Effects of acute exposure to microcystins on hypothalamic-pituitary-adrenal (HPA), -gonad (HPG) and -thyroid (HPT) axes of female rats

Chen, Liang; Shi, Ting; Wang, Yuting; He, Jun; Zhao, Xiangui; Wang, Yeke; Giesy, John P.; Chen, Feng; Chen, Yang; Tuo, Xun; Chen, Jun; Xie, Ping

doi:10.1016/j.scitotenv.2021.145196

Cited by 43 publications

(22 citation statements)

References 105 publications

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“…Knowing that T3 is the main transcriptionally active TH, we next assessed hippocampal T3 availability by measuring the main actors in TH signalling as well as the regulation of T3 target genes, as already widely described in the literature [ 34 , 35 , 36 , 40 , 41 ]. In the hippocampus, we observed a decrease in T3 target gene expression only in the C57BL/6J mouse strain.…”

Section: Discussionmentioning

confidence: 99%

A Fine Regulation of the Hippocampal Thyroid Signalling Protects Hypothyroid Mice against Glial Cell Activation

Chamas¹,

Seugnet²,

Poirier

et al. 2022

IJMS

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Adult-onset hypothyroidism is associated with learning and cognitive dysfunctions, which may be related to alterations in synaptic plasticity. Local reduced levels of thyroid hormones (THs) may impair glia morphology and activity, and promote the increase of pro-inflammatory cytokine levels mainly in the hippocampus. Given that neuroinflammation induces memory impairments, hypothyroidism-related glia dysfunction may participate in brain disorders. Thus, we investigated the mechanisms linking hypothyroidism and neuroinflammation, from a protective perspective. We induced hypothyroidism in adult C57BL/6J and wild-derived WSB/EiJ male mice by a seven-week propylthiouracil (PTU) treatment. We previously showed that WSB/EiJ mice were resistant to high-fat diet (HFD)-induced obesity, showing no neuroinflammatory response through adaptive abilities, unlike C57BL/6J. As PTU and HFD treatments are known to induce comparable inflammatory responses, we hypothesized that WSB/EiJ mice might also be protected against hypothyroidism-induced neuroinflammation. We showed that hypothyroid WSB/EiJ mice depicted no hippocampal neuroinflammatory response and were able to maintain their hippocampal thyroid signalling despite low circulatisng TH levels. In contrast, C57BL/6J mice exhibited disturbed hippocampal TH signalling, accompanied by neuroinflammation and memory impairment. Our results reinforce the preponderance of the hippocampal TH regulatory system over TH circulating levels in the hippocampal glial reactivity.

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Section: Discussionmentioning

confidence: 99%

A Fine Regulation of the Hippocampal Thyroid Signalling Protects Hypothyroid Mice against Glial Cell Activation

Chamas¹,

Seugnet²,

Poirier

et al. 2022

IJMS

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“…The mechanisms of MCs neurotoxicity were reviewed by different researchers [ 282 , 283 ]. Thus, MC-LR can induce apoptosis and atrophy of gonadotropin-releasing hormone (GnRH) neurons in rats’ hypothalamus [ 284 , 285 ]. Although the molecular mechanism of MC-LR- induced apoptosis remains elusive, growing evidence supports that MCs and other cyanobacterial toxins, such as cylindrospermopsin, act as endocrine disruptors [ 286 , 287 ].…”

