Evidence map›Paper›PMID 41854129›Full record

ArticleCurrent protocols2026

Analysis of Reactive Oxygen Species-Induced Cellular Damage in Cervical Cancer.

Hoi Ching Cherry Chan, Sachin Bhoora, Esther Zhou, Sumari Marais, Rivak Punchoo

Abstract read
In one paragraph

Article in Current protocols, 2026. 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
–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

1 citing paper in PubMed.

  1. 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.

Hoi Ching Cherry ChanDepartment of Chemical Pathology, Faculty of Health Sciences, University of Pretoria, Pretoria, Gauteng, South Africa.ORCID https://orcid.org/0009-0008-8858-8633
Sachin BhooraVitamin D Cancer Group, Division of Chemical Pathology, Department of Pathology, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.ORCID https://orcid.org/0000-0001-7050-4974
Esther ZhouVitamin D Cancer Group, Division of Chemical Pathology, Department of Pathology, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa.ORCID https://orcid.org/0000-0003-3652-1193
Sumari MaraisDepartment of Physiology, Faculty of Health Sciences, University of Pretoria, Pretoria, Gauteng, South Africa.ORCID https://orcid.org/0000-0002-3953-227X
Rivak PunchooDepartment of Chemical Pathology, Faculty of Health Sciences, University of Pretoria, Pretoria, Gauteng, South Africa.ORCID https://orcid.org/0000-0003-1570-3959

Funding

South African Medical Research Council (SAMRC)
6 · The paper itself

Abstract

Reactive oxygen species (ROS) are highly reactive oxygen-based molecules comprising hydrogen peroxide, hydroxyl radicals, superoxide anion, and singlet oxygen. These species are produced intracellularly and play an important role in cellular signaling and metabolism. Their high reactivity damages intracellular macromolecules such as lipids and DNA. In cancer biology, ROS display a dual role: they promote cancer cell proliferation at low to moderate levels, whereas excessive accumulation overwhelms antioxidant defenses, causing oxidative stress and apoptosis. This has resulted in therapeutic strategies that selectively increase ROS in cancer cells to induce apoptosis. Vitamin D has demonstrated anti-cancer properties, with one proposed mechanism involving ROS-mediated apoptosis. This article outlines a workflow to investigate ROS-induced cellular damage by vitamin D

Indexed as

Reactive Oxygen SpeciesUterine Cervical NeoplasmsAntioxidantsApoptosisCholecalciferolFemaleHeLa CellsHumansLipid PeroxidationMembrane Potential, MitochondrialOxidative StressSignal TransductionAntioxidantsCholecalciferolReactive Oxygen Speciesantioxidant defensecellular stress responseoxidative stressreactive oxygen speciesvitamin D‐induced apoptosis

Identifiers

PMID41854129
PMCPMC13001131

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.