Camel Milk Counteracts Cadmium-Induced Testicular Injury in Mice more than Bovine Milk by Further Regulating Oxidative Stress, Inflammation, and Apoptosis

Abstract

Background: Cadmium (Cd) is an extensively examined heavy metal that inflicts testicular damage inducing oxidative stress (OS), inflammation, apoptosis, and compromised spermatogenesis. Here, we investigated how bovine milk (BM) and camel milk (CM) protect mice from Cd-stimulated testicular damage. Methods: Adult male BALB/C mice were allocated into control, CdCl2, CdCl2+BM, and CdCl2+CM. Sperm count and motility, serum testosterone, OS markers (ROS, GSH, SOD), inflammatory cytokines (IL-1β, TNF-α), and histopathological alterations were assessed. Cleaved caspase-3 levels were measured by an ELISA kit. Furthermore, immunohistochemical analyses of PPAR-α, NF-κB, and PCNA expression levels were performed. Results: CdCl2 intoxication drastically reduced sperm count, motility, and testosterone levels, while it elevated OS indicators, and pro-inflammatory cytokines. Moreover, CdCl2 exposure raised the NF-κB and caspase-3 expression but reduced the PPAR-α and PCNA expression. BM or CM administration markedly mitigated the cytotoxic impact of CdCl2 intoxication. BM and CM improved sperm parameters and testosterone levels, decreased OS and inflammation indicators, and preserved testicular architecture. BM and CM modulated the NF-κB, PPAR-α, caspase-3, and PCNA expression levels that were affected by CdCl2 exposure. In all measured parameters, CM showed more improvement than BM. Conclusion: Both BM and CM counteracted testicular toxicity induced by CdCl2 intoxication; however, CM exhibited a greater defense impact. These findings point to CM as a promising therapeutic option for mitigating cadmium-induced male reproductive dysfunction.