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Cattani, D., Pierozan, P., Zamoner, A., Brittebo, E. B. & Karlsson, O. (2023). Long-Term Effects of Perinatal Exposure to a Glyphosate-Based Herbicide on Melatonin Levels and Oxidative Brain Damage in Adult Male Rats. Antioxidants, 12(10), Article ID 1825.
Open this publication in new window or tab >>Long-Term Effects of Perinatal Exposure to a Glyphosate-Based Herbicide on Melatonin Levels and Oxidative Brain Damage in Adult Male Rats
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2023 (English)In: Antioxidants, ISSN 2076-3921, Vol. 12, no 10, article id 1825Article in journal (Refereed) Published
Abstract [en]

Concerns have been raised regarding the potential adverse health effects of the ubiquitous herbicide glyphosate. Here, we investigated long-term effects of developmental exposure to a glyphosate-based herbicide (GBH) by analyzing serum melatonin levels and cellular changes in the striatum of adult male rats (90 days old). Pregnant and lactating rats were exposed to 3% GBH (0.36% glyphosate) through drinking water from gestational day 5 to postnatal day 15. The offspring showed reduced serum melatonin levels (43%) at the adult age compared with the control group. The perinatal exposure to GBH also induced long-term oxidative stress-related changes in the striatum demonstrated by increased lipid peroxidation (45%) and DNA/RNA oxidation (39%) together with increased protein levels of the antioxidant enzymes, superoxide dismutase (SOD1, 24%), glutamate-cysteine ligase (GCLC, 58%), and glutathione peroxidase 1 (GPx1, 31%). Moreover, perinatal GBH exposure significantly increased the total number of neurons (20%) and tyrosine hydroxylase (TH)-positive neurons (38%) in the adult striatum. Mechanistic in vitro studies with primary rat pinealocytes exposed to 50 mu M glyphosate demonstrated a decreased melatonin secretion partially through activation of metabotropic glutamate receptor 3 (mGluR3), while higher glyphosate levels (100 or 500 mu M) also reduced the pinealocyte viability. Since decreased levels of the important antioxidant and neuroprotector melatonin have been associated with an increased risk of developing neurodegenerative disorders, this demonstrates the need to consider the melatonin hormone system as a central endocrine-related target of glyphosate and other environmental contaminants.

Place, publisher, year, edition, pages
MDPI, 2023
Keywords
developmental exposure, glyphosate, pesticides, melatonin, striatum, oxidative stress
National Category
Pharmacology and Toxicology Psychiatry
Identifiers
urn:nbn:se:uu:diva-516649 (URN)10.3390/antiox12101825 (DOI)001096036700001 ()37891904 (PubMedID)
Available from: 2023-11-28 Created: 2023-11-28 Last updated: 2023-11-28Bibliographically approved
Dunlop, R. A., Banack, S. A., Bishop, S. L., Metcalf, J. S., Murch, S. J., Davis, D. A., . . . Bradley, W. G. (2021). Is Exposure to BMAA a Risk Factor for Neurodegenerative Diseases?: A Response to a Critical Review of the BMAA Hypothesis. Neurotoxicity research, 39(1), 81-106
Open this publication in new window or tab >>Is Exposure to BMAA a Risk Factor for Neurodegenerative Diseases?: A Response to a Critical Review of the BMAA Hypothesis
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2021 (English)In: Neurotoxicity research, ISSN 1029-8428, E-ISSN 1476-3524, Vol. 39, no 1, p. 81-106Article, review/survey (Refereed) Published
Abstract [en]

