Abstract
Acute and chronic effects of cadmium exposure on spermatozoan choline acetyl transferase (ChAT) were studied to investigate the mechanism of cadmium induced sterility. Cadmium at dosages of 1 mg/kg and 2 mg/kg given orally inhibited ChAT in all segments of spermatozoa obtained from rat epididymis. Maximum inhibition was observed about 72 hr after treatment. Decreased ChAT activity was seen in chronic experiments where animals were exposed to cadmium via drinking water; surprisingly, a greater decrease was observed at the lower dosage. Cadmium also inhibited ChAT activity of rat cauda spermatozoa, and human spermatozoa when they were incubatedin vitro at a concentration of 5 × 10−4M. Cadmium decreased human spermatozoan motility when incubated at a concentration of 5 × 10−4M. Acetyl-choline (ACh) and physostigmine (a cholinesterase inhibitor), however, increased spermatozoan motility. The results indicate that cadmium may produce sterility by inhibiting spermatozoan choline acetyltransferase, decreasing acetyl choline synthesis, and impairing spermatozoan motility, and could be a potential reproductive hazard to humans.
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