Deferasirox protects against hydrogen peroxide-induced cell apoptosis by inhibiting ubiquitination and degradation of p21WAF1/CIP1

Miao, Junhua; Xu, Mutao; Kuang, Yuhuan; Pan, Shuhong; Hou, Jianyuan; Cao, Pengxiu; Duan, Xingguang; Chang, Yan‐Zhong; Habelhah, Hasem; Zhou, Nan; Tan, Karsoon; Fan, Yumei

doi:10.1016/j.bbrc.2020.01.155

Cited by 2 publications

(2 citation statements)

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“…As Bip is involved in protein folding, this may also explain why after DFX stimulation of testicular Bip content we recorded an improved histone to protamine exchange in late differentiating germ cells, a process that requires marked protamine synthesis and ER maturation events [50]. We should point out that our observations contradict earlier reports, which have shown that DFX decreases cellular apoptosis via the 13 Oxidative Medicine and Cellular Longevity inhibition of P-JNK signaling and mitochondrial-dependent cell death [20,51].…”

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confidence: 72%

“…Two molecules of DFX can form a complex with ferric iron (Fe-[DFX]), to reduce iron overload in the body and prevent further iron deposition [18]. In this respect, Miao et al (2020) demonstrated that DFX can prevent the Fenton reaction and the associated overproduction of reactive oxygen species (ROS) [20]. Our approach to investigate the effect of DFX in the VCL rat model is based on previous studies showing excess iron in the male reproductive tissue of infertile individuals and, in particular, VCL patients [9][10][11].…”

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confidence: 99%

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Deferasirox, an Iron‐Chelating Agent, Improves Testicular Morphometric and Sperm Functional Parameters in a Rat Model of Varicocele

Rahmani

Tavalaee

Hosseini

et al. 2021

Oxidative Medicine and Cellular Longevity

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Varicocele is characterized by testicular dysfunction that originates from hyperthermia and hypoxia, leading to defects in testicular tissue and altered spermatozoa structure and function. The varicocele testis is characterized by the presence of intracellular iron deposits that contribute to the associated oxidative stress. Therefore, we tested the hypothesis that administration of an iron-chelating agent, such as deferasirox (DFX), could potentially mitigate the consequences of varicocele on testicular tissue and spermatozoa. Using a well-established rat model of varicocele (VCL), we show that treatment with DFX partially improved the structure and function of the testis and spermatozoa. In particular, sperm motility was markedly restored whereas abnormal sperm morphology was only partially improved. No significant improvement in sperm count was observed that could be associated with the proapoptotic response observed following iron chelation treatment. No reduction in oxidative damage to spermatozoa was observed since lipid peroxidation and DNA integrity were not modified. This was suggested to be a result of increased oxidative stress. Finally, we also saw no indication of attenuation of the endoplasmic reticulum/unfolded protein (ER/UPR) stress response that we recently found associated with the VCL testis in rats.

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confidence: 72%