Effects of environmental toxicants on the efferent ducts, epididymis and fertility.

Many of the reproductive toxicants have primary effects on the testis, which potentially overshadow effects downstream on the efferent ducts and epididymis. The specific target of these effects depends upon the dosage and time response. It is often necessary to design experiments that separate testosterone-dependent responses arising in the testis from direct effects on epididymal tissues and spermatozoa, to uncover the mechanisms of toxicity in excurrent ducts. Recent studies have confirmed that chemicals can also alter the time required for sperm transport through the epididymis. Currently there are approximately twenty chemicals that can be classified as epididymal toxicants. There are fewer toxicants reported for the efferent ducts, but a few overlap with epididymal effects. The benzimidazole carbamates, like many efferent ductal toxicants, induce occlusions and subsequent testicular atrophy. The mechanisms appear to be related to fluid reabsorption, sperm stasis, followed by leukocyte chemotaxis, sperm granulomas, fibrosis and often the formation of abnormal microcanals. Disruption of oestrogen receptor function in the efferent ducts also interferes with fluid reabsorption and results in testicular swelling and seminiferous tubular atrophy. Thus, studies in which testicular atrophy occurs after chronic or subchronic exposures should be examined for lesions in efferent ducts and head of the epididymis. Such lesions can lead to permanent infertility.