaluation of weak genotoxicity of hydroxychloroquine in human TK6 cells.

Xilin Li, Yuan Le, Yuxi Li, Si Chen, Lei Guo, Xin Fu, Mugimane G Manjanatha, Nan Mei

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Toxicology letters, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.5field-weighted citation impact, top 39% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Development of a TK6-derived cell line expressing four human cytochrome P450s for genotoxicity testing.Toxicology in vitro : an international journal published in association with BIBRA · 2025
    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

8 authors at 2 institutions in 1 country.

Xilin LiDivision of Genetic and Molecular Toxicology, National Center for Toxicological Research, Jefferson, AR 72079, USA. Electronic address: xilin.li@fda.hhs.gov.
Yuan LeDivision of Genetic and Molecular Toxicology, National Center for Toxicological Research, Jefferson, AR 72079, USA.
Yuxi LiDivision of Genetic and Molecular Toxicology, National Center for Toxicological Research, Jefferson, AR 72079, USA.
Si ChenDivision of Biochemical Toxicology, National Center for Toxicological Research, Jefferson, AR 72079, USA.
Lei GuoDivision of Biochemical Toxicology, National Center for Toxicological Research, Jefferson, AR 72079, USA.
Xin FuDivision of Pharmacology Toxicology Review, Office of Safety and Clinical Evaluation, Center for Drug Evaluation and Research, Silver Spring, MD 20993, USA.
Mugimane G ManjanathaDivision of Genetic and Molecular Toxicology, National Center for Toxicological Research, Jefferson, AR 72079, USA.
Nan MeiDivision of Genetic and Molecular Toxicology, National Center for Toxicological Research, Jefferson, AR 72079, USA. Electronic address: nan.mei@fda.hhs.gov.
National Center for Toxicological Research · USCenter for Drug Evaluation and Research · US

Funding

Intramural FDA HHS FD999999
6 · The paper itself

Abstract

Hydroxychloroquine (HCQ), a derivative of chloroquine (CQ), is an antimalarial and antirheumatic drug. Since there is limited data available on the genotoxicity of HCQ, in the current study, we used a battery of in vitro assays to systematically examine the genotoxicity of HCQ in human lymphoblastoid TK6 cells. We first showed that HCQ is not mutagenic in TK6 cells up to 80 μM with or without exogenous metabolic activation. Subsequently, we found that short-term (3-4 h) HCQ treatment did not cause DNA strand breakage as measured by the comet assay and the phosphorylation of histone H2A.X (γH2A.X), and did not induce chromosomal damage as determined by the micronucleus (MN) assay. However, after 24-h treatment, both CQ and HCQ induced comparable and weak DNA damage and MN formation in TK6 cells; upregulated p53 and p53-mediated DNA damage responsive genes; and triggered apoptosis and mitochondrial damage that may partially contribute to the observed MN formation. Using a benchmark dose (BMD) modeling analysis, the lower 95% confidence limit of BMD

Indexed as

HydroxychloroquineTumor Suppressor Protein p53ChloroquineComet AssayDNA DamageHumansChloroquineHydroxychloroquineTumor Suppressor Protein p53ApoptosisChloroquineChromosomal damageDNA damageHydroxychloroquineTK6 cells

Identifiers

PMID38311193
PMCPMC11369915
OpenAlexW4391469587

What OpenQuestion holds

Textmetadata
LicenceTDM
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.