P-008 Acetate ameliorates doxorubicin-induced testicular toxicity by modulating Nrf2/NFkB pathway and apoptotic signaling

Abstract Study question Will acetate treatment ameliorate doxorubicin-induced testicular toxicity when used concomitantly? Summary answer Acetate ameliorated by modulating Nrf2/NFkB and apoptotic signaling. What is known already Doxorubicin an antineoplastic agent that effective in the management of several forms cancers. However, a major limitation this drug its toxicity. Studies have revealed doxorubicin impairs male fertility inducing injury via downregulation Nrf2 upregulation NFkB On other hand, upregulates downregulates Yet, no study has reported impact on design, size, duration This prospective experimental using animal model. Thirty two sexually mature litter-mate Wistar rats comparable weight were for study. The lasted 8 weeks. Participants/materials, setting, methods Animals acclimatized weeks, then randomized into four groups (n = 8). control received 0.5mL distilled water as vehicle p.o 14 days, acetate-treated 200 mg/kg/day doxorubicin-treated 7 mg/kg i.p day 8, while + doxorubicin-treated. doses drugs Human Equivalent rats. Main results role chance rise activities gamma glutamyl transferase, lactate dehydrogenase activity, levels. Also, decline superoxide dismutase catalase, glutathione concentrations. also alleviated MPO activities, malondialdehyde, TNF-α, IL-1β, NF-kB More so, reduction spermatogenic indices sperm quality, circulatory levels FSH, LH, testosterone, concentrations 3β-HSD, 17β-HSD, testosterone. These events associated with dampening Bax, caspase 3 9 BCl-2 acetate. Limitations, reasons caution was conducted rat model; therefore present should be extrapolated to human caution. Clinical trials are recommended validate these findings. Wider implications findings demonstrated ameliorative effect provide substantive evidence possible protective Trial registration number Not applicable