Summary: Highly active antiretroviral therapy has evolved over the years, leading to a boost in the quality of life in people living withHIVandAIDS. However, growing evidence has shown that highly active antiretroviral therapy has deleterious effects on the testes and the overall reproductive capacity. Therefore, this study is to determine the adjuvant potential of Naringenin on highly active antiretroviral therapy‐induced perturbations in fertility of male Sprague‐Dawley rats. Thirty adult male Sprague‐Dawley rats were divided into six groups viz – Control; H: 30 mg/kg of highly active antiretroviral therapy (EFV, 600 mg +FTC, 200 mg +TDF, 300 mg); N40: Naringenin, 40 mg/kg; N80: Naringenin, 80 mg/kg;HN40: highly active antiretroviral therapy + Naringenin, 40 mg/kg;HN80: highly active antiretroviral therapy + Naringenin, 80 mg/kg. The rats were euthanized after 4 weeks. Results showed that there was a significant decrease in sperm count (p < 0.001), spermatozoa with normal morphology (p < 0.001) and progressive sperm motility (p < 0.05) of H compared to the control and theHNgroups. Likewise, fragmentations increased (p < 0.05) in tail lengths of spermDNAin H compared to control.HN40 andHN80 decreased tail lengths compared to H (p < 0.001). There was also a decrease in %tailDNAand tail moment inHN40 (p < 0.001) compared to H. Luteinizing hormone significantly increased (p < 0.05) inHN40,HN80, and N40 (p < 0.001) but decreased in H (p < 0.05) compared to control. The diameter of the seminiferous tubules also decreased (p < 0.05) in H compared to control, N80, andHN40. Likewise, the area of the seminiferous tubules in group H decreased (p < 0.05) compared to N80 andHN80. The seminiferous tubules epithelium increased (p < 0.05) in N40 andHN40 compared to H. This study establishes that highly active antiretroviral therapy has deleterious effects on the testicular microanatomy, sperm parameters, and spermDNAof Sprague‐Dawley rats, which may impair fertility but Naringenin is a potential complimentary adjuvant.

Objective: To investigate the short-term effects of Kigelia africana fruit extract (KAFE) on cisplatin-induced testicular histo-morphometric changes in Sprague–Dawley (SD) rats. Design: This is an experimental animal study. Materials and methods: Fifty-seven male SD rats were acclamatized and grouped into 10 of five rats per group. Each rat was administered either KAFE in 100 and 500mg/kg doses orally or cisplatin 10mg/kg i.p. or normal saline to controls. Experiment was terminated after 28days by i.p. injection of ketamin 50mg/kg. Testicular tissue was processed for histological and morphometric analyses while catalase enzyme activity, lipid peroxidation and glutathione levels were assayed accordingly. Sperm count/motility was also assessed. Results: Cisplatin treatment caused over 37.5% mortality of SD rats. Qualitative histological assessment showed no deleterious changes following treatment with KAFE alone or as a pre-treatment with cisplatin. KAFE post-treatment resulted in focal vacuolar changes in the seminiferous tubules (ST) of the SD rats. Cisplatin-treatment negatively affected the histoarchitecture of the seminiferous tubules with massive loss of spermatogenic cells. There was also a significant reduction in testicular weight/volume, ST diameter and cross-sectional areas (P<0.001) but KAFE positively improved these parameters. KAFE alone and as prophylaxis significantly increased body weight, serum testosterone and follicle-stimulating hormone (P<0.001). It showed a significant elevation in catalase activity, decline in malondialdehyde and up-regulated glutathione levels (P<0.001). These parameters were negatively affected by cisplatin treatment. Conclusion: The cytoprotection against cisplatin-induced testicular damage by KAFE is likely via an antioxidant modulatory pathway. Also, it is possible that KAFE possesses an androgen-stimulating property

The increased accessibility of antiretroviral therapy continues to positively drive the reduction in viral load and survival of patients despite the attendant reproductive toxicities. We propose that testicular damage caused by highly active antiretroviral therapy (HAART) can be attenuated by antioxidant treatment by investigating the testicular histomorphologic and stereological effects of antiretroviral drugs and its interaction with antioxidants using an experimental animal model. Sprague–Dawley rats were divided into seven groups of six rats per group (A, B… G) using simple random sampling and treated orally with 0.9% normal saline as placebo, a HAART cocktail of stavudine, lamivudine and nevirapine using the adjusted human therapeutic doses of 200, 600 and 350–400 mg/day, respectively, and antioxidants ascorbic acid (vitamin C) and I.M α‐tocopherol (vitamin E). Animals were killed after 4 weeks and testicular tissue harvested and processed for light microscopy and stereological evaluations. The results were interpreted by a Veterinary pathologist blinded to the study. No animal died during the experimental period. The histopathological assessment of the testis of animals treated with placebo, ascorbic acid alone and α‐tocopherol alone as well as vitamin E + HAART displayed normal testicular microanatomy. Groups treated with HAART alone, HAART + vitamin C + vitamin E and vitamins C + HAART showed extensive seminiferous tubular atrophy, necrosis and hypocellularity in the histoarchitectural patterns. While testicular cross‐sectional area of seminiferous tubules remained unaffected by HAART, epithelial heights significantly decreased (p < 0.05) when compared with controls. There was marked (p < 0.05) increased in testicular‐body weight ratio in HAART group. The results show that vitamin E could be useful in protecting testicular tissue from toxicities of HAART regimes as these results mirrors stereological data for the groups. HAART presents with deleterious histopathological changes in the testes causing tubular atrophy with altered morphometric indices. Supplementation with vitamin E appears to be a better adjuvant antioxidant that ameliorates these deleterious effects.

Oluwatosin O Ogedengbe, Ayoola I Jegede, Ismail O Onanuga, Ugochukwu Offor, Edwin CS Naidu, Aniekan I Peter, and Onyemaechi O Azu. ToxicolRes 2016;32:317-25. https://doi.org/10.5487/TR.2016.32.4.317

To study the protective effect of Red Palm Oil (RPO) on testicular damage induced by administration of lead acetate on male Sprague-Dawley rats, 28 rats divided into four groups of 7 animals each were used. They were administered orally with RPO (1 mL and 2 mL) and lead acetate (i.p.) 6 mg/kg body weight/day, respectively. Treatment was conducted for 8 weeks, and 24 hrs after the last treatment the rats were sacrificed using cervical dislocation. Sperms collected from epididymis were used for seminal fluid analyses; while the testes sample was used for ROS and oxidative enzyme activities assessment. Statistical analysis was carried out using GraphPad Prism 5.02 statistical analysis package. Administration of lead acetate increased generation of reactive oxygen species (ROS) significantly (p<0.05) as evidenced by the elevated value of H₂O₂and LPO and decreased GSH level. Also there was reduced epididymal sperm count, poor grade of sperm motility, and lower percentage of normal sperm morphology significantly. Coadministration with RPO, however, has a protective effect against lead toxicity by decreasing H₂O₂production, increased GSH level, and increased sperm qualities especially. This shows that RPO has a potential to attenuate the toxic effect of lead on testicular cells preventing possible resultant male infertility.