Abstract

Parathion is a widely used organophosphoric pesticide which has also been reported to interfere with mouse spermatogenesis. Moreover it has been related to prenatal toxicity in mammals. Sixteen A/ Snell mice were sacrificed at day 17 of pregnancy. Testes and epididymides of the male fetuses were implanted in the allantochorion of chicken eggs. Three experimental conditions of the egg injections were considered: Group I: 1 ml of parathion (0.5 mg/ml), Group II: 1 ml of parathion (1 mg/ml), and Group III: 1 ml distilled water (control group). The implanted subjects continued their development for 4 days (i.e. to complete the gestational period for mice). The cell proliferation and differentiation of the epithelial cells of the epididymis were evaluated with the use of the monoclonal antiproliferating cell nuclear antigen (PCNA-cyclin) antibody, and the AE1 keratin complex antibody. Parathion altered the allantochorion, as 15% of the chicken embryos died in Group I and 40% in Group II, vs. only 8% in controls (Group III). However, no malformations were seen in the surviving embryos. In the testicular implants, the seminiferous cords of Group I had the same cytological characteristics of germ and pre-Sertoli cells as the control, except for involuting Leydig cells. Contrarily, in the cases with higher doses of parathion (Group II), there was a complete disorganisation of the seminiferous cords and the interstitium. In some testes, hyaline degeneration of the seminiferous cords was observed. No cell proliferation was evident, and the epididymal morphology was apparently unaffected. Therefore, parathion seems to interfere with normal testicular differentiation. However, in spite of interstitial damage, the epididymal development seems unaltered. Since the epididymis is an androgen-dependent organ, it may be postulated that testosterone production is still sufficient to support epididymal development but not spermatogenic cell line differentiation.

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