The Possible Ameliorative Effect Of Dimethyl Dicarboxylate Biphenyl (DDB) Against Mancozeb–Induced Testicular Toxicity In Rats

Abstract

Mancozeb, an organocarbamate fungicide, has been widely used for several decades. Despite the wide scope of exposure to this compound, up till now, there is a scarcity in published studies on the toxicity of mancozeb and its impacts on cell structure and functions. Thus the present study was designed to investigate the possible counteracting effect of dimethyl dicarboxylate biphenyl (DDB) in reducing the hazards caused by mancozeb in the testies. The effects of mancozeb given separately or simultaneously with DDB on rat testis were studied histologically and ultra structurally. Twenty-one male albino rats were divided into three groups, 7 rats each. The first group was given orally 0.5 ml of distilled water and served as control. Animals of the second group were given mancozeb orally at a dose level of 500 mg/kg b.wt for 15 consecutive days. Animals of the third group received the same dose of mancozeb as in the second group and simultaneously given DDB (50 mg/kg b.wt) through the same route of administration. Mancozeb treatment induced cellular damage manifested as exfoliation and destruction of the spermatogenic lineage. Destructed spermatids and Leydig cells were also pronounced. The ultra structural observations revealed marked cytoplasmic vacuolation in Sertoli cells and spermatogonia. Some cytoplasmic organelles of the spermatogonia and primary spermatocytes were degenerated. Moreover, destructed spermatids were pronounced in most of the seminiferous tubules. The interstitial cells appeared devoid of lipid droplets and the mitochondria appeared with disintegrated cristae. Administration of DDB simultaneously with mancozeb ameliorated most of the testicular tissue damage. This was reflected as restoration of the normal appearance of the spermatogenic lineage. Numerous spermatids were demonstrated in the lumens of the seminiferous tubules, most of them showed similar structure to those of the control group. In conclusion, it is possible to suggest that DDB might have ameliorated and amended the abnormalities caused by mancozeb.