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Taken together, these findings indicate that NSBSO treatment leads to GSH depletion and inhibition of GSH biosynthesis, which in turn inhibits GPX4 activity and resulting ferroptosis in 4T1 cells
This, in turn, protects the liver from the harmful effects of toxic compounds and promotes their neutralization.Exposure to high levels of toxins exhausts glutathione faster than the body can produce or absorb from nutrition
In addition, the better effects of LCLN or QTLN than their conventional form may contribute to the enhanced cell permeability and availability 19,118 , which confirmed our findings
