Related Experiment Videos
Developmental toxicity of desbromoleptophos in chicks: enzyme inhibition, malformations and functional deficits
M Farage-Elawar1, J S Duffy, B M Francis
1Department of Veterinary Biosciences, University of Illinois, Urbana-Champaign 61801.
Abstract:
The relationship among inhibition of acetylcholinesterase (AChE), inhibition of neuropathy target enzyme (NTE), and developmental toxicity of the organophosphorus ester desbromoleptophos (DBL) was evaluated in chicks exposed on day 3 or day 15 of incubation or 10 days posthatching. DBL induced prolonged inhibition of AChE and NTE when administered either early or late in incubation, structural malformations if administered before organogenesis, posthatching paresis if administered after organogenesis, and delayed deficits of gait if administered after hatching. The posthatching paresis and abnormal gait are not determined solely by either AChE inhibition of NTE inhibition, since they occur in the absence of the latter and are not invariably seen in the presence of the former (Toxicology 49: 253-261; 1988).
Insights
Organophosphorus ester desbromoleptophos (DBL) causes developmental toxicity in chicks. Neurological effects like paresis and gait deficits are not solely explained by acetylcholinesterase (AChE) or neuropathy target enzyme (NTE) inhibition.
Area of Science:
- Toxicology
- Neuroscience
- Developmental Biology
Background:
- Organophosphorus esters (OPs) are widely used pesticides.
- Understanding their toxicological mechanisms, including neurotoxicity and developmental effects, is crucial.
- Desbromoleptophos (DBL) is an OP ester whose specific toxicological profile requires detailed investigation.
Purpose of the Study:
- To investigate the relationship between acetylcholinesterase (AChE) inhibition, neuropathy target enzyme (NTE) inhibition, and the developmental toxicity of DBL.
- To determine the timing of DBL exposure and its impact on toxicity and neurological outcomes.
- To elucidate the specific roles of AChE and NTE inhibition in DBL-induced posthatching neurological deficits.
Main Methods:
- Chicks were exposed to DBL at different developmental stages: day 3 or 15 of incubation, and 10 days posthatching.
- Acetylcholinesterase (AChE) and neuropathy target enzyme (NTE) activities were measured.
- Developmental toxicity, including structural malformations, paresis, and gait abnormalities, was assessed.
Main Results:
- DBL induced prolonged inhibition of both AChE and NTE, regardless of exposure timing (early or late incubation).
- Exposure before organogenesis resulted in structural malformations.
- Exposure after organogenesis led to posthatching paresis.
- Exposure after hatching caused delayed gait deficits.
- Posthatching paresis and gait abnormalities were not solely dependent on AChE or NTE inhibition.
Conclusions:
- DBL exhibits significant developmental toxicity and neurotoxicity in chicks.
- The timing of DBL exposure critically influences the type of toxicity observed.
- The observed neurological effects suggest a complex mechanism of toxicity not fully explained by AChE or NTE inhibition alone.