Elaidic acid induces testicular oxidative stress, inflammation, Wnt/β-catenin disruption and abnormalities in steroidogenesis, spermatogenesis and histo-architecture in Sprague Dawley rats.

Elaidic Acid (EA) is a major trans-fatty acid that has garnered significant attention due to its potential role in inducing systemic toxicity. The current investigation was conducted to assess the toxic effects of EA (50 mg/kg, 100 mg/kg, and 150 mg/kg) on testicular tissues of Sprague Dawley rats. EA intoxication disrupted Wnt/β-catenin via downregulating the expression of WNT3A and TCF7L2 while upregulating the expression of AXIN1 and GSK-3β. The activities of antioxidant enzymes were reduced while the levels of cellular oxidative stress were escalated following the EA exposure. EA administration disrupted the process of steroidogenesis as well as spermatogenesis through the downregulation of CYP11A1, 5α-reductase, 3β-HSD, CYP17A1, and StAR while elevating spermatogenic abnormalities in head, tail and neck of sperm cells. The levels of LH, androgen binding protein, FSH, inhibin B, plasma testosterone and estradiol were lowered after EA administration. Testicular tissues showed inflammatory responses after EA exposure that is evident by elevated levels of TNF-α, IL-1β, COX-2, IL-6 and NF-κB. The expressions of Bax and Caspase-3 were upsurged while expression of Bcl-2 was reduced following the EA intoxication. These findings showed EA exerted toxic effects on testicular tissues via elevating oxidative stress, inflammation and apoptosis.