Neurotoxicity of ochratoxin A: Molecular mechanisms and neurotherapeutic strategies

Obafemi, Blessing A.; Adedara, Isaac A.; Rocha, Joao B.T.

doi:10.1016/j.tox.2023.153630

Cited by 6 publications

(2 citation statements)

References 129 publications

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“…It is prevalently found in food, feed, and other commodities. , Due to its neurotoxic, nephrotoxic, teratogenic, and carcinogenic toxicities and potential risks to human and animal health, OTA has been listed as a 2B carcinogen by the International Agency for Research on Cancer . Consumption of OTA-contaminated products will inevitably lead to tissue bioaccumulation and serious harm . For safeguarding human health from OTA, the regulatory guidelines and maximum residue levels (MRLs) regarding it in certain commodities have been stipulated in the world .…”

Section: Introductionmentioning

confidence: 99%

“… 4 Consumption of OTA-contaminated products will inevitably lead to tissue bioaccumulation and serious harm. 5 For safeguarding human health from OTA, the regulatory guidelines and maximum residue levels (MRLs) regarding it in certain commodities have been stipulated in the world. 6 To meet these strict requirements and lower the risk of OTA consumption, effective and reliable approaches and analytical methods are urgently required for the sensitive detection of OTA at trace levels (ppt–ppb) in diverse matrices.…”

Section: Introductionmentioning

confidence: 99%

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Establishment of a Dual-Signal Enhanced Fluorescent Aptasensor for Highly Sensitive Detection of Ochratoxin A

Li,

Zhang

et al. 2024

ACS Omega

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A robust and versatile dual-signal enhanced fluorescent aptasensor was developed for ochratoxin A (OTA) detection based on fluorescence resonance energy transfer between 5-carboxyfluorescein (FAM) and Super Green I (SG) fluorophores as the donor and graphene oxide (GO) nanosheet as the acceptor. Abundant SG probes were adsorbed into the FAM-complementary DNA (cDNA)-aptamer double-stranded structure to achieve remarkably enhanced fluorescence responses. Without OTA, the FAM-cDNA-SG conjugates coexisted with GO nanosheets, exhibiting strong fluorescence signals. In the presence of OTA, it was captured by the aptamers to release cDNA-FAM and SG probes, which were adsorbed by GO, leading to OTA-dependent fluorescence quenching. The changed fluorescence intensity was measured for accurate quantitation of OTA. Under optimum conditions, the dual-signal enhanced fluorescent aptasensor realized fascinating sensitivity with a limit of detection of 0.005 ng/mL and a wide concentration range of 0.02−20 ng/mL, as well as high selectivity for OTA over other interfering substances, excellent accuracy with average recoveries of 91.37−116.83% in the fortified malt matrices, and superior reliability and practicability in actual samples. This FAM-cDNA-aptamer-SG/GO nanosheet-based aptasensing platform could be extended to monitor other contaminants or trace molecules in food, environmental, and diagnostic fields by altering the corresponding aptamers.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Establishment of a Dual-Signal Enhanced Fluorescent Aptasensor for Highly Sensitive Detection of Ochratoxin A

Li,

Zhang

et al. 2024

ACS Omega

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Investigation of the mechanisms behind ochratoxin A‐induced cytotoxicity in human astrocytes and the protective effects of N‐acetylcysteine

Chu,

Chen,

Liang

2024

J of Applied Toxicology

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Ochratoxin A (OTA) is a type of mycotoxin commonly found in raw and processed foods. It is essential to be aware of this toxin, as it can harm your health if consumed in high quantities. OTA can induce toxic effects in various cell models. However, a more comprehensive understanding of the harmful effects of OTA on human astrocytes is required. This study evaluated OTA's neurotoxic effects on the Gibco® Human Astrocyte (GHA) cell line, its underlying mechanisms, and the antioxidant N‐acetylcysteine (NAC) ability to prevent them. OTA exposure within 5–30 μM has induced concentration‐dependent cytotoxicity. In the OTA‐treated cells, the levels of reactive oxygen species (ROS) were found to be significantly increased, while the glutathione (GSH) contents were found to decrease considerably. The western blotting of OTA‐treated cells has revealed increased Bax, cleaved caspase‐9/caspase‐3 protein levels, and increased Bax/Bcl‐2 ratio. In addition, exposure to OTA has resulted in the induction of antioxidant responses associated with the protein expressions of Nrf2, HO‐1, and NQO1. On the other hand, the pretreatment with NAC has partially alleviated the significant toxic effects of OTA. In conclusion, our findings suggest that oxidative stress and apoptosis are involved in the OTA‐induced cytotoxicity in GHA cells. NAC could act as a protective agent against OTA‐induced oxidative damage.

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HIF-1α is a “brake” in JNK-mediated activation of amyloid protein precursor and hyperphosphorylation of tau induced by T-2 toxin in BV2 cells

Zhao,

Valis,

Wang

et al. 2024

Mycotoxin Res

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Mycotoxins have the capacity of triggering neurodegenerative conditions like Alzheimer's disease (AD), which is marked by β-amyloid (Aβ) deposition and hyperphosphorylation of tau (P-tau). However, there is no evidence of an exact molecular mechanism to prove the above point. Due to the high toxicity and broad contamination of T-2 toxin, we assessed how T-2 toxin exposure alters amyloid precursor protein (APP) and P-tau formation in BV2 cells, and determined the underlying roles of HIF-1α and JNK3 signaling. The ndings revealed that T-2 toxin stimulated the expression of HIF-1α and hypoxic stress factors in addition to increasing the expression of APP and P-tau. Additionally, HIF-1α acted as a "brake" on the induction of APP and P-tau expression by negatively regulating these proteins. Notably, T-2 toxin activated JNK3 signaling, which broke this "brake" to promote the formation of APP and P-tau. Furthermore, the cytoskeleton was an essential target for T-2 toxin to exert cytotoxicity, and JNK3/HIF-1α participated in this damage. Collectively, when the T-2 toxin induces the production of APP and P-tau, JNK3 might interfere with HIF-1α's protective function. This study will provide clues for further research on the neurotoxicity of mycotoxins.

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Neurotoxicity of ochratoxin A: Molecular mechanisms and neurotherapeutic strategies

Cited by 6 publications

References 129 publications

Establishment of a Dual-Signal Enhanced Fluorescent Aptasensor for Highly Sensitive Detection of Ochratoxin A

Establishment of a Dual-Signal Enhanced Fluorescent Aptasensor for Highly Sensitive Detection of Ochratoxin A

Investigation of the mechanisms behind ochratoxin A‐induced cytotoxicity in human astrocytes and the protective effects of N‐acetylcysteine

HIF-1α is a “brake” in JNK-mediated activation of amyloid protein precursor and hyperphosphorylation of tau induced by T-2 toxin in BV2 cells

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