ArticleMolecular biology reports2012
Hydroquinone-induced apoptosis of human lymphocytes through caspase 9/3 pathway.
Article in Molecular biology reports, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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.
Who cites it
7 citing papers in PubMed, 31 citations in OpenAlex.
- Health Implications of Colorism: A Narrative Review of the Literature.Journal of racial and ethnic health disparities · 2026Review
- Article
- Anti-apoptotic HAX-1 suppresses cell apoptosis by promoting c-Abl kinase-involved ROS clearance.Cell death & disease · 2022Article
- Article
- Resvega Alleviates Hydroquinone-Induced Oxidative Stress in ARPE-19 Cells.International journal of molecular sciences · 2020Article
- Hydroquinone: environmental pollution, toxicity, and microbial answers.BioMed research international · 2013Review
- Resveratrol inhibited hydroquinone-induced cytotoxicity in mouse primary hepatocytes.International journal of environmental research and public health · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hydroquinone (HQ) is a major benzene metabolite, which is produced after benzene biotransformation. In this study, we investigated the toxic effect of HQ on lymphocytes. HQ significantly induced the apoptosis of lymphocytes isolated from normal peripheral blood in both dose and time dependent courses. Volatile organic compounds such as benzene, phenol, formaldehyde, o- and p-xylene, and toluene have no effect on lymphocyte apoptosis. HQ induced the cleavage of procaspase 3 and procaspase 9, indicating activation of the pro-apoptotic enzymes. Supernatant was collected from normal lymphocytes after HQ treatment and it significantly induced the apoptosis of normal lymphocytes as compared to supernatant collected from normal lymphocytes without HQ treatment. HQ reduced the secretion of MCP-1, IL-6 and IL-8 increased by in vitro incubation, although benzene and phenol are not effective in cytokine production. HQ increased the intracellular ROS production of lymphocytes. Benzene and phenol also increased the ROS production. In summary, HQ has a cytotoxic effect on lymphocytes by apoptosis induction and the pro-apoptotic signaling is involved in caspase 9/3 pathway. Our results demonstrated that HQ induces apoptosis by activating caspases 9/3 pathway and that the toxic effect seems to be dependent on lymphocyte metabolism.
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Registered trials
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.