ArticleCell stress & chaperones2007
Cadmium induces an apoptotic response in sea urchin embryos.
Article in Cell stress & chaperones, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Impact of near-future ocean acidification on echinoderms.Ecotoxicology (London, England) · 2010Pooled it
- Remodeling of Embryo Architecture in Response to Vanadium and Increased Temperatures: From Morphometric to Molecular Changes.Journal of xenobiotics · 2025Article
- Between Life and Death: Sea Urchin Embryos Undergo Peculiar DNA Fragmentation after Exposure to Vanadium, Cadmium, Gadolinium, and Selenium.Life (Basel, Switzerland) · 2024Article
- Vanadium Toxicity Is Altered by Global Warming Conditions in Sea Urchin Embryos: Metal Bioaccumulation, Cell Stress Response and Apoptosis.Journal of xenobiotics · 2024Article
- Toxicity of Vanadium during Development of Sea Urchin Embryos: Bioaccumulation, Calcium Depletion, ERK Modulation and Cell-Selective Apoptosis.International journal of molecular sciences · 2022Article
- Cadmium stress effects indicating marine pollution in different species of sea urchin employed as environmental bioindicators.Cell stress & chaperones · 2019Review
- Autophagy as a defense strategy against stress: focus on Paracentrotus lividus sea urchin embryos exposed to cadmium.Cell stress & chaperones · 2016Review
- Maternal Exposure to Cadmium and Manganese Impairs Reproduction and Progeny Fitness in the Sea Urchin Paracentrotus lividus.PloS one · 2015Article
- Humoral and haemocytic responses of Litopenaeus vannamei to Cd exposure.TheScientificWorldJournal · 2014Article
- Effects of cadmium exposure on sea urchin development assessed by SSH and RT-qPCR: metallothionein genes and their differential induction.Molecular biology reports · 2013Article
- Article
- Axial patterning interactions in the sea urchin embryo: suppression of nodal by Wnt1 signaling.Development (Cambridge, England) · 2012Article
- Stress response induced by carbon nanoparticles in Paracentrotus lividus.International journal of molecular and cellular medicine · 2012Article
- Transcriptional increase and misexpression of 14-3-3 epsilon in sea urchin embryos exposed to UV-B.Cell stress & chaperones · 2010Article
- Dose-dependent effects of chlorpyriphos, an organophosphate pesticide, on metamorphosis of the sea urchin, Paracentrotus lividus.Ecotoxicology (London, England) · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cadmium is a heavy metal toxic for living organisms even at low concentrations. It does not have any biological role, and since it is a permanent metal ion, it is accumulated by many organisms. In the present paper we have studied the apoptotic effects of continuous exposure to subacute/sublethal cadmium concentrations on a model system: Paracentrotus lividus embryos. We demonstrated, by atomic absorption spectrometry, that the intracellular amount of metal increased during exposure time. We found, using terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling assay, that long treatments with cadmium triggered a severe DNA fragmentation. We demonstrated, by immunocytochemistry on whole-mount embryos, that treatment with cadmium causes activation of caspase-3 and cleavage of death substrates alpha-fodrin and lamin A. Incubating the embryos since fertilization with Z-DEVD FMK, a caspase-3 inhibitor, we found, by immunocytochemistry, that cleavage by caspase-3 and cleavage of death substrates were inactivated.
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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.