Ochratoxin A (OTA) causes intestinal aging damage through the NLRP3 signaling pathway mediated by calcium overload and oxidative stress

© 2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature..

Ochratoxin A (OTA) is a widespread environmental toxin that poses a serious threat to human and animal health. OTA has been shown to cause cellular and tissue damage and is a global public health problem. However, the effects of OTA on gastrointestinal aging have not been reported. The aim of this study was to investigate the effects of OTA on intestinal aging in vitro and in vivo. In vitro experiments showed that OTA induced cellular inflammation through calcium overload and oxidative stress, significantly up-regulated the expression of P16, P21, and P53 proteins, markedly increased senescence-associated β-galactosidase activity (SA-β-gal) positive cells, and obviously decreased the expression of proliferating cell nuclear antigen (PCNA) proteins, which led to intestinal cell senescence. Meanwhile, we found that treatment with β-carotene ameliorated OTA-induced intestinal cell senescence. Consistent with the results of the in vitro experiments, in vivo studies showed that the intestinal aging of mice fed OTA was significantly higher than that of the control group. In conclusion, OTA may induce intestinal aging through calcium overload, oxidative stress and inflammation. This study lays a foundation for further research on the toxicological effects of OTA.

Medienart:

E-Artikel

Erscheinungsjahr:

2024

Erschienen:

2024

Enthalten in:

Zur Gesamtaufnahme - year:2024

Enthalten in:

Environmental science and pollution research international - (2024) vom: 25. März

Sprache:

Englisch

Beteiligte Personen:

Wang, Guoxia [VerfasserIn]
Zhang, Shuai [VerfasserIn]
Lan, Hainan [VerfasserIn]
Zheng, Xin [VerfasserIn]

Links:

Volltext

Themen:

β-carotene
IEC6 cells
Inflammation, Oxidative stress
Intestinal aging
Journal Article
Ochratoxin A

Anmerkungen:

Date Revised 25.03.2024

published: Print-Electronic

Citation Status Publisher

doi:

10.1007/s11356-024-32696-1

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM370162870