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Ferroptosis contributes to cyclophosphamide-induced hemorrhagic cystitis
Zhimin Mao1, Kun Zhong1, Xiaojun Liu1
1Institute of Reproductive Medicine, Medical School, Nantong University, Nantong, Jiangsu, China.
Chemico-Biological Interactions
|September 10, 2023
Summary
Cyclophosphamide (CYP) causes bladder toxicity by inducing ferroptosis, a cell death pathway. Inhibiting ferroptosis with dexrazoxane (DXZ) protected against this damage, suggesting new therapeutic strategies for chemotherapy side effects.
Area of Science:
- Oncology
- Toxicology
- Molecular Biology
Background:
- Cyclophosphamide (CYP) is a widely used chemotherapy agent.
- CYP's clinical use is limited by severe bladder toxicity (cystitis).
- Acrolein (ACR), a CYP metabolite, is implicated in cystitis via lipid peroxidation and ferroptosis.
Purpose of the Study:
- To investigate if ferroptosis is a key mechanism in CYP-induced cystitis.
- To evaluate the therapeutic potential of targeting ferroptosis for bladder protection.
Main Methods:
- Mice were injected with CYP to induce cystitis.
- Bladder tissues were analyzed for oxidative stress, inflammation, cell injury, and ferroptosis markers (FPN1, ACSL4, SLC7A11, GPX4).
- Mice were treated with the ferroptosis inhibitor dexrazoxane (DXZ) post-CYP injection.
Main Results:
- CYP injection caused significant bladder hemorrhage, edema, oxidation, inflammation, and cell injury.
- These pathological changes correlated with altered expression of key ferroptosis markers.
- DXZ treatment ameliorated ferroptosis and prevented CYP-induced bladder damage.
Conclusions:
- Ferroptosis is a critical molecular mechanism driving cyclophosphamide-induced cystitis.
- Targeting ferroptosis pathways represents a promising therapeutic strategy to mitigate CYP-induced bladder toxicity.
