Abstract

Aim: A role of thyroid disruption in developmental neurotoxicity of monocrotophos (MCP) and lead is studied.

Materials and Methods: A total of 24 female rats after conception were randomized into four groups of six each and treated as follows: Group I - Sham was administered distilled water orally. Group II - A positive control was administered methyl methimazole at 0.02% orally in drinking water. Group III - MCP orally at 0.3 mg/kg and Group IV - Lead acetate at 0.2% orally in drinking water. The drug was administered from gestation day 3 through post-natal day 21 in all the groups. Acetylcholinesterase (AChE) inhibition, thyroid profile (thyroid stimulating hormone, T3 and T4), neurodevelopment (brain wet weights, DNA, RNA and protein), and neurobehavioral (elevated plus maze, photoactometry, and Morris water maze) parameters were assessed in pups. A histopathology of thyroid of dams and brain of progeny was conducted.

Results: Inhibition of AChE was <20%. Thyroid profile decreased in the treatment groups. Neurodevelopmental and neurobehavioral parameters did not reveal any significant changes. Thyroid architecture was affected significantly with MCP and lead. Cortical layers too were affected. The three layers of cerebellum either had abnormal arrangement or decreased cellularity in all treated groups relating to thyroid disruption.

Conclusion: MCP and lead might have affected the development of cerebrum and cerebellum via thyroid disruption leading to developmental neurotoxicity.

Details

Title
Developmental neurotoxicity of monocrotophos and lead is linked to thyroid disruption
Author
Developmental neurotoxicity of monocrotophos; lead is linked to thyroid disruption -
Pages
133-141
Publication year
2016
Publication date
Feb 2016
Publisher
Veterinary World
ISSN
09728988
e-ISSN
22310916
Source type
Scholarly Journal
Language of publication
English
ProQuest document ID
1776874620
Copyright
Copyright Veterinary World Feb 2016