Dietary Ochratoxin A Contamination Modulates Oxidative Stress, Inflammation Processes and Causes Fibrosis in in vitro and in vivo Lung Models

Abstract

Background: The prevalence of aging-related diseases has increased significantly and this imposes a burden on both families and society. The lung is one of the few internal organs that is continuously exposed to the external environment, and lung aging is associated with a number of lung diseases. Ochratoxin A (OTA) is a toxin that is widely present in food and the environment but an effect for OTA on lung aging has not been reported. Methods: Using both cultured lung cell and in vivo model systems, we studied the effect of OTA on lung cell senescence using flow cytometry, indirect immunofluorescence, western blotting, and immunohistochemistry. Results: Results obtained showed that OTA caused significant lung cell senescence in cultured cells. Furthermore, using in vivo models, results showed that OTA caused lung aging and aging fibrosis. Mechanistic analysis showed that OTA upregulated the levels of inflammation and oxidative stress, and that this may be the molecular basis of OTA-induced lung aging. Conclusions: Taken together, these findings indicate that OTA causes significant aging damage to the lung, which lays an important foundation for the prevention and treatment of lung aging.

Keywords

• ochratoxin a
• lung aging
• lung fibrosis
• inflammation
• oxidative stress