ArticleNeurotoxicity research2010
Mechanism of the specific neuronal toxicity of a type I ribosome-inactivating protein, trichosanthin.
Article in Neurotoxicity research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed, 8 citations in OpenAlex.
- Trichosanthin elicits antitumor activity via MICU3 mediated mitochondria calcium influx.Journal of advanced research · 2025Article
- Cytotoxicity Effect of Quinoin, Type 1 Ribosome-Inactivating Protein from Quinoa Seeds, on Glioblastoma Cells.Toxins · 2021Article
- Trichosanthin cooperates with Granzyme B to restrain tumor formation in tongue squamous cell carcinoma.BMC complementary medicine and therapies · 2021Article
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 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim was to study the mechanism of neuronal toxicity, the cellular pathway, and the glial cell reactions induced by trichosanthin (TCS), a type I ribosome-inactivating protein (RIP). Ricin A chain (RTA) was included for comparison. TCS, RTA, and fluorescein isothiocyanate (FITC)-labeled TCS and RTA were separately injected into rat eyes. Saline or pure FITC was used as the control. Electron microscopy, confocal microscopy, and lectin and immunohistochemical staining were used to study the neurotoxic mechanism. TCS mainly induced apoptosis by causing degeneration of the mitochondria. TCS was able to enter the Müller and pigment cells. It caused a change in cell number of the following types of glial cells: a decrease in Müller cells, an increase in astrocytes, and little change in microglia. In contrast, RTA mainly induced necrosis and entered vascular endothelial cells. Astrocyte and microglia reactions were stronger in the RTA-treated retinas than those in the TCS-treated retinas. In conclusion, TCS appears to selectively enter and destroy Müller and pigment epithelia cells, which subsequently induce the death of photoreceptors. Degeneration of mitochondria is involved in the pathways of apoptosis of the photoreceptors caused by TCS. In sharp contrast, RTA can enter vascular endothelial cells and damage the vascular endothelium, resulting in retinitis and necrosis.
Indexed as
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.