Caffeic acid protects against DNA damage, oxidative and inflammatory mediated toxicities, and upregulated caspases activation in the hepatorenal system of rats treated with aflatoxin B1

Toxicon ◽  
2022 ◽  
Vol 207 ◽  
pp. 1-12
Solomon E. Owumi ◽  
Chioma E. Irozuru ◽  
Uche O. Arunsi ◽  
Adegboyega K. Oyelere
2018 ◽  
Vol 26 ◽  
pp. 42-48 ◽  
Grace A. Odongo ◽  
Nina Schlotz ◽  
Susanne Baldermann ◽  
Susanne Neugart ◽  
Benard Ngwene ◽  

Franziska Ferk ◽  
Karl Speer ◽  
Miroslav Mišík ◽  
Armen Nersesyan ◽  
Siegfried Knasmüller

2020 ◽  
Vol 10 (11) ◽  
pp. 3929-3947
Nick St. John ◽  
Julian Freedland ◽  
Henri Baldino ◽  
Francis Doyle ◽  
Cinzia Cera ◽  

Exposure to the mycotoxin aflatoxin B1 (AFB1) strongly correlates with hepatocellular carcinoma (HCC). P450 enzymes convert AFB1 into a highly reactive epoxide that forms unstable 8,9-dihydro-8-(N7-guanyl)-9-hydroxyaflatoxin B1 (AFB1-N7-Gua) DNA adducts, which convert to stable mutagenic AFB1 formamidopyrimidine (FAPY) DNA adducts. In CYP1A2-expressing budding yeast, AFB1 is a weak mutagen but a potent recombinagen. However, few genes have been identified that confer AFB1 resistance. Here, we profiled the yeast genome for AFB1 resistance. We introduced the human CYP1A2 into ∼90% of the diploid deletion library, and pooled samples from CYP1A2-expressing libraries and the original library were exposed to 50 μM AFB1 for 20 hs. By using next generation sequencing (NGS) to count molecular barcodes, we initially identified 86 genes from the CYP1A2-expressing libraries, of which 79 were confirmed to confer AFB1 resistance. While functionally diverse genes, including those that function in proteolysis, actin reorganization, and tRNA modification, were identified, those that function in postreplication DNA repair and encode proteins that bind to DNA damage were over-represented, compared to the yeast genome, at large. DNA metabolism genes also included those functioning in checkpoint recovery and replication fork maintenance, emphasizing the potency of the mycotoxin to trigger replication stress. Among genes involved in postreplication repair, we observed that CSM2, a member of the CSM2(SHU) complex, functioned in AFB1-associated sister chromatid recombination while suppressing AFB1-associated mutations. These studies thus broaden the number of AFB1 resistance genes and have elucidated a mechanism of error-free bypass of AFB1-associated DNA adducts.

Toxins ◽  
2016 ◽  
Vol 9 (1) ◽  
pp. 9 ◽  
Wei-Hong Feng ◽  
Kathy Xue ◽  
Lili Tang ◽  
Phillip Williams ◽  
Jia-Sheng Wang

2013 ◽  
Vol 31 (8) ◽  
pp. 692-697 ◽  
Mustafa Akçam ◽  
Reha Artan ◽  
Aygen Yilmaz ◽  
Sebahat Ozdem ◽  
Tekinalp Gelen ◽  

2015 ◽  
Vol 83 ◽  
pp. 54-60 ◽  
J. Zhang ◽  
N. Zheng ◽  
J. Liu ◽  
F.D. Li ◽  
S.L. Li ◽  

Sign in / Sign up

Export Citation Format

Share Document