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

Aims: The aim of this study was to investigate the potential antioxidant, anti-inflammatory, and sperm functionpreserving 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 degrees 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-alpha, IL-1 beta, IL-6, NFkB, HIF-1 alpha, and VCAM-1. In addition, acetate treatment alleviated T/D-induced decline in sperm quality (count, motility, viability, and normal morphology) and testicular 3 beta-HSD, 17 beta-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.