Open Access
Research
(Published
online:
08-02-2016)
5.
Developmental neurotoxicity of
monocrotophos and lead is linked to thyroid disruption -
B. Kala Kumar, A. Gopala Reddy, A. Vamsi Krishna, S. S. Y. H.
Quadri and P. Shiva Kumar
Veterinary World, 9(2): 133-141
doi:
10.14202/vetworld.2016.133-141
B. Kala Kumar:
Department of Veterinary Pharmacology & Toxicology, College of
Veterinary Science, Sri P.V. Narsimha Rao Telangana State
University for Veterinary, Animal and Fishery Science, Hyderabad
- 500 030, Telangana, India; bkalakumar@rediffmail.com
A. Gopala Reddy:
Department of Veterinary Pharmacology & Toxicology, College of
Veterinary Science, Sri P.V. Narsimha Rao Telangana State
University for Veterinary, Animal and Fishery Science, Hyderabad
- 500 030, Telangana, India; gopalaredddy123@rediffmail.com
A. Vamsi Krishna:
Department of Bio-technology, Ministry of Science & Technology,
New Delhi, India; vk.addanki@nic.in
S. S. Y. H. Quadri:
Department of Pathology, National Institute of Nutrition (ICMR),
Hyderabad, Telangana, India; ssyhq@yahoo.com
P. Shiva Kumar:
Sri P.V. Narsimha Rao Telangana State University for Veterinary,
Animal and Fishery Science, Hyderabad - 500 030, Telangana,
India; drshiva40@gmail.com
Received: 01-08-2015, Revised: 14-12-2015, Accepted: 25-12-2015,
Published online: 08-02-2016
Corresponding author:
P. Shiva Kumar, e-mail: drshiva40@gmail.com
Citation:
Kumar BK, Reddy AG, Krishna AV, Quadri SSYH, Kumar PS (2016)
Developmental neurotoxicity of monocrotophos and lead is linked
to thyroid disruption,
Veterinary World 9(2):
133-141.
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.
Keywords:
behavioral alterations, developmental neurotoxicity, lead,
monocrotophos, thyroid disruption.
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