TY - JOUR
T1 - Effects of multiple dosing of fenthion, fenitrothion, and desbromoleptophos in young chicks
AU - Farage-Elawar, Miranda
AU - Magnus Francis, B.
N1 - Funding Information:
This work was supported by the Research Board of the University of Illinois, and by the Toxicology Program of The Institute for Environmental Studies of the University of Illinois. We wish to thank Dr. R. L Metcalf for providing desbromoleptophos for the treatments, as well as desbromoleptophosoxon and phenylvalerate for the NTE assays, and Dr. L C. Hansen for his valuable advice. Requests for reprints should be sent to B. Magnus Francis, Institute for Environmental Studies, University of Illinois, 408 South Goodwin Avenue, Urbana, Illinois 61801.
PY - 1988/2
Y1 - 1988/2
N2 - The effects of multiple doses of desbromoleptophos, fenitrothion, and pure fenthion on brain acetylcholinesterase (AChE), brain neurotoxic esterase (NTE), and walking were investigated in immature chicks, below the age of sensitivity to organophosphorusester-induced delayed neurotoxicity (OPIDN). Ten milligrams per kilogram per day of delayed neurotoxicant desbromoleptophos (DBL), 15 mg/kg·d of the nonneurotoxicant fenitrothion (FTR), and 3 mg/kg·d of the suspected neurotoxicant fenthion (FEN) were given orally for 7 d to 3-d-old chicks. Behavioral testing was performed for treated and control chicks on various days after treatment. Brain NTE and AChE assays were carried out for treated and control chicks on each day of behavioral testing. DBL altered gait and inhibited both NTE and AChE; FEN altered gait and inhibited AChE but not NTE; and FTR did not affect gait, while inhibiting AChE but not NTE. NTE and AChE inhibition were 70% and 55%, respectively, 24 h after the last treatment, for the chicks treated with DBL. NTE returned to normal levels by around d 25 and AChE by 20 d after the last treatment. FTR caused more than 50% AChE inhibition but no NTE inhibition, 24 h after last treatment. NTE inhibition for the FEN-treated chicks never exceeded 11% during the whole period of the experiment, whereas 54% inhibition of AChE was seen 1 d after last treatment. DBL and FEN significantly altered the gait of treated chicks, but the non-OPIDN-inducing FTR did not. This study confirms that alterations in the gait of young chicks are not direct consequences of either NTE or AChE inhibition, and that fenthion-induced functional deficits can be distinguished from classical OPIDN.
AB - The effects of multiple doses of desbromoleptophos, fenitrothion, and pure fenthion on brain acetylcholinesterase (AChE), brain neurotoxic esterase (NTE), and walking were investigated in immature chicks, below the age of sensitivity to organophosphorusester-induced delayed neurotoxicity (OPIDN). Ten milligrams per kilogram per day of delayed neurotoxicant desbromoleptophos (DBL), 15 mg/kg·d of the nonneurotoxicant fenitrothion (FTR), and 3 mg/kg·d of the suspected neurotoxicant fenthion (FEN) were given orally for 7 d to 3-d-old chicks. Behavioral testing was performed for treated and control chicks on various days after treatment. Brain NTE and AChE assays were carried out for treated and control chicks on each day of behavioral testing. DBL altered gait and inhibited both NTE and AChE; FEN altered gait and inhibited AChE but not NTE; and FTR did not affect gait, while inhibiting AChE but not NTE. NTE and AChE inhibition were 70% and 55%, respectively, 24 h after the last treatment, for the chicks treated with DBL. NTE returned to normal levels by around d 25 and AChE by 20 d after the last treatment. FTR caused more than 50% AChE inhibition but no NTE inhibition, 24 h after last treatment. NTE inhibition for the FEN-treated chicks never exceeded 11% during the whole period of the experiment, whereas 54% inhibition of AChE was seen 1 d after last treatment. DBL and FEN significantly altered the gait of treated chicks, but the non-OPIDN-inducing FTR did not. This study confirms that alterations in the gait of young chicks are not direct consequences of either NTE or AChE inhibition, and that fenthion-induced functional deficits can be distinguished from classical OPIDN.
UR - http://www.scopus.com/inward/record.url?scp=0023845314&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0023845314&partnerID=8YFLogxK
U2 - 10.1080/15287398809531108
DO - 10.1080/15287398809531108
M3 - Article
C2 - 2449534
AN - SCOPUS:0023845314
SN - 0098-4108
VL - 23
SP - 217
EP - 228
JO - Journal of Toxicology and Environmental Health
JF - Journal of Toxicology and Environmental Health
IS - 2
ER -