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.

Spermatotoxic effect of carbendazim.

Carbendazim, suspended in sunflower oil, was administered to Wistar male rats through an oral intubation at a daily dose of 25 mg/kg body weight for 48 days, and the cauda epididymal sperm were analysed on day 49 for counts, motility and abnormalities. The study indicates that carbendazim affects the cauda epididymal sperm as seen in decreased sperm counts, inhibition of motility and increased incidence of abnormalities.

Carbendazim generates symplasts in rat spermatogenic clones.

In order to find non-microtubular targets in the seminiferous epithelium for the fungicide and reproductive toxicant carbendazim, it was administered to 90 days old male Wistar rat in a single bolus dose of 400 mg/kg body weight through an oral intubation. A parallel control group was maintained. Rats were sacrificed 48 days after the treatment and the testes were analysed for histopathological changes adopting routine histological methods, when symplasts were localised. The maximum diameter of five largest symplasts was measured, and the number of nuclei in these symplasts was also determined. As it is known that symplasts of spermatogenic cells are produced due to opening up of the intercellular bridges between cells in a clone consequent upon disruption of actin microfilaments, the present study shows that actin microfilaments would also be targets in the seminiferous epithelium for carbendazim toxicity.

Male reproductive toxicity of phosphamidon: histopathological changes in epididymis.

Phosphamidon, a neurotoxic insecticide, was tested for male reproductive toxicity with special reference to the epididymis. The insecticide was fed to Wistar strain male albino rat at 35 ppm concentration in drinking water ad libitum for 30 days. After vascular perfusion, thin slices of caput and cauda epididymidis were embedded in plastic, cut at 1 micron thickness and stained in toluidine blue for light microscopic observation. Principal cells of the caput epididymidis were vacuolarized and seen to pinch off fragments apically. In the proximal cauda the clear cells increased in height and in the size of the secondary lysosomal granules. In the distal cauda the clear cells appeared swollen out of proportion. Phosphamidon appears to affect the principal cells indirectly through its toxic effect on the Leydig cells; the clear cells of the cauda appear to be directly vulnerable to the toxic action of the pesticide.

Specific effect of vincristine on epididymis.

Wistar strain male albino rats were administered with vincristine (VCR) sulphate (10 micrograms/day for 15 days); epithelial cell types of the caput (zone II) and cauda (zone V) were studied light microscopically adopting semithin sectioning. VCR caused conspicuous pathological changes in the principal and apical cells of the caput and the clear cells of the cauda. The study points to toxic effect of VCR on these cell types, suggesting impairment of epididymal function, particularly concerning sperm maturation and endocytotic removal of the contents of the cytoplasmic droplets and dead sperm.

Reproductive toxicity of vincristine in male rats.

Gross morphological and gravimetric changes were observed in the male reproductive system of sexually mature rats as well as rats in pubertal transition, given a continuous treatment of vincristine at dose levels of 10/20 and 5/10 micrograms respectively per day, for 15 days. The treatment resulted in a drastic regression of entire male reproductive system, suggesting that vincristine would cause male reproductive toxicity.

Anti-spermatogenic effect of Vinca rosea Linn.

Regressive changes in seminiferous tubules and Leydig cells, increased cholesterol content in testis, and degeneration of all germinal elements other than spermatogonia were observed in the male Swiss albino mice, treated with aqueous extract of V. rosea leaves for 24 days. While the results reflect antiandrogenic and antispermatogenic action of V. rosea, the selective retention of the spermatogonia provides scope for the much desired revival of spermatogenesis on cessation of the treatment.

Antifertility effect of Andrographis paniculata (Nees) in male albino rat.

Dry leaf powder of A. paniculata, when fed orally to male albino rats, at a dose level of 20 mg powder per day for 60 days, resulted in cessation of spermatogenesis, degenerative changes in the seminiferous tubules, regression of Leydig cells and regressive and/or degenerative changes in the epididymis, seminal vesicle, ventral prostate and coagulating gland. There was reduction in the weight and fluid content of the accessory glands. The treatment also resulted in accumulation of glycogen and cholesterol in the testis, and increased activities of lactate dehydrogenase in testis and alkaline phosphatase in testis and ventral prostate. The results suggest antispermatogenic and/or antiandrogenic effect of the plant.

Utilization of seminal proteins by house gecko, Hemidactylus brooki(Gray), sperm for motility.

Five protein fractions of medium electrophoretic mobility were observed in the seminal plasma of H. brooki. On incubation of sperm in phosphate buffered saline and Zn and Mg free buffer, both containing seminal plasma, two of the protein fractions disappeared while a third fraction had become weak. The results suggest that H. brooki sperm utilize seminal proteins for motility.