Assessing the Reducing Effect of Coenzyme Q10 on Carbendazim-Induced Testicular Tissue Dysfunction Through Modulation of miR-202-5p/Apoptosis Signaling in Rats: A Histological and Immunohistochemical Study

Widespread application of carbendazim (Carb) in agriculture and veterinary is a major environmental concern because of its residues that disrupt spermatogenesis. Recently, coenzyme Q10 (CoQ10) supplementation has demonstrated various health benefits due to its anti-apoptosis and anti-inflammatory nature. Thus, the present study aimed to investigate the possible mechanistic pathway of CoQ10 in Carb-induced reproductive dysfunction in male rats. Adult male Wistar rats were orally exposed to Carb (150 mg/kg) singly or in combination with CoQ10 (200 mg/kg). The rats received their treatments daily for 9 weeks. At the end of the work, the testis specimens were excised for histological (H & E staining), immunohistochemical, hormonal, and molecular (real-time quantitative PCR) assessments. The Carb group showed adverse testicular alterations confirmed by immunostaining and demonstrated a significant upregulation of Bax and Caspase-3 expression, while exhibiting a notable reduction in the immunopositivity of Bcl-2 protein within the testes of rats. Real-time PCR analysis revealed that Carb treatment decreased the expression of miR-202-5p with a concomitant decline in concentrations of testosterone and LH hormones. Conversely, in Carb-treated rats, co-treatment with CoQ10 restored the tissue architecture, hormonal disturbance, and declined apoptotic index to near control level. In addition, high expression of miR-202-5p was observed in the Carb + CoQ10 group, and testicular tissues returned to nearly normal histological architecture. We concluded that Carb causes adverse testicular alterations via miR-202-5p/apoptosis pathway, and CoQ10 may prove useful in combating Carb-induced adverse effects via its anti-apoptotic and gene regulatory effects.