Bisphenol F

Bisphenol F is an orally active endocrine disruptor. Bisphenol F promotes ROS generation, upregulates p-AKT/p-GSK3β, and induces Apoptosis. Bisphenol F interferes with glucose metabolism, affects neurodevelopment and reproductive function. Bisphenol F reduces social novelty preference in mouse offspring. Bisphenol F can be used in bone, blood, and fat-related studies. Bisphenol F is used as a substitute for Bisphenol A (HY-18260)^{[1][2][3][4][5][6][7][8]}. In Vitro:Bisphenol F (0-100 µM; 24 h) significantly reduces cell viability, induces oxidative stress (increased ROS, decreased antioxidant enzyme activity) in human granulosa KGN cells^[1].
Bisphenol F (0.1-10 µM; 24 h) significantly inhibits proliferation via apoptosis induction in human osteoblasts, reducing alkaline phosphatase activity and mineralization capacity^[2].
Bisphenol F (0.1-500 µg/mL; 1-24 h) induces ROS in human red blood cells^[3].
Bisphenol F (10 nM-1 µM; 12 d) inhibits late differentiation gene expression and reduces lipid accumulation in 3T3-L1 preadipocytes^[4].
In Vivo:Bisphenol F (administered to pregnant female mice; 40-4000 μg/kg; p.o. via drinking water; from gestation to F1 generation 3 weeks old) induces testicular injury, decreases testosterone levels, and impairs sperm quality in F1 generation male Kunming mice^[6].
Bisphenol F (100 µg/kg; i.g.; every other day; 5 months) improves glucose tolerance, insulin sensitivity, inhibits hepatic gluconeogenesis, and increases TCA cycle metabolites in high-fat diet-fed mice^[7].
Bisphenol F (50 µg/kg; s.c.; daily) decreases social novelty preference in C57BL/6J mouse offspring without affecting anxiety/depression-like behaviors^[8].