Environmentally relevant level of aflatoxin B1 and the role of (non)oxidative immuno-/neurodysregulation and toxicity

Toxicology ◽  
2021 ◽  
pp. 165-179
Author(s):  
Jalil Mehrzad
Keyword(s):  
Author(s):  
Khalid M. Mahrose ◽  
Izabela Michalak ◽  
Mohamed Farghly ◽  
Abdelmotaleb Elokil ◽  
Runxiang Zhang ◽  
...  
Keyword(s):  

2010 ◽  
Vol 59 (3) ◽  
pp. 393-406 ◽  
Author(s):  
Inés Nicolás-Vázquez ◽  
Abraham Méndez-Albores ◽  
Ernesto Moreno-Martínez ◽  
René Miranda ◽  
Miguel Castro

2018 ◽  
Vol 13 (1) ◽  
pp. 60 ◽  
Author(s):  
HasnaaA Radwan ◽  
IbrahimM Farag ◽  
HanaaM Roshdy ◽  
InasS Ghaly ◽  
SherifaH Salah ◽  
...  

2018 ◽  
Vol 156 ◽  
pp. 177-185 ◽  
Author(s):  
Haoran Jiang ◽  
Jun Wu ◽  
Feiyong Zhang ◽  
Jikai Wen ◽  
Jun Jiang ◽  
...  

Toxicology ◽  
2001 ◽  
Vol 162 (3) ◽  
pp. 209-218 ◽  
Author(s):  
M.H. Salem ◽  
K.I. Kamel ◽  
M.I. Yousef ◽  
G.A. Hassan ◽  
F.D. EL-Nouty

2014 ◽  
Vol 2014 ◽  
pp. 1-13 ◽  
Author(s):  
Yi-Xiao Liu ◽  
Xi-Dai Long ◽  
Zhi-Feng Xi ◽  
Yun Ma ◽  
Xiao-Ying Huang ◽  
...  

MicroRNA-24 (miR-24) may be involved in neoplastic process; however, the role of this microRNA in the hepatocellular carcinoma (HCC) related to aflatoxin B1 (AFB1) has not been well elaborated. Here, we tested miR-24 expression in 207 pathology-diagnosed HCC cases from high AFB1 exposure areas and HCC cells. We found that miR-24 was upregulated in HCC tumor tissues relative to adjacent noncancerous tissue samples, and that the high expression of miR-24 was significantly correlated with larger tumor size, higher microvessel density, and tumor dedifferentiation. Additionally, this microRNA overexpression modified the recurrence-free survival (relative hazard ratio [HR], 4.75; 95% confidence interval [CI], 2.66–8.47) and overall survival (HR=3.58, 95% CI = 2.34–5.46) of HCC patients. Furthermore, we observed some evidence of joint effects between miR-24 and AFB1 exposure on HCC prognosis. Functionally, miR-24 overexpression progressed tumor cells proliferation, inhibited cell apoptosis, and developed the formation of AFB1-DNA adducts. These results indicate for the first time that miR-24 may modify AFB1-related HCC prognosis and tumorigenesis.


2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Qingqiang Xu ◽  
Wenwen Shi ◽  
Pan Lv ◽  
Wenqi Meng ◽  
Guanchao Mao ◽  
...  

AbstractAflatoxin B1 (AFB1) is a potent hepatocarcinogen in humans and exposure to AFB1 is known to cause both acute and chronic hepatocellular injury. As the liver is known to be the main target organ of aflatoxin, it is important to identify the key molecules that participate in AFB1-induced hepatotoxicity and to investigate their underlying mechanisms. In this study, the critical role of caveolin-1 in AFB1-induced hepatic cell apoptosis was examined. We found a decrease in cell viability and an increase in oxidation and apoptosis in human hepatocyte L02 cells after AFB1 exposure. In addition, the intracellular expression of caveolin-1 was increased in response to AFB1 treatment. Downregulation of caveolin-1 significantly alleviated AFB1-induced apoptosis and decreased cell viability, whereas overexpression of caveolin-1 reversed these effects. Further functional analysis showed that caveolin-1 participates in AFB1-induced oxidative stress through its interaction with Nrf2, leading to the downregulation of cellular antioxidant enzymes and the promotion of oxidative stress-induced apoptosis. In addition, caveolin-1 was found to regulate AFB1-induced autophagy. This finding was supported by the effect that caveolin-1 deficiency promoted autophagy after AFB1 treatment, leading to the inhibition of apoptosis, whereas overexpression of caveolin-1 inhibited autophagy and accelerated apoptosis. Interestingly, further investigation showed that caveolin-1 participates in AFB1-induced autophagy by regulating the EGFR/PI3K-AKT/mTOR signaling pathway. Taken together, our data reveal that caveolin-1 plays a crucial role in AFB1-induced hepatic cell apoptosis via the regulation of oxidation and autophagy, which provides a potential target for the development of novel treatments to combat AFB1 hepatotoxicity.


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