Pyrrolidine Dithiocarbamate (PDTC) Inhibits DON-Induced Mitochondrial Dysfunction and Apoptosis via the NF-κB/iNOS...

Area of Science:

• Biochemistry
• Cell Biology
• Toxicology

Background:

• Oxidative stress is implicated in cellular toxicity under normal and pathological conditions.
• Deoxynivalenol (DON) induces stress responses, mitochondrial dysfunction, and apoptosis via oxidative stress.
• The NF-κB pathway is a key signaling pathway in DON-induced toxicity and a potential therapeutic target.

Purpose of the Study:

• To investigate the protective effects of pyrrolidine dithiocarbamate (PDTC) against DON toxicity.
• To explore the role of the NF-κB pathway in DON-induced cellular damage.

Main Methods:

• Rat anterior pituitary GH3 cells were treated with DON and PDTC.
• NF-κB activation, oxidative stress markers, mitochondrial function, and apoptosis were assessed.
• Transmission electron microscopy (TEM) and cell apoptosis assays were utilized.
• iNOS expression and activity were measured.

Main Results:

• DON activated NF-κB transcription factors, increased oxidative stress, impaired mitochondrial function, and induced apoptosis.
• PDTC treatment prevented DON-induced mitochondrial dysfunction and apoptosis.
• PDTC inhibited the translocation of NF-κB p65 into the nucleus.
• PDTC suppressed DON-induced iNOS expression and activity.

Conclusions:

• PDTC exhibits protective effects against DON toxicity in GH3 cells.
• PDTC likely functions by inhibiting the NF-κB pathway and iNOS expression.
• These findings highlight PDTC as a potential agent for mitigating DON-induced cellular damage.