Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Groups of 10 F344/N rats and B6C3F1 mice of each sex were exposed to cobalt sulfate heptahydrate aerosols of 0, 0.3, 1.0, 3.0, 10, or 30 mg/m3, 6 hr per day, 5 days per week, for 13 weeks. All rats and female mice and all but 2/10 male mice exposed at the top concentration survived to the end of the studies. Polycythemia was observed in exposed rats but not in mice. Sperm motility was decreased in mice exposed at 3 mg/m3 (the lowest concentration evaluated) and at higher concentrations, and increased numbers of abnormal sperm and decreased testis and epididymal weights occurred in mice exposed to 30 mg/m3. Cobalt content in the urine of rats increased with increasing atmospheric cobalt exposure. Primary histopathologic effects were limited to the respiratory tract. Lesions in rats and mice included degeneration of the olfactory epithelium, squamous metaplasia of the respiratory epithelium, and inflammation in the nose; inflammation, necrosis, squamous metaplasia, ulcers (rats), and inflammatory polyps (rats) of the larynx; metaplasia of the trachea (mice); and fibrosis, histiocytic infiltrates, bronchiolar epithelial regeneration, and epithelial hyperplasia in the alveoli of the lung. The most sensitive tissue was the larynx, with squamous metaplasia observed in rats and mice at the lowest exposure concentration of 0.3 mg/m3. Thus, a no-observed-adverse-effect level was not reached in these studies.
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PMID:Inhalation toxicity studies of cobalt sulfate in F344/N rats and B6C3F1 mice. 222 61

It was possible to demembrante and reactivate not only freshly collected testicular, cauda epididymal, and ejaculated ram sperm but also sperm that had been stored for several days at 0 degrees C and for several months at -196 degrees C in rete testis fluid or egg yolk citrate media. Sperm were usually washed free of seminal plasma before demembranation, but this was not essential for reactivation. Bovine serum albumin (1.0%) in the wash medium increased the survival of sperm, but more than 0.25% in the extraction medium decreased reactivation. A macro-molecular component of cauda epididymal fluid also inhibited the reactivation of testicular sperm. Triton X-100 concentrations between 0.01% and 1.00% in the extraction medium were satisfactory for demembranating the sperm. Rapid cooling (i.e., cold shock) mimicked the effect of detergent in making the sperm responsive to added ATP and demonstrated that damage to ram sperm in cold shock does not involve the axoneme. Ejaculated and cauda sperm were reactivated immediately on addition of ATP and activity persisted for up to 10 min. Testicular sperm, on the other hand, required about 4 min to become fully reactivated. The optimal ATP concentration for activation of sperm was 0.1-1.0 mM. Magnesium ions (0.1-1.0 mM) were important for reactivation, and testicular sperm required a higher magnesium concentration than did cauda or ejaculated sperm. Manganese ions were almost as effective as magnesium for reactivating cauda epididymal and ejaculated sperm. Cobalt and cadmium ions were much less active for cauda and ejaculated sperm and none of these ions were effective for testicular sperm. Fluoride (25-50 mM) inhibited reactivation. The presence of 50 microM cAMP in the extraction medium or preincubation of testicular sperm with theophylline or caffeine increased low levels of activation, but this was not evident with ejaculated or cauda sperm. We conclude that the motor apparatus is already functionally assembled in spermatozoa on leaving the testis, but some fine adjustment must take place during maturation in the epididymis.
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PMID:ATP-induced reactivation of ram testicular, cauda epididymal, and ejaculated spermatozoa extracted with Triton X-100. 395 35

Toxicology studies of cobalt sulfate heptahydrate (99%percnt; pure) were conducted by exposing groups of F344/N rats and B6C3F1 mice of each sex to a cobalt sulfate heptahydrate aerosol 6 hours per day, 5 days per week, for 16 days or 13 weeks. In 16-day studies, all rats and mice exposed at the top concentration of 200 mg cobalt sulfate/m3 died (5 animals per group); partial survival was seen in the 50 mg/m(3) exposure groups. Degeneration of the olfactory epithelium and necrotizing inflammation occurred in the nose of all rats and mice that died and in animals exposed to 50 mg/m(3). Necrotizing inflammation was observed in the larynx and trachea of rats and mice at concentrations as low as 5 mg/m(3), and a similar lesion was present in the bronchi at exposure concentrations of 50 mg/m(3) or higher. Regenerative and inflammatory lesions, including peribronchial and septal fibrosis in the lung, were found in rats and mice exposed to 50 mg/m(3). In 13-week studies, all rats, all female mice, and all but 2 male mice exposed at the top concentration survived to the end of the studies (target exposure concentrations of 0, 0.3, 1, 3, 10, and 30 mg/m(3), 10 animals per group). Rats and mice exposed to 30 mg/m(3) lost weight during the first exposure week and then gained weight at the same rate as controls. Lung weights were increased over those of controls in rats exposed at concentrations as low as 1 mg/m(3) and in mice exposed to 10 mg/m(3) or more. Polycythemia was observed in rats exposed to cobalt sulfate but not in mice. Sperm motility was decreased in mice exposed at 3 mg/m(3) or at higher concentrations (lower concentrations were not evaluated), and increased numbers of abnormal sperm were found in mice exposed to 30 mg/m(3). Testis and epididymal weights were decreased in mice exposed to 30 mg/m(3). Cobalt content in the urine of rats increased with increasing atmospheric cobalt exposure. Lesions seen in the respiratory tract in 13-week studies in rats and mice included degeneration of the olfactory epithelium, squamous metaplasia of the respiratory epithelium, and inflammation in the nose; inflammation, necrosis, squamous metaplasia, ulcers (rats), and inflammatory polyps (rats) of the larynx; squamous metaplasia of the trachea (mice); and histiocytic infiltrates, bronchiolar regeneration, peribronchiolar and septal fibrosis, and epithelial hyperplasia in the alveoli of the lung. The most sensitive tissue was the larynx, with squamous metaplasia observed in rats and mice at the lowest exposure concentration of 0.3 mg/m(3). Thus, a no-observed-adverse-effect level was not reached in these studies. (NOTE: These studies were supported in part by funds from the Comprehensive Environmental Response, Compensation, and Liability Act trust fund (Superfund) by an interagency agreement with the Agency for Toxic Substances and Disease Registry, U.S. Public Health Service.)
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PMID:NTP technical report on the toxicity studies of Cobalt Sulfate Heptahydrate in F344/N Rats and B6C3F1 Mice (Inhalation Studies) (CAS No. 10026-24-1). 1220 63