Evaluation of the Effect of Date Palm [Phoenix dactylifera] Fruit Extract on Methotrexate-Induced Reproductive Toxicity in Male Rats

Abstract

Background: Phoenix dactylifera L. in the Palmae family (Arecaceae) is commonly known as Date palm. Its fruit is popularly consumed as food and also used as a herbal remedy for fertility enhancing effects in males. Aim: The present study was designed to explore the effect of P. dactylifera fruit extract (PDFE) on methotrexate (MTX)-induced reproductive toxicity in male rat models. Study Design: An experimental study which lasted for 19 days. Place and Duration of Study: Department of Medical Laboratory Sciences and Animal House, College of Medicine, University of Nigeria, Enugu Campus, between April 2019 and November 2019. Methodology: Sixteen (16) rats were divided into four groups (n=4) namely: Normal control (NC), MTX control, MTX+200mg/kg PDFE and MTX+400mg/kg PDFE. PDFE was administered by oral gavage, once daily, for 10 days. MTX injection (20mg/kg i.p.) was administered to rats in the three test groups on the fifth day. All the rats were sacrificed on Day 11 and the testes and epididymides of all rats were excised and histologically processed for light microscopical examination. Caudal epididymal sperm concentration was also determined. Results: MTX induced a marked depletion and degeneration of spermatogenic series in the testicular tissues of MTX-control rats whereas PDFE treatment offered some cyto-architectural preservation in a dose-dependent manner. Similarly, a decreased number of spermatozoa within the lumen of epididymal tubules was observed with MTX treatment compared to the normal control and PDFE-treated rats. Treatment with PDFE caused a slight improvement in caudal epididymal sperm concentration although not statistically significant (p>0.05) when compared with the controls. Conclusion: Data from the present study has revealed that oral treatment with P. dactylifera fruit extracts ameliorates the deleterious effects of methotrexate-induced reproductive toxicity in rats.