Abstract
It is well known that cadmium damages the testes of experimental animals although the mechanism of action has not been completely clucidated. Two possibilities have been postulated for the primary mechanism of toxicity: 1) circulatory failure due to vascular damage and 2) decreased utilization of zinc by spermatogenic cells due to a competitive action of cadmium. The velocity sedimentation cell separation technique was used to identify the spermatogenic cell types which incorporate cadmium and zinc and to study the interaction of these two metals. Cadmium-109 and zinc-65 were used to monitor the cellular incorporation. After intraperitoneal administration of either cadmium on zinc, peak radioactivity was present in the spermatogenic cell fraction which sediments at 2.2 mm/hr (late elongated spermatids). The affinity of cadmium for these cells was 2.5 to 2.9 times that of zinc at equimolar concentrations. The incorporation of these two metals into the late elongated spermatids appeared to be competitive. Cadmium chloride (1 mg/kg i.p.) immediately inhibited thymidine uptake into spermatogonial cells by 42 and 52% of control on days 1 and 7, but cadmium failed to affect the incorporation of uridine and L-leucine into early and late elongated spermatids, respectively. Similar results were obtained with in vitro studies. In vivo serial mating fertility studies indicated that cadmium affected all spermatogenic cell types, with the exception of mature spermatozoa and significantly decreased fertility during a 55-day period after a single cadmium injection. Pretreatment of mice with ZnCl2 (1 mg/kg) prior to cadmium treatment completely blocked the biochemical and functional effect of cadmium on spermiogenic cells but not on spermatogonial cells. Therefore, the primary action of cadmium seems to be both an effect on zinc utilization by spermiogenic cells as well as an inhibition of deoxyribonucleic acid synthesis by spermatogonial cells.
Footnotes
- Received February 1, 1973.
- Accepted July 20, 1973.
- © 1973 by The Williams & Wilkins Co.
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