Acute toxicity and urinary excretion of diphenyldiselenide.
The acute toxicity of diphenyldiselenide (DPDS) in the male Swiss mouse was found to be enhanced by pretreatment with phenobarbital of SKF-525A. DPDS decreased hepatic glutathione content by 50% at 1 h after administration. Following administration of 14C-DPDS, labelled metabolites were found in urine but not in bile or feces. Analysis of the urinary metabolites of 14C-DPDS showed that selenium-containing metabolites elute from a DEAE-Sephadex column in two fractions: the first has not been chemically characterized, while the second peak contained the glucuronide conjugates of C6H4(OH)SeH and C6H5SeH. Virtually all of the administered selenium is excreted within 5 days, while only about 36% of the 14C is excreted in the same time period. This discrepancy indicates metabolic scission of the carbon-selenium bond.
Pharmacology Department, Jefferson Medical College, Philadelphia, PA 19107.
W J
WJ
Adams
J J
JJ
Kocsis
R
R
Snyder
D000818:Animals; D001555:Benzene Derivatives / Q000633:toxicity*; D005978:Glutathione / Q000032:analysis; D008099:Liver / Q000032:analysis; D008297:Male; D051379:Mice; D016566:Organoselenium Compounds; D011335:Proadifen / Q000494:pharmacology; D012643:Selenium / Q000633:toxicity* / Q000652:urine
D001555:Benzene Derivatives; D016566:Organoselenium Compounds; C061132:diphenyldiselenide; D011335:Proadifen; D005978:Glutathione; D012643:Selenium