Chronic exposure of zearalenone inhibits antioxidant defense and results in aging-related defects associated with DAF-16/FOXO in Caenorhabditis elegans

Acrolein Promotes Aging and Oxidative Stress via the Stress Response Factor DAF-16/FOXO in Caenorhabditis elegans

“…After 100 µM ACR exposure, the expression levels of daf-16 , ctl-1 , and ctl-2 were significantly downregulated by 25.5%, 15.3%, and 28.3%, respectively ( p < 0.05). The downregulation of these gene expressions was similar to the previous study that chronic exposure to the high concentration of zearalenone increased the ROS level and decreased the proportion of DAF-16::GFP in the nucleus, while decreasing the expression levels of ctl-1 and ctl-2 genes [ 41 ]. In summary, it could be inferred that excessive ROS caused by excessive exposure to toxins disrupted antioxidant defense systems and further promoted the production of ROS, as well as resulted in aging acceleration.…”

“…It was consistent with the findings that exposure to pharmaceuticals which induce oxidative stress, such as H 2 O 2 , N , N ′ bis-(2-mercaptoethyl) isophthalamide, juglone, and so on, could lead to the DAF-16 nuclear translocation [ 38 , 39 , 40 ]. It is worth noting that, with high exposure to ACR, the percentages of DAF-16 nuclear localization were decreased significantly (50 μM, 43.8%; 100 μM, 16.0%) ( p < 0.01) as compared to those treated with 25 μM of ACR, and this is similar to what was found in chronic exposure of zearalenone [ 41 ]. The previous experimental results of this paper had found that, when exposing to 12.5 μM of ACR, the locomotion behavior, e.g., head thrashes, was slightly affected, indicating that low dose exposure hardly affected the normal physiological functions of worms, but activated their own immune defense system.…”

Zearalenone Induces Dopaminergic Neurodegeneration via DRP-1-Involved Mitochondrial Fragmentation and Apoptosis in a Caenorhabditis elegans Parkinson’s Disease Model

“…The potential neurotoxicity of ZEN such as locomotion defects has been suggested in our previous study . Herein, we investigated the damage on specific neurons associated with neurodegenerative disease and found that the PD-related dopaminergic neurons were injured upon the ZEN exposure (Figure A,C).…”

“…Our previous study has shown that 1.25, 10, and 50 μM ZEN significantly decreased the frequency of locomotive behaviors including body bends and head thrashes in C. elegans . Since PD is associated with dopamine-involved locomotive defects and motor symptoms, we used 1.25, 10, and 50 μM concentrations of ZEN exposure in the following dopaminergic neurodegeneration and dopamine-dependent behavior assays.…”

“…Studies have shown that ZEN affected mitochondrial metabolism and increased cell apoptosis to cause different toxic effects . A recent study has demonstrated that ZEN could induce aging-related defects and accelerate aging in vivo . However, the relationship between ZEN exposure and neurodegenerative disease, such as PD, is still largely unknown in vivo .…”