Aflatoxin B1-Induced Testosterone Biosynthesis Disorder via the ROS/AMPK Signaling Pathway in Male Mice.
J Agric Food Chem
; 72(11): 5955-5965, 2024 Mar 20.
Article
in En
| MEDLINE
| ID: mdl-38451160
ABSTRACT
The worldwide prevalence of Aflatoxin B1 (AFB1), which contaminates feedstock and food, is on the rise. AFB1 inhibits testosterone (T) biosynthesis, but the mechanism is not yet clear. By establishing in vivo and in vitro models, this study found the number of Leydig cells (LCs), T content, and the expression of T biosynthesis key enzymes were suppressed after AFB1 treatment. AFB1 exposure also increased reactive oxygen species (ROS) and promoted mitochondrial injury and mitochondrial pathway apoptosis. Moreover, the AMPK signaling pathway was activated, and using an AMPK inhibitor relieved apoptosis and the suppressed T biosynthesis key enzymes of LCs caused by AFB1 through regulating downstream p53 and Nur77. Additionally, adding ROS intervention could inhibit AMPK activation and alleviate the decreased T content caused by AFB1. In summary, AFB1 promotes the apoptosis of LCs and inhibits T biosynthesis key enzyme expression via activating the ROS/AMPK signaling pathway, which eventually leads to T synthesis disorder.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Aflatoxin B1
/
AMP-Activated Protein Kinases
Limits:
Animals
Language:
En
Journal:
J Agric Food Chem
/
J. agric. Food chem
/
Journal of agricultural and food chemistry
Year:
2024
Document type:
Article
Affiliation country:
Country of publication: