This study demonstrates that impaired chromatin compaction and slightly increased chromosome aneuploidies are found in spermatozoa with an elongated head, suggesting possible mechanisms such as meiotic non-disjunctions or spermiogenesis anomalies.

Ninety-day-old Sprague-Dawley rats were intoxicated for 70 d with lead, given either as 0.3% lead acetate in drinking water or by inhalation as 5 mg m-3 lead oxide. Direct or transmitted lead toxicity for the male reproductive system was assessed in the rats and their offspring from pituitary and genital organ weights after exposure, the numbers of Sertoli and germ cells, the number, motility and morphology of epididymal spermatozoa, the levels of plasma testosterone, LH and FSH and fertility tests. Whole blood lead levels were similar after lead ingestion and after inhalation (58.0 ± 1.7 μg dl-1 vs. 51.1 ± 1.8 μg dl-1). Lead acetate ingestion did not affect the reproductive system or fertility of rats. Inhalation of lead oxide did not affect fertility either, but seminal vesicle weight dropped significantly, which might suggest an alteration in the pattern of testosterone secretion. In the male progeny of sires that inhaled lead, the number of epididymal spermatozoa decreased but this did not interfere with fertility. Our results show that for the doses studied, lead inhalation and lead ingestion do not produce strikingly different effects on the male rat's reproductive system. Differences between the present findings and those of others might be due to difference of rat strain or of age at exposure.

The reproductive toxicity of lead was investigated in NMRI mice exposed to 0.5% lead acetate in drinking water from day 1 of intra-uterine life until 60 days after birth. Compared with control mice, the weights of lead- exposed fetuses and subsequently of the lead-exposed weaned pups, male and female, diminished by 11 and 13% respectively. The lead-exposed male and female offspring of lead-exposed dams were mated with unexposed females and males, to examine the effect of lead exposure on reproductive function. Male fertility was not affected but reduced female fertility was observed: litters were smaller and a smaller number of implantation sites was found in lead-exposed females. In lead-exposed males, the weights of the body, testes and epididymes diminished by about 13%, and seminal vesicle and ventral prostate weights, by about 29%. Testicular histology and the number and mor phology of epididymal spermatozoa were normal. The lev els of plasma FSH, LH and testosterone, and of testicular testosterone, were not modified. These results suggest that the hypothalamic-pituitary-testicular axis is not adverse ly affected by the above lead exposure, and that therefore the decreased seminal vesicle and ventral prostate weights might not be the consequence of reduced testosterone lev els. The hypothesis that lead has a direct effect on these organs as well as a secondary effect resulting from possi bly reduced food consumption by lead-exposed mice can not be excluded. Consequently, in male NMRI mice, expo sure to lead might affect reproductive function by acting directly and/or indirectly on accessory sex organs.

It has often been suggested that determination of free L(-)-carnitine in seminal plasma may provide a good indication of epididymal function. However, there has been disagreement regarding the origin of L(-)-carnitine (epididymis and seminal vesicles) and its concentration in human seminal plasma. In this study, free L(-)-carnitine was determined after deproteinization with an enzymatic spectrophotometric method. In 29 semen samples from fathers and with normal spermiograms (semen volume between 2 and 6 ml, sperm count over 20.10(6)/ml, more than 50% motile spermatozoa), the total free L(-)-carnitine in the seminal plasma was 1010 nmoles (SD: +/- 480), in 16 samples from vasectomized men it was 131 nmoles (SD: +/- 77), and in 5 from men with agenesis of the vas deferens and seminal vesicles it was 21 nmoles (SD: +/- 25). These results suggest that free L(-)-carnitine in the seminal fluid is predominantly of epididymal origin. The results of free L(-)-carnitine determinations in split ejaculates and the absence of a correlation between L(-)-carnitine and fructose concentrations in semen from normal subjects indicate that the seminal vesicles make only on minor contribution to L(-)-carnitine in the seminal plasma.