A serious adverse effect of the broad-spectrum anticancer drug cyclophosphamide is haemorrhagic cystitis. The physiological properties of hydrogen sulfide, an endogenous gas transmitter, include neuromodulation, anti-oxidation, and anti-inflammation. We examined the effects of NaHS pretreatment on bladder dysfunction in CYP-treated rats in this study. Before cytometry, male Wistar rats underwent intraperitoneal pretreatment with NaHS or vehicle once daily for seven days, and CYP or saline was given intraperitoneally for two days. The bladder tissues were collected for haematoxylin and eosin staining after cytometry. A subcutaneous injection of capsaicin, which has the ability to desensitize CAP-sensitive afferent nerves, was given to some rats four days before cystometry. In comparison to the saline-treated control group, CYP increased the number of non-voiding contractions and reduced intercontraction intervals as well as bladder compliance. The CYP-induced changes were improved by NaHS pretreatment in a dose-dependent manner. While NaHS had no effect on these CYP-induced changes, CYP raised histological scores for neutrophil infiltration, haemorrhage, and oedema in bladder tissues. CAP had a tendency to prevent ICI-induced changes caused by CYP. NaHS-induced improvement in CYP-induced changes in urodynamic parameters were not detected in CAP-treated rats. These discoveries recommend that NaHS pretreatment forestalled bladder brokenness in CYP-treated rodents by stifling CAP-delicate bladder afferent nerves, however not by smothering bladder aggravation. As a result, H2S is a fresh possibility as a preventative medication for HC-induced bladder dysfunction, a CYP chemotherapy side effect. Men are most likely to die from prostate cancer. Prostate carcinogenesis has been linked to inflammation and inducible nitric oxide synthase overexpression. The hypothesis that nitric oxide NO has pro-tumorigenic effects on prostate cells at physiologically relevant levels and contributes to carcinogenesis was the focus of our investigation. We investigated how cell proliferation and the activation of DNA damage repair pathways were affected when normal immortalized prostate cells were acutely exposed to NO. In addition, we investigated the long-term effects of chronic NO exposure on the migration, invasion, and transformational characteristics of RWPE-1 cells. As evidenced by H2AX foci and p53 activation, a damage repair protein, our findings indicate that NO damages DNA. Adaptation to NO overtime increases resistance to chemotherapy, acquires anchorage-independent growth, and increases migration and invasion potential.PC3 and DU145 prostate cancer cells, which were exposed to NO for an extended period of time, displayed an increase in cell migration, colony formation, and chemotherapeutic resistance

Home Page Link: https://digestive-diseases.imedpub.com

With Regards,
Sara Giselle
Associate Managing Editor
Global  Journal of Digestive Diseases