ArticleToxicology research2016
Gene expression profiling to identify the toxicities and potentially relevant disease outcomes due to endosulfan exposure.
Article in Toxicology research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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
1 citing paper in PubMed, 13 citations in OpenAlex.
- Persistent organic pollutants and prostate cancer: multiple mechanisms and comprehensive control strategies.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endosulfan, one of the most toxic organochlorine pesticides, belongs to a group of persistent organic pollutants. Gene expression profiling offers a promising approach in health hazard identification of chemicals. The aim of this study was to use gene expression profiling to identify the toxicities and potentially relevant human diseases due to endosulfan exposure. We performed DNA microarray analysis to analyze gene expression profiles in human endothelial cells exposed to 20, 40 and 60 μM endosulfan in combination with an endothelial phenotype. Microarray results showed that endosulfan increased the number of altered genes in a dose-dependent manner, and changed the expression of 161 genes across all treatment groups. qRT-PCR closely matched the microarray data for the genes tested. Significantly enriched biological processes for overlapping down-regulated genes include the neurological system process, signal transduction, and homeostatic process in all the dose groups. These down-regulated genes were associated with cytoskeleton organization and DNA repair at low doses, and involved in cell cycle, apoptosis, p53 pathway and carcinogenesis at high doses. Those up-regulated genes were linked to the inflammatory response and transcriptional misregulation in cancer at higher doses. These findings are consistent with our established endothelial phenotypes. Endosulfan may be relevant to human diseases including liver cancer, prostate cancer and leukemia using the NextBio Human Disease Atlas. These results provide molecular evidence supporting the toxicities and carcinogenic potential of endosulfan in humans.
Identifiers
What OpenQuestion holds
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.