Sodium acetate prevents testicular damage in Wistar rats subjected to testicular ischaemia/reperfusion injury.

Exp Mol Pathol

Department of Physiology, Ladoke Akintola University of Technology, Ogbomoso, Oyo State, Nigeria; Reproductive Biology and Toxicology Research Laboratory, Oasis of Grace Hospital, Osogbo, Osun State, Nigeria. Electronic address:

Published: June 2024

AI Article Synopsis

  • The study aimed to explore how sodium acetate (ACE), an HDAC inhibitor, could protect sperm function and reduce inflammation and oxidative stress in a rat model of testicular torsion/detorsion (T/D).
  • Wistar rats were subjected to T/D with one group receiving ACE treatment before detorsion, while a control group was given distilled water, followed by analysis of their testes after 72 hours.
  • Results indicated that ACE treatment reduced various harmful biochemical markers and improved sperm quality and testicular health, suggesting that sodium acetate could help preserve fertility during post-ischaemic conditions.

Article Abstract

Aims: The aim of this study was to investigate the potential antioxidant, anti-inflammatory, and sperm function-preserving properties of sodium acetate (ACE), a histone deacetylase (HDAC) inhibitor, in a rat model of testicular torsion/detorsion (T/D).

Main Methods: Littermate Wistar rats of identical weight were subjected to sham surgery or testicular T/D by rotating the left testis at 720° around its axis along the spermatic cord clockwise and fixing it in this position for two and a half hours. 1 h before detorsion, T/D + ACE-treated rats were treated with ACE (200 mg/kg/day, per os) while T/D rats were vehicle-treated by administering 0.5 mL of distilled water. After 72 h, animals were euthanized, and the left testes were harvested for bio-molecular and histological analysis.

Key Findings: Acetate administration attenuated T/D-induced rises in serum and testicular HDAC and testicular xanthine oxidase, uric acid, MDA, GSSG, MPO, TNF-α, IL-1β, IL-6, NFkB, HIF-1α, and VCAM-1. In addition, acetate treatment alleviated T/D-induced decline in sperm quality (count, motility, viability, and normal morphology) and testicular 3β-HSD, 17β-HSD, testosterone, GSH, GSH/GSSG, SOD, catalase, GPx, GST, Nrf2, and HO-1. Furthermore, acetate prevented T/D-distorted testicular histoarchitecture and spermatogenic germ cell loss.

Significance: Sodium acetate during the post-ischaemic phase of testicular T/D may be beneficial in preventing I/R injury and maintaining fertility.

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Source
http://dx.doi.org/10.1016/j.yexmp.2024.104901DOI Listing

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