Effect of methotrexate (MTX) administration on spermatogenesis: an experimental on animal model.

An experiment was conducted to observe histomorphometric and cellular toxicity on rat testes after sixty days of methotrexate administration intraperitoneally (ip). Total 30 adult male rats were divided into one control and two experimental groups containing 10 rats in each group. Experimental groups received methotrexate in two different doses i.e 25 ig and 50 ig, whereas control one received normal saline intraperitoneally. At the end of the experiment, animals were sacrificed and testes were processed for paraffin sectioning and stained in haematoxylin and eosin. Further microscopic study of seminiferous tubules, interstitial spaces, primary spermatocytes and spermatids were carriedout. Results revealed decreased diameter of seminiferous tubules, increased interstiial spaces in experimental groups in dose dependent manner and found to be statistically significant (p < 0.05) as well as distortion of morphology of Leydig cells in experimental group. Therefore, it can be concluded that these qualitative and quantitative changes in male gonads may alter the reproductive performance of animals.

Male reproductive toxic effects of carbendazim: hitherto unreported targets in testis.

Carbendazim (MBC), a widely used fungicide, is toxic to male reproductive mechanisms. Various cellular targets in the testis for MBC action are being understood only recently and still more targets have been conceived. The present study was aimed at finding such newer targets. Male rats were administered through oral route a single dose of carbendazim (400 mg/kg) and the testis was studied adopting routine histological technique. It has been observed that pachytene spermatocytes could also be targets for MBC action in the testis. The study also reports selective loss of step 14 spermatids, asynchrony of the stages in the spermatogenic cycle and development of Sertoli cell fibrosis of the seminiferous tubules of carbendazim-treated rats. From the different kinds of responses seen in the seminiferous tubules in the same testis to MBC, particularly in the Sertoli cell, MBC action in the testis appears dependent on the stage in the spermatogenic cycle at first exposure.

Stage specific effect during one seminiferous epithelial cycle following ethylene glycol monomethyl ether exposure in rats.

Stage specific effect of single oral dose (500 mg/kg body wt) of ethylene glycol monomethyl ether (EGME) was characterised during one cycle of seminiferous epithelium in rats. Maximum peritubular membrane damage and germinal epithelial distortion were observed at stages IX-XII. Cell death occurred during conversion of zygotene to pachytene spermatocytes (stage XIII) and between dividing spermatocytes and step I spermatids (stage late XIII-XIV). Profound effect was noted during first meiotic division than during second meiotic division. Presence of multinucleated secondary spermatocytes indicated cytokinesis arrest. The spermatogenesis was delayed and consequently frequency of tubules at stages I-VIII was reduced by day 10. Many of the tubules were devoid of round spermatids on day 12. Possibly, EGME (or it's metabolite) distorted the barrier system at stages IX-XIV and damaged the cells mostly at stages XII-early XIV.

Cytogenetic effect of thioridazine hydrochloride in mice and in human lymphocyte chromosomes.

Thioridazine hydrochloride, a drug of the phenothiazine group with a piperidine side chain is widely used in human medicine as a psycho-relaxant and anxiolytic agent. The mutagenic effects of thioridazine hydrochloride were studied in Swiss albino mice. The animals were treated with 4, 6 and 8 mg/kg of thioridazine hydrochloride for the micronucleus test, analysis of chromosomes in germ cells, and for sperm morphology assay. Human lymphocyte cultures were treated in vitro with 0.75, 1.25 and 1.75 mg/culture of thioridazine hydrochloride for 24, 48 and 72 hours. The study showed no significant increase in the frequency of micronuclei, chromosomal aberrations in germ cells and sperm head abnormalities in mice, or chromosomal aberrations in human lymphocyte cultures.