In a literature survey, Chernoff et al. (2017) dismissed the hypothesis that chronic exposure to beta-N-methylamino-L-alanine (BMAA) may be a risk factor for progressive neurodegenerative disease. They question the growing scientific literature that suggests the following: (1) BMAA exposure causes ALS/PDC among the indigenous Chamorro people of Guam; (2) Guamanian ALS/PDC shares clinical and neuropathological features with Alzheimer's disease, Parkinson's disease, and ALS; (3) one possible mechanism for protein misfolds is misincorporation of BMAA into proteins as a substitute for L-serine; and (4) chronic exposure to BMAA through diet or environmental exposures to cyanobacterial blooms can cause neurodegenerative disease. We here identify multiple errors in their critique including the following: (1) their review selectively cites the published literature; (2) the authors reported favorably on HILIC methods of BMAA detection while the literature shows significant matrix effects and peak coelution in HILIC that may prevent detection and quantification of BMAA in cyanobacteria; (3) the authors build alternative arguments to the BMAA hypothesis, rather than explain the published literature which, to date, has been unable to refute the BMAA hypothesis; and (4) the authors erroneously attribute methods to incorrect studies, indicative of a failure to carefully consider all relevant publications. The lack of attention to BMAA research begins with the review's title which incorrectly refers to BMAA as a "non-essential" amino acid. Research regarding chronic exposure to BMAA as a cause of human neurodegenerative diseases is emerging and requires additional resources, validation, and research. Here, we propose strategies for improvement in the execution and reporting of analytical methods and the need for additional and well-executed inter-lab comparisons for BMAA quantitation. We emphasize the need for optimization and validation of analytical methods to ensure that they are fit-for-purpose. Although there remain gaps in the literature, an increasingly large body of data from multiple independent labs using orthogonal methods provides increasing evidence that chronic exposure to BMAA may be a risk factor for neurological illness.

Place, publisher, year, edition, pages
SpringerSPRINGER, 2021
Keywords
BMAA, Neurodegeneration, ALS, ALS/PDC, Cyanobacteria, Neurodegenerative diseases
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:uu:diva-454742 (URN)10.1007/s12640-020-00302-0 (DOI)000615127800001 ()33547590 (PubMedID)
Available from: 2021-10-03 Created: 2021-10-03 Last updated: 2024-01-15Bibliographically approved
Cattani, D., Struyf, N., Steffensen, V., Bergquist, J., Zamoner, A., Brittebo, E. B. & Andersson, M. (2021). Perinatal exposure to a glyphosate-based herbicide causes dysregulation of dynorphins and an increase of neural precursor cells in the brain of adult male rats. Toxicology, 461, Article ID 152922.
Open this publication in new window or tab >>Perinatal exposure to a glyphosate-based herbicide causes dysregulation of dynorphins and an increase of neural precursor cells in the brain of adult male rats
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2021 (English)In: Toxicology, ISSN 0300-483X, E-ISSN 1879-3185, Vol. 461, article id 152922Article in journal (Refereed) Published
Abstract [en]

Glyphosate, the most used herbicide worldwide, has been suggested to induce neurotoxicity and behavioral changes in rats after developmental exposure. Studies of human glyphosate intoxication have reported adverse effects on the nervous system, particularly in substantia nigra (SN). Here we used matrix-assisted laser desorption ionization (MALDI) imaging mass spectrometry (IMS) to study persistent changes in peptide expression in the SN of 90-day-old adult male Wistar rats. The animals were perinatally exposed to 3 % GBH (glyphosate-based herbicide) in drinking water (corresponding to 0.36 % of glyphosate) starting at gestational day 5 and continued up to postnatal day 15 (PND15). Peptides are present in the central nervous system before birth and play a critical role in the development and survival of neurons, therefore, observed neuropeptide changes could provide better understanding of the GBH-induced long term effects on SN. The results revealed 188 significantly altered mass peaks in SN of animals perinatally exposed to GBH. A significant reduction of the peak intensity (P < 0.05) of several peptides from the opioid-related dynorphin family such as dynorphin B (57 %), alpha-neoendorphin (50 %), and its endogenous metabolite des-tyrosine alpha-neoendorphin (39 %) was detected in the GBH group. Immunohistochemical analysis confirmed a decreased dynorphin expression and showed a reduction of the total area of dynorphin immunoreactive fibers in the SN of the GBH group. In addition, a small reduction of dynorphin immunoreactivity associated with non-neuronal cells was seen in the hilus of the hippocampal dentate gyrus. Perinatal exposure to GBH also induced an increase in the number of nestin-positive cells in the subgranular zone of the dentate gyrus. In conclusion, the results demonstrate long-term changes in the adult male rat SN and hippocampus following a perinatal GBH exposure suggesting that this glyphosate-based formulation may perturb critical neurodevelopmental processes.

