Effects of Environmental Pollutants on Calcium Release and Uptake by Rat Cortical Microsomes
Open accessAbstract
Dysregulation of neuronal intracellular Ca2+ homeostasis can play a crucial role in many neurotoxic effects, including impaired brain development and behavioral dysfunctions. This study examined 40 suspected neurotoxicants from different chemical classes for their capacity to alter Ca2+ release and uptake from rat cortical microsomes. First, ten suspected neurotoxicants have been tested using a well-established cuvette-based Ca2+ flux assay. Five out of ten compounds (TOCP, endosulfan, PCB-95, chlorpyrifos and BDE-49) showed a significant, concentration-dependent alteration of Ca2+ release and uptake in adult rat cortical microsomes. The original cuvette assay was downscaled and customized to a fast, higher throughput microplate method and the 40 suspected neurotoxicants were screened for their effects on intracellular Ca2+homeostasis. In decreasing order of potency, the 15 test compounds that showed the strongest alteration of Ca2+ levels in adult rat microsomes were TOCP, endosulfan, BDE-49, 6-OH-BDE-47, PCB-95, permethrin, alpha-cypermethrin, chlorpyrifos, bioallethrin, cypermethrin, RDP, DEHP, DBP, BDE-47, and PFOS. Results from co-exposure experiments with selective inhibitors suggested that for some compounds Ca2+ releasing effects could be attributed to RyR activation (PFOS, DBP, and DEHP) or to SERCA inhibition (a potential novel mechanism of action for all four tested pyrethroid insecticides). The effects of the two most potent compounds, endosulfan and TOCP, were not blocked by any of the inhibitors tested, indicating other possible mechanism of action. For all other potent test compounds, a combined effect on RyR, IP3R, and/or SERCA has been observed. PFOS and 6-OH-BDE-47 caused increased Ca2+ release from adult but not from neonatal rat brain microsomes, indicating age-dependent difference in susceptibility to these test compounds. The current study suggests that the neurotoxic potential of compounds belonging to different chemical classes could partly be attributed to the effects on intracellular Ca2+ release and uptake. Although further validation is required, the downscaled method developed in this study presents technical advance that could be used for the future screening of suspected intracellular Ca2+ disruptors.
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PFAS-induced increases in neuronal Ca2+ have been observed in both in vivo and in vitro studies.
“PFAS-induced increases in neuronal Ca2+ have been observed in both in vivo and in vitro studies”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Dusza et al., 2018
The Introduction and section 4.1.1 report elevated calcium in cultured hippocampal neurons exposed to PFOS, supporting the in vitro part. The paper also reports increased calcium release from isolated rat cortical microsomes. Although its References list a study titled as finding calcium overload in rat offspring, our copy does not establish that increased neuronal calcium was observed in vivo. (LLM, conf=0.82)
Experimental — accuracy not yet measuredPFAS-induced neuronal Ca2+ increases appear to be driven by Ca2+ influx from the extracellular space and intracellular Ca2+ storage organelles such as mitochondria and endoplasmic reticulum.
“appear to be driven by Ca2+ influx from the extracellular space and intracellular Ca2+ storage organelles, such as the mitochondria and endoplasmic reticulum”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Dusza et al., 2018
Section 4.1.1 reports that PFOS caused calcium release from rat cortical microsomes through RyR-mediated mobilization of intracellular stores. It does not establish calcium influx from extracellular space or release from mitochondria as drivers of PFAS-induced neuronal calcium increases. The methods in Section 2.4 studied isolated microsomes rather than influx into intact neurons; page numbers were unavailable in our copy. (LLM, conf=0.88)
Experimental — accuracy not yet measuredSeveral Ca2+ dependent signaling molecules, including CaMKII, CREB, and calcineurin, have been shown to be sensitive to PFAS exposure.
“Several Ca2+ dependent signaling molecules, including Ca2+/calmodulin-dependent protein kinase II (CaMKII), cAMP-response element binding protein (CREB), and calcineurin (CaN) have also been shown to be sensitive to PFAS exposure”
From A Critical Review and Meta-Analysis of Impacts of Per- and Polyfluorinated Substances on the Brain and Behavior (2022) · cites this paper as Dusza et al., 2018
Section 4.1.1 reports that PFOS increased calcium release from rat cortical microsomes, but it does not address whether CaMKII, CREB, or calcineurin are sensitive to PFAS exposure. Searches for the three molecule names and their expanded forms found no passage establishing the attributed claim. (LLM, conf=0.73)
Experimental — accuracy not yet measured
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- Authors
- Dusza, H. M., Cenijn, P. H., Kamstra, J. H., Westerink, R. H. S., Leonards, P. E. G., & Hamers, T.
- Affiliations
- Utrecht University (NL)
- Vrije Universiteit Amsterdam (NL)
- Norwegian University of Life Sciences (NO)
- Corresponding author
- Hamers, Timo
- ORCID
- Venue
- NeuroToxicology
- Publisher
- Elsevier BV
- Published
- 2018-12
- Volume
- 69
- Pages
- 266-277
- ISSN
- 0161-813X (ISSN-L)
- OpenAlex
- W2884092761
- Cited by
- 38
- References
- 71
- Citations by year
- 2026: 6 · 2025: 4 · 2024: 7 · 2023: 6 · 2022: 3 · 2021: 5 · 2020: 4 · 2019: 3
- FWCI
- 2.65
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Locations
- NeuroToxicology (publishedVersion, cc-by)
- PubMed (publishedVersion)
- VU Research Portal (publishedVersion, other-oa)
- BIBSYS Brage (BIBSYS (Norway)) (acceptedVersion, cc-by-nc-nd)
- Utrecht University Repository (Utrecht University) (submittedVersion, other-oa)
- NORA - Norwegian Open Research Archives (submittedVersion, cc-by-nc-nd)
- Data Archiving and Networked Services (DANS) (submittedVersion, other-oa)
- Funders
- DENAMIC
- Topics
- Life Sciences › Agricultural and Biological Sciences › Plant Science › Pesticide Exposure and Toxicity
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Toxic Organic Pollutants Impact
- Physical Sciences › Environmental Science › Health, Toxicology and Mutagenesis › Effects and risks of endocrine disrupting chemicals
- Keywords
- environmental pollutants, neurotoxicity, intracellular calcium homeostasis, calcium release, calcium uptake, pyrethroid insecticides, PFOS, endosulfan, triphenyltin, PCB 95, chlorpyrifos, BDE-49, SERCA inhibition, ryanodine receptor, IP3 receptor, microplate assay, age-related susceptibility
- MeSH terms
- Animals, Calcium, Cerebral Cortex, Environmental Pollutants, Female, Microsomes, Rats, Wistar, Rats, Sarcoplasmic Reticulum Calcium-Transporting ATPases
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