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

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. Our findings suggest that oxidative stress and apoptosis are involved in the ochratoxin A (OTA)‐induced cytotoxicity in Gibco® Human Astrocyte (GHA) cells. N‐acetylcysteine (NAC) could act as a protective agent against OTA‐induced oxidative damage. This study has reported that NAC could alleviate the OTA‐induced cytotoxicity in GHA cells for the first time. It has also elucidated some of its mechanisms, providing a new perspective for treating OTA‐induced neurotoxicity.