The current study was conducted to investigate the protective properties of Eucalyptus globulus leaves methanolic extract (EGLME) against diclofenac sodium (DS) induced hepatorenal and testicular toxicity in male rats. A total of 40 rats were equally divided into 4 groups, Control, Diclofenac sodium (DS), EGLME and DS + EGLME groups, respectively. DS and EGLME were administered orally at dose rate 2.5 and 100 mg/kg BW, 4 times/week for 8 weeks, respectively. Administration of DS distorted hepatorenal functions manifested by alteration of serum levels of ALT, AST, total protein and albumin, creatinine and urea with changes of histological architectures. DS caused reproductive toxicity represented by minimized sperm count, individual sperm motility and viability; depleted concentration of reduced glutathione (GSH) in testicular tissue; and decreased testosterone level with alteration in testicular histological features. In contrast, co-treatment of DS intoxicated rats with EGLME protected rats against the adverse effects of DS revealing enhancing properties of EGLME on rats’ liver, kidney and testes. In conclusion, we demonstrated that EGLME had a potent protecting property against DS induced hepatic, renal and testicular toxicity in male rats, with special concern to testicular tissue via modulation of GSH as an oxidant marker. (classification by EVISE): Diclofenac sodium toxicity (hepatorenal and testicular toxicity), co-treatment with natural herbal extract, blood biochemical assays, tissue anti-oxidants assay, histopathology and reproductive indices analyses.

This study examined the protective effect of earthworm extract (EE) on acrylamide (ACR)-induced reproductive dysfunction. Forty male rats were allocated into four groups (n = 10). The G I (control) group received distilled water (D.W.). The G II group received ACR (5 mg kg⁻¹ B.W. in D.W.) 5 days per week, orally, for 3 weeks. The G III group was administered EE (300 mg kg⁻¹ B.W in D.W.) 5 days per week, orally, for 3 weeks. The G IV group was pretreated with EE for 3 weeks and then co-treated with EE and ACR for an additional 3 weeks. ACR decreased the number of sperm, sperm viability, and total motility. However, it increased testosterone levels with no effect on the FSH or LH levels. Moreover, ACR increased the concentrations of malondialdehyde (MDA) and nitric oxide (NO). Meanwhile, it decreased the glutathione (GSH) concentration in testicular tissues. Notably, the expression levels of p53 and Ki-67 were increased in the degenerated spermatogenic cells and in the hyperplastic Leydig cells of the testis of the ACR-treated group, respectively. Acrylamide induced alterations in the testicular tissue architecture. Interestingly, EE restored the sperm parameters and recovered the testicular histological structures and the biochemical alterations induced by ACR. In conclusion, earthworm extract ameliorated ACR-induced reproductive toxicity via restoring the testicular antioxidant balance and suppressing p53 and Ki-67 expressions in testicular tissues.

This study was designed to examine the effect of the intrauterine infusion of platelet-rich plasma (PRP) or equine lyophilized growth factor (L-GF^equina) on the follicular growth, endometrial thickness, estrus cycle length, and pregnancy rate in purebred Arabian mares. A total of 73 purebred Arabian mares who experienced repeat breeding for three successive cycles were randomly divided into the following three groups: control group, without treatment; second Group (PRP group), in which mares were intrauterine infused with 20 mL of fresh PRP on the second day after the end of physic estrus phase; and the third group (L-GF^equina Group), consisting of mares that were intrauterine infused with 20 mL of reconstituted lyophilized horse platelets growth factors (L-GF^equina) on the second day after the estrus phase. The results showed no significant difference between control and treated groups in the diameter of the preovulatory follicles during the post treatment cycle. The endometrium thickness increased significantly in the L-GF^equina and PRP groups ahead of the non-treated group. Intrauterine L-GF^equina or PRP administration shortened the estrus cycle length. A higher pregnancy rate was recorded in the L-GF^equina and PRP treated mares. In conclusion, the intrauterine infusion of L-GF^equina or PRP increased the endometrial thickness and pregnancy rate and could be used to improve fertility in Arabian purebred mares who experienced from repeat breeding.