Place, publisher, year, edition, pages
ElsevierELSEVIER IRELAND LTD, 2021
Keywords
Glyphosate-based herbicide, MALDI IMS, Substantia nigra, Hippocampus, Dynorphin, Nestin
National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:uu:diva-456934 (URN)10.1016/j.tox.2021.152922 (DOI)000696272700022 ()34474092 (PubMedID)
Funder
Swedish Research Council, 2011-4423Swedish Research Council, 2015-4870
Available from: 2021-10-25 Created: 2021-10-25 Last updated: 2024-01-15Bibliographically approved
Pierozan, P., Piras, E., Brittebo, E. B. & Karlsson, O. (2020). The cyanobacterial neurotoxinbeta-N-methylamino-L-alanine (BMAA) targets the olfactory bulb region. Archives of Toxicology, 94(8), 2799-2808
Open this publication in new window or tab >>The cyanobacterial neurotoxinbeta-N-methylamino-L-alanine (BMAA) targets the olfactory bulb region
2020 (English)In: Archives of Toxicology, ISSN 0340-5761, E-ISSN 1432-0738, Vol. 94, no 8, p. 2799-2808Article in journal (Refereed) Published
Abstract [en]

Olfactory dysfunction is implicated in neurodegenerative disorders and typically manifests years before other symptoms. The cyanobacterial neurotoxin beta-N-methylamino-l-alanine (BMAA) is suggested as a risk factor for neurodegenerative disease. Detection of BMAA in air filters has increased the concern that aerosolization may lead to human BMAA exposure through the air. The aim of this study was to determine if BMAA targets the olfactory system. Autoradiographic imaging showed a distinct localization of radioactivity in the right olfactory mucosa and bulb following a unilateral intranasal instillation of H-3-BMAA (0.018 mu g) in mice, demonstrating a direct transfer of BMAA via the olfactory pathways to the brain circumventing the blood-brain barrier, which was confirmed by liquid scintillation. Treatment of mouse primary olfactory bulb cells with 100 mu M BMAA for 24 h caused a disruption of the neurite network, formation of dendritic varicosities and reduced cell viability. The NMDA receptor antagonist MK-801 and the metabotropic glutamate receptor antagonist MCPG protected against the BMAA-induced alterations, demonstrating the importance of glutamatergic mechanisms. The ionotropic non-NMDA receptor antagonist CNQX prevented the BMAA-induced decrease of cell viability in mixed cultures containing both neuronal and glial cells, but not in cultures with neurons only, suggesting a role of neuron-glial interactions and glial AMPA receptors in the BMAA-induced toxicity. The results show that the olfactory region may be a target for BMAA following inhalation exposure. Further studies on the relations between environmental olfactory toxicants and neurodegenerative disorders are warranted.

Place, publisher, year, edition, pages
Springer, 2020
Keywords
BMAA, Olfactory bulb, mGluR, NMDAR, Neurodegenerative diseases, ALS, PDC, Intranasal, Air pollution
National Category
Pharmacology and Toxicology
Research subject
Pharmaceutical Science
Identifiers
urn:nbn:se:uu:diva-421163 (URN)10.1007/s00204-020-02775-6 (DOI)000534456100001 ()32435914 (PubMedID)
Funder
Swedish Research Council Formas
Available from: 2020-10-06 Created: 2020-10-06 Last updated: 2020-11-05Bibliographically approved
Klint, H., Lejonklou, M. H., Karimullina, E., Rönn, M., Lind, L., Lind, P. M. & Brittebo, E. (2017). Low-dose exposure to bisphenol A in combination with fructose increases expression of genes regulating angiogenesis and vascular tone in juvenile Fischer 344 rat cardiac tissue. Upsala Journal of Medical Sciences, 122(1), 20-27
Open this publication in new window or tab >>Low-dose exposure to bisphenol A in combination with fructose increases expression of genes regulating angiogenesis and vascular tone in juvenile Fischer 344 rat cardiac tissue
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2017 (English)In: Upsala Journal of Medical Sciences, ISSN 0300-9734, E-ISSN 2000-1967, Vol. 122, no 1, p. 20-27Article in journal (Refereed) Published
Abstract [en]

OBJECTIVES: Epidemiological studies report associations between exposure to the high-volume chemical and endocrine disruptor bisphenol A (BPA) and cardiovascular disorders, but there is a lack of experimental studies addressing the mechanisms of action of BPA on the cardiovascular system. In the present study, effects on markers for cardiovascular function of exposure to BPA and fructose in vivo in rat cardiac tissues, and of BPA exposure in human cardiomyocytes in vitro, were investigated.