Section: Mechanisms Of Brain Toxicitymentioning

confidence: 99%

Freshwater Cyanobacterial Toxins, Cyanopeptides and Neurodegenerative Diseases

Nugumanova

Ponomarev

Askarova

et al. 2023

Toxins

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Cyanobacteria produce a wide range of structurally diverse cyanotoxins and bioactive cyanopeptides in freshwater, marine, and terrestrial ecosystems. The health significance of these metabolites, which include genotoxic- and neurotoxic agents, is confirmed by continued associations between the occurrence of animal and human acute toxic events and, in the long term, by associations between cyanobacteria and neurodegenerative diseases. Major mechanisms related to the neurotoxicity of cyanobacteria compounds include (1) blocking of key proteins and channels; (2) inhibition of essential enzymes in mammalian cells such as protein phosphatases and phosphoprotein phosphatases as well as new molecular targets such as toll-like receptors 4 and 8. One of the widely discussed implicated mechanisms includes a misincorporation of cyanobacterial non-proteogenic amino acids. Recent research provides evidence that non-proteinogenic amino acid BMAA produced by cyanobacteria have multiple effects on translation process and bypasses the proof-reading ability of the aminoacyl-tRNA-synthetase. Aberrant proteins generated by non-canonical translation may be a factor in neuronal death and neurodegeneration. We hypothesize that the production of cyanopeptides and non-canonical amino acids is a more general mechanism, leading to mistranslation, affecting protein homeostasis, and targeting mitochondria in eukaryotic cells. It can be evolutionarily ancient and initially developed to control phytoplankton communities during algal blooms. Outcompeting gut symbiotic microorganisms may lead to dysbiosis, increased gut permeability, a shift in blood-brain-barrier functionality, and eventually, mitochondrial dysfunction in high-energy demanding neurons. A better understanding of the interaction between cyanopeptides metabolism and the nervous system will be crucial to target or to prevent neurodegenerative diseases.

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“…MC-LR is the most distributed variant, followed by MC-RR and MC-YR from over 270 identified MCs variants [11][12][13]147]. For MC congeners, other than MC-LR, there are limited data concerning their toxicity and occurrence in the scientific literature [148].…”

Section: Variants Other Than Mc-lrmentioning

confidence: 99%

“…Among various classes of cyanotoxins, MCs are the most widespread in freshwater environments. Until now, over 270 different MC congeners have been determined, and Microcystin-LR (MC-LR), Microcystin-RR (MC-RR), and Microcystin-YR (MC-YR) are the three of most concern and widely studied [11][12][13]. The molecular formula and molecular weight of the three commonly distributed MCs are shown in Figure 2.…”

Section: Introductionmentioning

confidence: 99%

Microcystin-Induced Immunotoxicity in Fishes: A Scoping Review

Wang

Hung

Kurobe

et al. 2021

Toxins

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Cyanobacteria (blue-green algae) have been present on Earth for over 2 billion years, and can produce a variety of bioactive molecules, such as cyanotoxins. Microcystins (MCs), the most frequently detected cyanotoxins, pose a threat to the aquatic environment and to human health. The classic toxic mechanism of MCs is the inhibition of the protein phosphatases 1 and 2A (PP1 and PP2A). Immunity is known as one of the most important physiological functions in the neuroendocrine-immune network to prevent infections and maintain internal homoeostasis in fish. The present review aimed to summarize existing papers, elaborate on the MC-induced immunotoxicity in fish, and put forward some suggestions for future research. The immunomodulatory effects of MCs in fish depend on the exposure concentrations, doses, time, and routes of exposure. Previous field and laboratory studies provided strong evidence of the associations between MC-induced immunotoxicity and fish death. In our review, we summarized that the immunotoxicity of MCs is primarily characterized by the inhibition of PP1 and PP2A, oxidative stress, immune cell damage, and inflammation, as well as apoptosis. The advances in fish immunoreaction upon encountering MCs will benefit the monitoring and prediction of fish health, helping to achieve an ecotoxicological goal and to ensure the sustainability of species. Future studies concerning MC-induced immunotoxicity should focus on adaptive immunity, the hormesis phenomenon and the synergistic effects of aquatic microbial pathogens.

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Effects of acute exposure to microcystins on hypothalamic-pituitary-adrenal (HPA), -gonad (HPG) and -thyroid (HPT) axes of female rats

Cited by 43 publications

References 105 publications

A Fine Regulation of the Hippocampal Thyroid Signalling Protects Hypothyroid Mice against Glial Cell Activation

A Fine Regulation of the Hippocampal Thyroid Signalling Protects Hypothyroid Mice against Glial Cell Activation

Freshwater Cyanobacterial Toxins, Cyanopeptides and Neurodegenerative Diseases

Microcystin-Induced Immunotoxicity in Fishes: A Scoping Review

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