Background: This study explored the effect of vitamin C (Vit-C) administration on the reproductive function of adult male Wistar rats injected with boldenone undecylenate (BOL). Methods: Rats were randomly assigned into control, vehicle control, Vit-C (120 mg/kg b.wt./day, orally), BOL (received 5 mg/kg b.wt./week, IM) and BOL+Vit-C-treated groups. After eight weeks, hormonal assay, semen evaluation, testicular enzymes, and antioxidants biomarkers were assessed. Besides, the histopathological and immunohistochemical investigations of the androgen receptor (AR) expression were performed. Results: The results revealed that serum testosterone, acid phosphatase, sorbitol dehydrogenase, sperm abnormalities, and testicular malondialdehyde were significantly incremented in the BOL-treated group. Testicular weight, sperm count, and sperm motility together with serum levels of luteinizing hormone, follicle-stimulating hormone, and estradiol, and testicular testosterone, catalase, superoxide dismutase, and reduced glutathione showed a significant decrease following BOL treatment. Besides, the AR immunoreactivity was significantly decreased in testicular tissues. Vit-C co-administration with BOL significantly relieved the BOL-induced sperm abnormalities, reduced sperm motility, testicular enzyme leakage, and oxidative damage. However, Vit-C could rescue neither BOL-induced hormonal disturbances nor AR down-regulation. Conclusions: The results provide further insight into the mechanisms of BOL-induced reproductive dysfunction and its partial recovery by Vit-C.

Herein, male juvenile rats (23th postnatal days (PND)) were exposed to chlorpyrifos (CPS) (7.5 mg/kg b.wt) and/or iprodione (IPD) (200 mg IPD /kg b.wt) until the onset of puberty (60th day PND). Our results demonstrated that IPD and/or CPS exposure considerably reduced locomotion and exploration. However, CPS single exposure induced anxiolytic effects. Yet, neither IPD nor IPD + CPS exposure significantly affected the anxiety index. Of note, IPD and/or CPS-exposed rats showed reduced swimming time. Moreover, IPD induced significant depression. Nonetheless, the CPS- and IPD + CPS-exposed rats showed reduced depression. The individual or concurrent IPD and CPS exposure significantly reduced TAC, NE, and AChE but increased MDA with the maximum alteration at the co-exposure. Moreover, many notable structural encephalopathic alterations were detected in IPD and/or CPS-exposed rat brain tissues. The IPD + CPS co-exposed rats revealed significantly more severe lesions with higher frequencies than the IPD or CPS-exposed ones. Conclusively, IPD exposure induced evident neurobehavioral alterations and toxic reactions in the brain tissues. IPD and CPS have different neurobehavioral effects, particularly regarding depression and anxiety. Hence, co-exposure to IPD and CPS resulted in fewer neurobehavioral aberrations relative to each exposure. Nevertheless, their simultaneous exposure resulted in more brain biochemistry and histological architecture disturbances.