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Related: About this forumDNA and RNA Adducts Formation from 3,4-Quinone Metabolites of Bisphenol F
There have been lots and lots of environmental and health concerns about resins containing bisphenol A, and as a result, increasingly it has been replaced with another compound bisphenol f. Both molecules contain planar hydroxyphenyl rings, but the substitution patterns differ.
Here's a paper about the consequence of this "improvement:"
DNA and RNA Adducts Formation from 3,4-Quinone Metabolites of Bisphenol F (Xiaoxiao Wang, Guodong Cao, Zhiyi Yang, Hongzhi Zhao, and Zongwei Cai Environmental Science & Technology Letters 2021 8 (11), 1009-1014)
Some commentary from the text:
...DNA adduct formation has been considered as predictor of cancer. (17) DNA adducts were detected in tissues of mice exposed to BPA. (18) The quinone metabolites of BPA were found to form a carcinogen-DNA adduct via Michael addition, (19) which might be the first critical step in BPA-induced cancer initiation. (20)...
Well, this substitution seems to have its own problems according to this diagram from the paper showing structures determined by LC/HRMS (Orbitrap QE Focus):
The caption:
Note that the compound in the center is not BPF, but its metabolite, but a quinone generated from it by oxidative metabolism. This quinone forms adducts with adenosine, guanosine, and cytosine, and their deoxy analogues, but not thymosine or uridine or their deoxyanalogues.
Oh well then...
Finding something different is not always finding something better, and as in the case with the misguided attempt to replace nuclear plants with so called "renewable energy," replacements can actually be worse than the original.
Whether BPF is worse, the same, or slightly better than BPA is not clear, but it seems to have some problematic properties.
Red Pest
(288 posts)The obvious and easy followup experiments will be to look at and compare the rates of mutagenesis when BPA or BPF is added to growth media for E. coli or yeast. Of course the E. coli and yeast might just not recognize the BPA and BPF and fail to transport it into the cells. The harder and longer studies will be to expose (feed) BPA and BPF to various model animals (Drosophila, mice, etc.) and look at the rates of mutagenesis or cancer.
One minor typo error in your commentary at the end - I think that you meant thymidine not thymosine
NNadir
(33,574 posts)...farts last night while jumping around on various topics, a kind of frenzy with a lot of stuff in my head while I caught up on some reading.
The worst was when I "calculated" the energy expenditure of refrigerators in Germany over in another forum.
Yes you are correct, I think; I'm not really a toxicologist, but have some good friends who are with whom I interact, but what you say seems reasonable. The follow up experiments will involve cell based assays including I assume proliferation assays, etc.
It probably would be simplest to use the same set of assays and experiments as were utilized with BPA, for example:
Bisphenol A inhibits proliferation and induces apoptosis in micromass cultures of rat embryonic midbrain cells through the JNK, CREB and p53 signaling pathways, Food and Chemical Toxicology, Volume 52, 2013, Pages 76-82
Alberto Izzotti, Stefano Kanitz, Francesco DAgostini, Anna Camoirano, Silvio De Flora, Formation of adducts by bisphenol A, an endocrine disruptor, in DNA in vitro and in liver and mammary tissue of mice, Mutation Research/Genetic Toxicology and Environmental Mutagenesis, Volume 679, Issues 12, 2009, Pages 28-32,
Lim et al., Biomolecules & Therapeutics 2017; 25(5): 545-552 https://doi.org/10.4062/biomolther.2017.148 Low-Dose Bisphenol A Increases Bile Duct Proliferation in Juvenile Rats: A Possible Evidence for Risk of Liver Cancer in the Exposed Population?
These are just a few that popped up. There is, I think, no reason to reinvent the wheel. I could be wrong, but probably that's the case.
Thanks for your comments.