In this study, we estimated the protective role of Moringa oleifera leaf ethanolic extract (MOLE) against obesity-associated testicular dysfunction. Fifty male albino rats were randomly assigned to five groups (n = 10): Group I (basal diet), group II (basal diet plus MOLE orally), group III (high-fat diet—HFD), group IV (HFD plus oral MOLE) and group V (HFD for 8 weeks followed by a basal diet plus oral MOLE for 6 weeks). The study duration extended for 14 weeks. Serum collected to investigate testosterone, FSH and LH levels. Testicular tissues were used to determine levels of SOD, glutathione, catalase and malondialdehyde. Semen was collected to estimate its quality (morphology, motility and concentration). Morphological changes in the testis were investigated by histopathological and immunohistochemical techniques. Compared with both control treatment and MOLE treatment, serum testosterone, FSH, LH, testicular enzymatic catalase, SOD, GSH, survivin immunoreactivity, sperm quality and testicular weight were all significantly decreased in rats treated with HFD, while there were significant increases in testicular malondialdehyde and caspase-3 immunoreactivity. MOLE improved all harmful effects of HFD. Improvements were more pronounced in the protected (G 4) than the treated (G 5) group. MOLE could be a potential solution for obesity-associated fertility problem.

The present study aimed to investigate the protective potential of naringin (NG) against di-n-butyl phthalate (DBP)- induced testicular damage and impairment of spermatogenesis in rats. Forty-two male Wistar albino rats were divided into six equal groups, and treated orally, 3 times weekly for 8 successive weeks. Control vehicle group was administrated olive oil, naringin-treated group was administered NG (80 mg/kg), DBP 250- and DBP 500- intoxicated groups received DBP (250 mg/kg) and (500 mg/kg), respectively, NG + DBP 250 and NG + DBP 500 groups received NG, an hour prior to DBP 250 and 500 administration. The results revealed that DBP induced dose-dependent male reproductive dysfunctions, included a significant decrease in the serum testosterone level concomitantly with significant decreases in the sperm count, viability, and total motility. Meanwhile, DBP significantly increased the testicular malondialdehyde level with significant reductions of glutathione content and catalase activity. Histopathologically, DBP provoked absence of spermatozoa, degenerative changes in the cell layers of seminiferous tubules and a significant decrease in the thickness of the seminiferous tubules epithelium. Conversely, the concomitant treatment with NG, one hour before DBP 250 or 500- intoxication mitigated the dose-dependent reproductive dysfunctions induced by DBP, evidenced by significant increases of serum testosterone level, sperm motility, count and viability along with marked improvement of the oxidant/antioxidant status and testicular histoarchitecture. In conclusion, the findings recorded herein proved that NG could mitigate DBP-induced testicular damage and impairment of spermatogenesis, suggesting the perspective of using NG as a natural protective and therapeutic agent for alleviating the reproductive dysfunctions and improving reproductive performance, mainly via its potent antioxidant activity.

The current study aimed to investigate the protective potential of Chlorella Vulgaris (CV) extract against the reproductive dysfunction induced by sodium nitrite toxicity. Forty‐five male Wistar albino rats were assigned into five groups (n = 9). Control group received normal saline orally for 3 months, CV‐treated: administered CV extract (70 mg/kg.BW) orally for 3 months, sodium nitrite‐treated: received sodium nitrite (80 mg/kg.BW) orally for 3 months, co‐treated: simultaneously received CV along with sodium nitrite treatment, orally, daily for 3 months, and CV‐pre‐treated: pre‐treated with CV extract for 4 weeks followed by simultaneous treatment with sodium nitrite and CV extract for additional 8 weeks. Treatment with sodium nitrite significantly decreased serum testosterone and follicle‐stimulating hormone concentrations, sperm count, motility, and viability. Besides, it decreased testicular superoxide dismutase and glutathione peroxidase activities while increased malondialdehyde concentration. This effect of sodium nitrite was associated with degenerative, necrotic, vascular, and inflammatory changes in testicular tissues. Treatment of sodium nitrite‐intoxicated rats with CV in co‐treated and pre‐treated groups significantly prevented sodium nitrite‐induced alterations of sperm parameters, hormonal concentrations, testicular oxidative–antioxidant status, and histological architecture. This study indicates that CV extract ameliorates the reproductive dysfunction induced by sodium nitrite toxicity via improving reproductive hormonal levels and testicular antioxidant activities.