Evidence map›Paper›PMID 39347848›Full record

ReviewBiometals : an international journal on the role of metal ions in biology, biochemistry, and medicine2024

Trace elements and metal nanoparticles: mechanistic approaches to mitigating chemotherapy-induced toxicity-a review of literature evidence.

Ademola C Famurewa, Mina Y George, Cletus A Ukwubile, Sachindra Kumar, Mehta V Kamal, Vijetha S Belle, Eman M Othman, Sreedhara Ranganath K Pai

Abstract readReview
PubMed Publisher
In one paragraph

Review in Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine, 2024. 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
–field-weighted citation impact
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.

  1. Review
  2. Review
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.

Ademola C FamurewaDepartment of Medical Biochemistry, Faculty of Basic Medical Sciences, College of Medical Sciences, Alex Ekwueme Federal University Ndufu-Alike Ikwo, Abakaliki, Ebonyi, Nigeria. ademola.famurewa@funai.edu.ng.
Mina Y GeorgeDepartment of Pharmacology and Toxicology, Faculty of Pharmacy, Ain Shams University, Cairo, Egypt.
Cletus A UkwubileDepartment of Pharmacognosy, Faculty of Pharmacy, University of Maiduguri, Bama Road, Maiduguri, Borno, Nigeria.
Sachindra KumarDepartment of Pharmacology, Manipal College of Pharmaceutical Science, Manipal Academy of Higher Education, Manipal, 576104, Karnataka, India.
Mehta V KamalDepartment of Biochemistry, Kasturba Medical College, Manipal, Manipal Academy of Higher Education, Manipal, 576104, Karnataka, India.
Vijetha S BelleDepartment of Biochemistry, Kasturba Medical College, Manipal, Manipal Academy of Higher Education, Manipal, 576104, Karnataka, India.
Eman M OthmanDepartment of Biochemistry, Faculty of Pharmacy, Minia University, Minia, 61519, Egypt.
Sreedhara Ranganath K PaiDepartment of Pharmacology, Manipal College of Pharmaceutical Science, Manipal Academy of Higher Education, Manipal, 576104, Karnataka, India.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anticancer chemotherapy (ACT) remains a cornerstone in cancer treatment, despite significant advances in pharmacology over recent decades. However, its associated side effect toxicity continues to pose a major concern for both oncology clinicians and patients, significantly impacting treatment protocols and patient quality of life. Current clinical strategies to mitigate ACT-induced toxicity have proven largely unsatisfactory, leaving a critical unmet need to block toxicity mechanisms without diminishing ACT's therapeutic efficacy. This review aims to document the molecular mechanisms underlying ACT toxicity and highlight research efforts exploring the protective effects of trace elements (TEs) and their nanoparticles (NPs) against these mechanisms. Our literature review reveals that the primary driver of ACT toxicity is redox imbalance, which triggers oxidative inflammation, apoptosis, endoplasmic reticulum stress, mitochondrial dysfunction, autophagy, and dysregulation of signaling pathways such as PI3K/mTOR/Akt. Studies suggest that TEs, including zinc, selenium, boron, manganese, and molybdenum, and their NPs, can potentially counteract ACT-induced toxicity by inhibiting oxidative stress-mediated pathways, including NF-κB/TLR4/MAPK/NLRP3, STAT-3/NLRP3, Bcl-2/Bid/p53/caspases, and LC3/Beclin-1/CHOP/ATG6, while also upregulating protective signaling pathways like Sirt1/PPAR-γ/PGC-1α/FOXO-3 and Nrf2/HO-1/ARE. However, evidence regarding the roles of lncRNA and the Wnt/β-catenin pathway in ACT toxicity remains inconsistent, and the impact of TEs and NPs on ACT efficacy is not fully understood. Further research is needed to confirm the protective effects of TEs and their NPs against ACT toxicity in cancer patients. In summary, TEs and their NPs present a promising avenue as adjuvant agents for preventing non-target organ toxicity induced by ACT.

Indexed as

Antineoplastic AgentsMetal NanoparticlesTrace ElementsAnimalsHumansNeoplasmsOxidative StressAntineoplastic AgentsTrace ElementsApoptosisCancerCancer therapyChemotherapyMetal nanoparticlesTrace elements

Identifiers

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.