Poster Session II. - J: Theoretical and Translational Medicine
Dr. Borsodi Kinga, PhD
IWA1O0
Institute of Translational Medicine
+36205740715
kingaborsodi@gmail.com
The Role of Dual Oxidase 1 Enzyme in Cyclophosphamide-Induced Cystitis in Mice
Kinga Borsodi1, Ádám Lénárt2, Helga Balla1, Péter József Molnár2, Kamilla Makk3, Gábor Sirokmány4, Miklós Geiszt4, Zoltán Benyó3
1: Institute of Translational Medicine
2: Department of Urology, Semmelweis University, Budapest
3: Institute of Translational Medicine, Semmelweis University, Budapest
4: Department of Physiology, Semmelweis University, Budapest
Poszter
Poster Session II. - J: Theoretical and Translational Medicine
English
Theoretical and Translational Medicine
Introduction: Overactive bladder (OAB) syndrome is commonly associated with oxidative stress and elevated hydrogen peroxide (H₂O₂). The cyclophosphamide (CYP)-induced cystitis mouse effectively mimics the symptoms of OAB. The dual oxidase 1 (DUOX1) enzyme is abundantly expressed in the urinary bladder, and it is often upregulated in conditions linked to oxidative stress. This suggests a potential role for DUOX1 enzyme in the pathomechanism of OAB.
Aims: This study aimed to investigate the role of DUOX1 enzyme in the CYP-induced mouse model of OAB.
Methods: We conducted in vivo cystometric measurements and void spot assays (VSA) on 90-120-day-old female DUOX1 wild type (WT) and DUOX1 knockout (KO) mice. OAB symptoms were induced via intraperitoneal CYP-administration (200 mg/kg). Bladders were filled transurethrally with physiological saline solution via a catheter before and 24 hours after CYP-treatment. The following parameters were assessed: voiding contraction (VC) frequency and amplitude, bladder capacity at first VC, bladder capacity at first voiding, average capacity before VC. In case of VSA, we investigated the size, number and location of void spots on filter paper before and after CYP-treatment.
Result: CYP-treatment increased bladder contractile activity in WT mice. We observed a higher VC frequency, reduced bladder capacity at first VC and first voiding and decreased average bladder capacity before VC. The amplitude of VCs remained unchanged. VSA measurements supported our findings, showing smaller and more frequent urine spots after CYP-treatment in WT mice. In contrast, CYP-treatment in DUOX1-KO mice did not induce bladder hyperactivity. All cystometric and VSA parameters were similar to those measured before the CYP-treatment.
Conclusion: CYP-treatment resulted in OAB-like symptoms in DUOX1-WT mice, as demonstrated by both cystometric parameters and VSA parameters. However, the absence of DUOX1 enzyme prevented the development of bladder hyperactivity following CYP-treatment. These findings suggest that DUOX1 plays a critical role in the pathophysiology of CYP-induced OAB Thus, DUOX1 enzyme serves as a potential target and we are planning further research to better understand its role in bladder dysfunction.
Funding: K-135683, K-139230, PD-143327; and Predoctoral Fellowship 2024/25, TKP2021-EGA-25 from the Hungarian NRDIO
Semmelweis University
Zoltán Benyó, MD, DSc
I do not give consent to the publication of my abstract on the website of the congress.
after finishing doctoral studies with absolutorium (PhD)
Szabad
elfogadva
poszter
nem rendelkezett róla
4811
18:36
18:42