MATERIALS: Juvenile female Fischer 344 rats were exposed to 5, 50, and 500 μg BPA/kg bodyweight/day in their drinking water from 5 to 15 weeks of age, in combination with 5% fructose. Further, cultured human cardiomyocytes were exposed to 10 nM BPA to 1 × 10(4) nM BPA for six hours. Expression of markers for cardiovascular function and BPA target receptors was investigated using qRT-PCR.

RESULTS: Exposure to 5 μg BPA/kg bodyweight/day plus fructose increased mRNA expression of Vegf, Vegfr2, eNos, and Ace1 in rat heart. Exposure of human cardiomyocytes to 1 × 10(4) nM BPA increased mRNA expression of eNOS and ACE1, as well as IL-8 and NFκβ known to regulate inflammatory response.

CONCLUSIONS: . Low-dose exposure of juvenile rats to BPA and fructose induced up-regulation of expression of genes controlling angiogenesis and vascular tone in cardiac tissues. The observed effects of BPA in rat heart were in line with our present and previous studies of BPA in human endothelial cells and cardiomyocytes. These findings may aid in understanding the mechanisms of the association between BPA exposure and cardiovascular disorders reported in epidemiological studies.

Keywords
Angiogenesis, bisphenol A, cardiomyocytes, cardiovascular disease, endocrine disruption, fructose, heart, vascular tone
National Category
Pharmacology and Toxicology General Practice
Identifiers
urn:nbn:se:uu:diva-311874 (URN)10.1080/03009734.2016.1225870 (DOI)000396476600003 ()27622962 (PubMedID)
Funder
Swedish Research Council Formas, 216-2009-972
Available from: 2017-01-03 Created: 2017-01-03 Last updated: 2018-01-13Bibliographically approved
Engskog, M. K. R., Ersson, L., Haglöf, J., Arvidsson, T., Pettersson, C. & Brittebo, E. (2017). β-N-Methylamino-L-alanine (BMAA) perturbs alanine, aspartate and glutamate metabolism pathways in human neuroblastoma cells as determined by metabolic profiling. Amino Acids, 49(5), 905-919
Open this publication in new window or tab >>β-N-Methylamino-L-alanine (BMAA) perturbs alanine, aspartate and glutamate metabolism pathways in human neuroblastoma cells as determined by metabolic profiling
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2017 (English)In: Amino Acids, ISSN 0939-4451, E-ISSN 1438-2199, Vol. 49, no 5, p. 905-919Article in journal (Refereed) Published
Abstract [en]

β-Methylamino-L-alanine (BMAA) is a non-proteinogenic amino acid that induces long-term cognitive deficits, as well as an increased neurodegeneration and intracellular fibril formation in the hippocampus of adult rodents following short-time neonatal exposure and in vervet monkey brain following long-term exposure. It has also been proposed to be involved in the etiology of neurodegenerative disease in humans. The aim of this study was to identify metabolic effects not related to excitotoxicity or oxidative stress in human neuroblastoma SH-SY5Y cells. The effects of BMAA (50, 250, 1000 µM) for 24 h on cells differentiated with retinoic acid were studied. Samples were analyzed using LC-MS and NMR spectroscopy to detect altered intracellular polar metabolites. The analysis performed, followed by multivariate pattern recognition techniques, revealed significant perturbations in protein biosynthesis, amino acid metabolism pathways and citrate cycle. Of specific interest were the BMAA-induced alterations in alanine, aspartate and glutamate metabolism and as well as alterations in various neurotransmitters/neuromodulators such as GABA and taurine. The results indicate that BMAA can interfere with metabolic pathways involved in neurotransmission in human neuroblastoma cells.

