Evidence map›Paper›PMID 36835302›Full record

ArticleInternational journal of molecular sciences2023

Adverse Toxic Effects of Tyrosine Kinase Inhibitors on Non-Target Zebrafish Liver (ZFL) Cells.

Katja Kološa, Bojana Žegura, Martina Štampar, Metka Filipič, Matjaž Novak

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
1.3field-weighted citation impact, top 23% 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

2 citing papers in PubMed, 9 citations in OpenAlex.

  1. Micronuclei: origins, assays, mechanisms, diseases and treatments.Signal transduction and targeted therapy · 2026
    Review
  2. 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

5 authors at 2 institutions in 1 country.

Katja KološaDepartment of Genetic Toxicology and Cancer Biology, National Institute of Biology, Večna Pot 111, 1000 Ljubljana, Slovenia.ORCID 0000-0002-2855-2793
Bojana ŽeguraDepartment of Genetic Toxicology and Cancer Biology, National Institute of Biology, Večna Pot 111, 1000 Ljubljana, Slovenia.ORCID 0000-0002-5731-0785
Martina ŠtamparDepartment of Genetic Toxicology and Cancer Biology, National Institute of Biology, Večna Pot 111, 1000 Ljubljana, Slovenia.
Metka FilipičDepartment of Genetic Toxicology and Cancer Biology, National Institute of Biology, Večna Pot 111, 1000 Ljubljana, Slovenia.ORCID 0000-0002-1437-2556
Matjaž NovakDepartment of Genetic Toxicology and Cancer Biology, National Institute of Biology, Večna Pot 111, 1000 Ljubljana, Slovenia.
National Institute of Biology · SIJožef Stefan International Postgraduate School · SI

Funding

Slovenian Research Agency J1-8140Slovenian Research Agency P1-0245Slovenian Research Agency Z1-1854
6 · The paper itself

Abstract

Over the past 20 years, numerous tyrosine kinase inhibitors (TKIs) have been introduced for targeted therapy of various types of malignancies. Due to frequent and increasing use, leading to eventual excretion with body fluids, their residues have been found in hospital and household wastewaters as well as surface water. However, the effects of TKI residues in the environment on aquatic organisms are poorly described. In the present study, we investigated the cytotoxic and genotoxic effects of five selected TKIs, namely erlotinib (ERL), dasatinib (DAS), nilotinib (NIL), regorafenib (REG), and sorafenib (SOR), using the in vitro zebrafish liver cell (ZFL) model. Cytotoxicity was determined using the MTS assay and propidium iodide (PI) live/dead staining by flow cytometry. DAS, SOR, and REG decreased ZFL cell viability dose- and time-dependently, with DAS being the most cytotoxic TKI studied. ERL and NIL did not affect viability at concentrations up to their maximum solubility; however, NIL was the only TKI that significantly decreased the proportion of PI negative cells as determined by the flow cytometry. Cell cycle progression analyses showed that DAS, ERL, REG, and SOR caused the cell cycle arrest of ZFL cells in the G0/G1 phase, with a concomitant decrease of cells in the S-phase fraction. No data could be obtained for NIL due to severe DNA fragmentation. The genotoxic activity of the investigated TKIs was evaluated using comet and cytokinesis block micronucleus (CBMN) assays. The dose-dependent induction of DNA single strand breaks was induced by NIL (≥2 μM), DAS (≥0.006 μM), and REG (≥0.8 μM), with DAS being the most potent. None of the TKIs studied induced micronuclei formation. These results suggest that normal non-target fish liver cells are sensitive to the TKIs studied in a concentration range similar to those previously reported for human cancer cell lines. Although the TKI concentrations that induced adverse effects in exposed ZFL cells are several orders of magnitude higher than those currently expected in the aquatic environment, the observed DNA damage and cell cycle effects suggest that residues of TKIs in the environment may pose a hazard to non-intentionally exposed organisms living in environments contaminated with TKIs.

Indexed as

Antineoplastic AgentsHepatocytesTyrosine Kinase InhibitorsAnimalsHumansLiverPhenylurea CompoundsPyridinesPyrimidinesSorafenibZebrafishAntineoplastic AgentsPhenylurea CompoundsPyridinesPyrimidinesregorafenibSorafenibTyrosine Kinase Inhibitorscell cyclecytotoxicityenvironmental hazardgenotoxicitytyrosine kinase inhibitorszebrafish liver cellsZFL

Identifiers

PMID36835302
PMCPMC9965539
OpenAlexW4320919540

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.