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Lead exposure causes altered spermiogenesis in rats.
Sharpnack-D; Childress-C; Moorman-W; Schrader-S; Chapin-R
Toxicologist 1997 Mar; 36(1)(Part 2):359
Testicular lesions that might explain lead-induced decreases in sperm counts in man and laboratory animals have not been described. Male Dutch-Belted rabbits (n = 95) were divided into 8 groups and administered lead acetate subcutaneously to achieve and hold target blood lead levels (0, 20, 40, 50, 70, 80, 90, 110 microg/dl; n = 22, 15, 15, 7, 7, 15, 7, 7, respectively) for 15 weeks. Animals were then sacrificed and necropsied. Mean testis weight was not altered. When seminiferous tubules of lead-exposed rabbits were examined by light microscopy, membrane-bound cytoplasmic bodies (CBs), containing >1 elongate spermatid(s), were seen on the luminal surfaces of the germinal epithelium. CBs were most frequently found in tubules that were at the stage of spermatid release. No treatment effect on either the quantity or quality of Sertoli cells or pre-spermatid germinal cells could be detected by light microscopy. The percent of animals with CBs in each treatment group were (from control to high dose) : 0%, 7%, 33%, 43%, 43%, 47%, 14%, and 100%, respectively. Lead exposure to male rabbits causes a lesion in spermiogenesis which is characterized by retention of spermatid cytoplasm.
Toxic-materials; Toxins; Exposure-assessment; Exposure-levels; Exposure-limits; Reproductive-effects; Reproductive-hazards; Reproductive-system; Reproductive-system-disorders; Animal-studies; Animals; Laboratory-animals; Lead-poisoning
Issue of Publication
The Toxicologist. Society of Toxicology 36th Annual Meeting, March 9-13, 1997, Cincinnati, Ohio
Page last reviewed: July 10, 2020
Content source: National Institute for Occupational Safety and Health Education and Information Division