Keywords
BMAA, Global metabolite profiling, MS, Metabolism, NMR, Neurotoxin
National Category
Pharmaceutical Sciences
Identifiers
urn:nbn:se:uu:diva-322142 (URN)10.1007/s00726-017-2391-8 (DOI)000399176200006 ()28161796 (PubMedID)
Funder
Swedish Research Council Formas
Available from: 2017-05-16 Created: 2017-05-16 Last updated: 2019-12-19Bibliographically approved
Andersson, M., Karlsson, O., Bergström, U., Brittebo, E. B. & Brandt, I. (2015). Correction: Maternal Transfer of the Cyanobacterial Neurotoxin β-N-Methylamino-L-Alanine (BMAA) via Milk to Suckling Offspring. PLOS ONE, 8(10), Article ID e78133.
Open this publication in new window or tab >>Correction: Maternal Transfer of the Cyanobacterial Neurotoxin β-N-Methylamino-L-Alanine (BMAA) via Milk to Suckling Offspring
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2015 (English)In: PLOS ONE, E-ISSN 1932-6203, Vol. 8, no 10, article id e78133Article in journal (Refereed) Published
National Category
Cell Biology Developmental Biology
Identifiers
urn:nbn:se:uu:diva-265863 (URN)10.1371/journal.pone.0133110 (DOI)000358194900136 ()26172384 (PubMedID)
Available from: 2015-11-03 Created: 2015-11-03 Last updated: 2021-06-14Bibliographically approved
Karlsson, O., Jiang, L., Ersson, L., Malmstrom, T., Ilag, L. L. & Brittebo, E. B. (2015). Environmental neurotoxin interaction with proteins: Dose-dependent increase of free and protein-associated BMAA (beta-N-methylamino-L-alanine) in neonatal rat brain. Scientific Reports, 5, Article ID 15570.
Open this publication in new window or tab >>Environmental neurotoxin interaction with proteins: Dose-dependent increase of free and protein-associated BMAA (beta-N-methylamino-L-alanine) in neonatal rat brain
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2015 (English)In: Scientific Reports, E-ISSN 2045-2322, Vol. 5, article id 15570Article in journal (Refereed) Published
Abstract [en]

beta-Methylamino-L-alanine (BMAA) is implicated in the aetiology of neurodegenerative disorders. Neonatal exposure to BMAA induces cognitive impairments and progressive neurodegenerative changes including intracellular fibril formation in the hippocampus of adult rats. It is unclear why the neonatal hippocampus is especially vulnerable and the critical cellular perturbations preceding BMAA-induced toxicity remains to be elucidated. The aim of this study was to compare the level of free and protein-associated BMAA in neonatal rat brain and peripheral tissues after different exposures to BMAA. Ultra-high performance liquid chromatography-tandem mass spectrometry analysis revealed that BMAA passed the neonatal blood-brain barrier and was distributed to all studied brain areas. BMAA was also associated to proteins in the brain, especially in the hippocampus. The level in the brain was, however, considerably lower compared to the liver that is not a target organ for BMAA. In contrast to the liver there was a significantly increased level of protein-association of BMAA in the hippocampus and other brain areas following repeated administration suggesting that the degradation of BMAA-associated proteins may be lower in neonatal brain than in the liver. Additional evidence is needed in support of a role for protein misincorporation in the neonatal hippocampus for long-term effects of BMAA.

National Category
Pharmacology and Toxicology
Identifiers
urn:nbn:se:uu:diva-267198 (URN)10.1038/srep15570 (DOI)000363397500001 ()26498001 (PubMedID)
Funder
Swedish Research Council Formas
Available from: 2015-11-19 Created: 2015-11-19 Last updated: 2022-09-15Bibliographically approved
Karlsson, O., Berg, A.-L., Hanrieder, J., Arnerup, G., Lindström, A.-K. & Brittebo, E. B. (2015). Intracellular fibril formation, calcification, and enrichment of chaperones, cytoskeletal, and intermediate filament proteins in the adult hippocampus CA1 following neonatal exposure to the nonprotein amino acid BMAA. Archives of Toxicology, 89(3), 423-436
Open this publication in new window or tab >>Intracellular fibril formation, calcification, and enrichment of chaperones, cytoskeletal, and intermediate filament proteins in the adult hippocampus CA1 following neonatal exposure to the nonprotein amino acid BMAA
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2015 (English)In: Archives of Toxicology, ISSN 0340-5761, E-ISSN 1432-0738, Vol. 89, no 3, p. 423-436Article in journal (Refereed) Published
Abstract [en]

