COGNITIVE AND NEURO-ENDOCRINE DISRUPTION OF LEAD AND MONOCROTOPHOS AND THEIR RELATION TO THYROTOXICITY IN PERINATALLY EXPOSED RATS

dc.contributor.advisorGOPALA REDDY, A (Major)
dc.contributor.advisorRAVI KUMAR, P
dc.contributor.advisorKONDAL REDDY, K
dc.contributor.advisorANAND KUMAR, A
dc.contributor.authorKALA KUMAR, B. D. P
dc.date.accessioned2017-06-10T17:40:11Z
dc.date.available2017-06-10T17:40:11Z
dc.date.issued2010-06
dc.descriptionTHESESen_US
dc.description.abstractABSTRACT : Thyroid hormone is essential for neuronal and glial genesis and also the time specific migration of neurons. Any change in the sequential neurodevelopment of foetus or the neonate would be manifested as behavioural abnormality in the adult life. In utero exposure to xenobiotics would interfere with the availability of maternal thyroid hormone to the foetus. Pesticides and heavy metals form a major chunk of the environmental pollutants that affect the behaviour of animals and human beings. Monocrotophos a widely used pesticide and lead a ubiquitous heavy metal are known neurotoxicants. The role of these two substances in thyroid disruption and subsequent developmental neurotoxicity was studied. Thirty pregnant female rats were divided into five groups. Group I was Sham. Methimazole (II), monocrotophos (III), lead acetate (IV) were administered singly and in combination (V) to assess the interaction. AChE, thyroid profile (TSH, T3 and T4), maternal behaviour, litter size, neonatal mortality, neurodevelopmental (brain wet weights, DNA, RNA and protein), neurobehavioural (auditory startle response, rope descent, mid air righting reflex, elevated plus maze, photoactometry and morris water maze) and neurochemical (acetyl choline and glutamate content of the brain) parameters were studied. Histopathology of thyroid and brain were conducted. Inhibition of AChE was < 20% in III and V. Thyroid profile decreased in II and T4 increased in IV. Maternal behaviour was significantly (p<0.01) interfered in III and V. Neurodevelopmental and neurobehavioural parameters did not reveal significant changes. Glutamate content was highest in group V indicating excitotoxicity. Thyroid was affected significantly in II, III and IV but not in V. Cerebral cortical layers were affected in groups II through V. The three layers of cerebellum either had abnormal arrangement or decreased cellularity in all treated groups. Thus, it is concluded that monocrotophos and lead acetate could act as thyroid disruptors and might have interfered with neurodevelopment during the perinatal exposure. Group V also affected neurodevelopment but did not affect thyroid histology suggesting other mechanisms could have contributed to the neurotoxicity.en_US
dc.identifier.urihttp://krishikosh.egranth.ac.in/handle/1/5810019316
dc.keywordsRATS; LEAD ; MONOCROTOPHOS; THYROTOXICITYen_US
dc.language.isoenen_US
dc.pages93en_US
dc.publisherSRI VENKATESWARA VETERINARY UNIVERSITY , TIRUPATI – 517502. (A.P.) INDIAen_US
dc.subVeterinary Pharmacologyen_US
dc.subjectnullen_US
dc.themeCOGNITIVE AND NEURO-ENDOCRINE DISRUPTION OF LEAD AND MONOCROTOPHOS AND THEIR RELATION TO THYROTOXICITY IN PERINATALLY EXPOSED RATSen_US
dc.these.typePh.Den_US
dc.titleCOGNITIVE AND NEURO-ENDOCRINE DISRUPTION OF LEAD AND MONOCROTOPHOS AND THEIR RELATION TO THYROTOXICITY IN PERINATALLY EXPOSED RATSen_US
dc.typeThesisen_US
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