OECD SIDS 5. TOXICITY
ID: 79-50-5 DATE: 18.01.2006
Short citation be judged.
250, 750, 1000, 1500, 2000 mg/
Route of admin.:
= 250 mg/kg bw
(1982), Molec Pharmacol 22:
Year: GLP: Test substance:
as described in Klunk et al. 438-443 1982 no data as prescribed by 1.1 - 1.4
Two or three mice per treatmen stated whether i.p., i.v. or i undescribed vehicle. Time to f contraction and relaxation) an (persistent contractions, usua recorded and compared with tha butyrolactones in order to det respectively important structu physiological action. Full det previous publication: Klunk WE
t group were injected (not .m.) with dl-lactone in irst clonic seizure (alternate d/or to first tonic seizure lly resulting in death) was t of other substituted ermine potency and mechanism ral determinants of ails of methods are given in a
et al. (1982), Molec Pharmacol
Mice per group
Time to first seizure of type _____________________________
287±174 (3/3) 39±126 (3/3)
"DL-Pantolactone (alpha-hydroxy-beta,beta-dimethyl-gamma-butyrolactone) was obtained from Chemical Procurement Laboratories (College Point, NY)." No further information given. dl-Lactone administered by injection leads to dose-dependent neurophysiological effects in mice. At 250 mg/kg bw no effects were observed (NOEL). All higher doses caused clonic convulsions with the first seizures appearing after a shorter delay the higher the dose; tonic convulsions started at a dose of 1000 mg/kg bw in one of three animals after more than 20 min while both higher doses caused tonic seizures in all animals of the respective treatment groups with a highly dose-dependent reaction time. However, in comparison with five other substituted butyrolactones, dl-lactone was the weakest neurotoxicant, by a factor of five to the next weakest, as measured by the dose in millimoles/kg bodyweight (full data in paper).
Peer-reviewed paper in scientific journal, clear presentation of results.