The environmental neurotoxin β-N-methylamino-L-alanine (BMAA) has been implicated in the etiology of neurodegenerative disease, and recent studies indicate that BMAA can be misincorporated into proteins. BMAA is a developmental neurotoxicant that can induce long-term learning and memory deficits, as well as regionally restricted neuronal degeneration and mineralization in the hippocampal CA1. The aim of the study was to characterize long-term changes (2 weeks to 6 months) further in the brain of adult rats treated neonatally (postnatal days 9-10) with BMAA (460 mg/kg) using immunohistochemistry (IHC), transmission electron microscopy, and laser capture microdissection followed by LC-MS/MS for proteomic analysis. The histological examination demonstrated progressive neurodegenerative changes, astrogliosis, microglial activation, and calcification in the hippocampal CA1 3-6 months after exposure. The IHC showed an increased staining for α-synuclein and ubiquitin in the area. The ultrastructural examination revealed intracellular deposition of abundant bundles of closely packed parallel fibrils in neurons, axons, and astrocytes of the CA1. Proteomic analysis of the affected site demonstrated an enrichment of chaperones (e.g., clusterin, GRP-78), cytoskeletal and intermediate filament proteins, and proteins involved in the antioxidant defense system. Several of the most enriched proteins (plectin, glial fibrillar acidic protein, vimentin, Hsp 27, and ubiquitin) are known to form complex astrocytic inclusions, so-called Rosenthal fibers, in the neurodegenerative disorder Alexander disease. In addition, TDP-43 and the negative regulator of autophagy, GLIPR-2, were exclusively detected. The present study demonstrates that neonatal exposure to BMAA may offer a novel model for the study of hippocampal fibril formation in vivo.

National Category
Pharmacology and Toxicology Neurosciences
Identifiers
urn:nbn:se:uu:diva-225453 (URN)10.1007/s00204-014-1262-2 (DOI)000350030200011 ()24798087 (PubMedID)
Available from: 2014-06-03 Created: 2014-06-03 Last updated: 2018-01-11Bibliographically approved
Hanrieder, J., Gerber, L., Persson Sandelius, A., Brittebo, E. B., Ewing, A. G. & Karlsson, O. (2014). High resolution metabolite imaging in the hippocampus following neonatal exposure to the environmental toxin BMAA using ToF-SIMS. ACS Chemical Neuroscience, 5(7), 568-575
Open this publication in new window or tab >>High resolution metabolite imaging in the hippocampus following neonatal exposure to the environmental toxin BMAA using ToF-SIMS
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2014 (English)In: ACS Chemical Neuroscience, E-ISSN 1948-7193, Vol. 5, no 7, p. 568-575Article in journal (Refereed) Published
Abstract [en]

The environmental neurotoxin β-N-methylamino-l-alanine (BMAA) is suggested to be linked with neurodegenerative disease. In a rat model, neonatal exposure to BMAA induced selective uptake in the hippocampus and caused cell loss, mineralization and astrogliosis as well as learning and memory impairments in adulthood. Moreover, neonatal exposure resulted in increased protein ubiquitination in the cornus ammonis 1 (CA1) region of the adult hippocampus indicating that BMAA may induce protein aggregation. Time-of-flight secondary ion mass spectrometry (ToF-SIMS) based imaging is a powerful technology for spatial profiling of small molecular weight compounds in biological tissues with high chemical specificity and high spatial resolution. The aim of this study was to characterize neurochemical changes in the hippocampus of six month-old rats treated neonatally (postnatal days 9-10) with BMAA. Multivariate data analysis of whole section ToF-SIMS scans was performed to delineate anatomical regions of interest based on their chemical distribution pattern. Further analysis of spectral data obtained from the outlined anatomical regions, including CA1 and dentate gyrus (DG) revealed BMAA-induced long-term changes. Increased levels of phospholipids and protein fragments in the histopathologically altered CA1 region as well as phosphate depletion in the DG were observed. Moreover, high resolution SIMS imaging revealed a specific localization of phosphatidylcholine lipids, protein signals and potassium in the histopathologically altered CA1. These findings demonstrate that ToF-SIMS based imaging is a powerful approach for probing biochemical changes in situ and might serve as promising technique for investigating neurotoxin-induced brain pathology.

National Category
Neurosciences Pharmacology and Toxicology
Identifiers
urn:nbn:se:uu:diva-225455 (URN)10.1021/cn500039b (DOI)000339226100013 ()24779349 (PubMedID)
Available from: 2014-06-03 Created: 2014-06-03 Last updated: 2023-08-28Bibliographically approved
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ORCID iD: ORCID iD iconorcid.org/0000-0002-7644-1967

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