Research progress on reactive oxygen species production mechanisms in tumor sonodynamic therapy

In recent years,because of the growing desire to improve the noninvasiveness and safety of tumor treatments,sonodynamic therapy has gradually become a popular research topic.However,due to the complexity of the therapeutic process,the relevant mechanisms have not yet been fully elucidated.One of the widely accepted possibilities involves the effect of reactive oxygen species.In this review,the mechanism of reactive oxygen species production by sonodynamic therapy(SDT)and ways to enhance the sonodynamic production of reactive oxygen species are reviewed.Then,the clinical application and limitations of SDT are discussed.In conclusion,current research on sonodynamic therapy should focus on the development of sonosensitizers that efficiently produce active oxygen,exhibit biological safety,and promote the clinical transformation of sonodynamic therapy.

Bisphenol A induces testicular oxidative stress in mice leading to ferroptosis

Bisphenol A is a common environmental factor and endocrine disruptor that exerts a negative impact on male reproductive ability.By exploring bisphenol A-induced testicular cell death using the Institute of Cancer Research(ICR)mouse model,we found that a ferroptosis phenomenon may exist.Mice were divided into six groups and administered different doses of bisphenol A via intragastric gavage once daily for 45 consecutive days.Serum was then collected to determine the levels of superoxide dismutase and malondialdehyde.Epididymal sperm was also collected for semen analysis,and testicular tissue was collected for ferritin content determination,electron microscope observation of mitochondrial morphology,immunohistochemistry,real-time quantitative polymerase chain reaction,and western blot analysis.Exposure to bisphenol A was found to decrease sperm quality and cause oxidative damage,iron accumulation,and mitochondrial damage in the testes of mice.In addition,bisphenol A was confirmed to affect the expression of the ferroptosis-related genes,glutathione peroxidase 4(GPX4),ferritin heavy chain 1(FTH1),cyclooxygenase 2(COX2),and acyl-CoA synthetase 4(ACSL4)in mouse testicular tissues.Accordingly,we speculate that bisphenol A induces oxidative stress,which leads to the ferroptosis of testicular cells.Overall,the inhibition of ferroptosis may be a potential strategy to reduce male reproductive toxicity caused by bisphenol A.