Evidence map›Paper›PMID 21113647›Full record

ArticleMolecular and cellular biochemistry2011

Butylated hydroxyanisole inhibits the growth of HeLa cervical cancer cells via caspase-dependent apoptosis and GSH depletion.

Hwa Jin Moon, Woo Hyun Park

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.6field-weighted citation impact, top 38% 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

4 citing papers in PubMed, 15 citations in OpenAlex.

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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

2 authors at 1 institution in 1 country.

Hwa Jin MoonDepartment of Physiology, Medical School, Chonbuk National University, JeonJu, Republic of Korea.
Woo Hyun Park
Jeonbuk National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Butylated hydroxyanisole (BHA), a synthetic antioxidant is commonly used as a preservative in food and pharmaceutical agents. Despite the assumed low toxicity of BHA, it exerts a variety of effects on tissues and cell functions. In this study, the authors investigated the effects of BHA on the growth inhibition and death of HeLa cervical cancer cells. Dose-dependent inhibition of cell growth was observed with an IC(50) of approximately 150 μM BHA at 24 h. In addition, this agent-induced apoptosis, which was accompanied by the loss of mitochondrial membrane potential (ΔΨ(m)) and caspase activation. Caspase-3 and -8 inhibitors markedly rescued HeLa cells from BHA-induced cell death. In addition, BHA decreased intracellular ROS levels in HeLa cells whereas it increased O(2)(∙-) levels among ROS. The number of glutathione (GSH)-depleted cells was increased in 150 μM BHA-treated cells, which was attenuated by caspase inhibitors. In conclusion, BHA inhibited the growth of HeLa cells via caspase-dependent apoptosis, which seemed to be related to increase in GSH depletion and O(2)(∙-) level.

Indexed as

ApoptosisButylated HydroxyanisoleCaspase InhibitorsCaspasesCell ProliferationCysteine Proteinase InhibitorsGlutathioneHeLa CellsHumansReactive Oxygen SpeciesButylated HydroxyanisoleCaspase InhibitorsCaspasesCysteine Proteinase InhibitorsGlutathioneReactive Oxygen Species

Identifiers

PMID21113647
OpenAlexW2038266856

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.