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Effects of Obesity on Cholinergic an...

Kondakala, Sandeep Reddy.

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Effects of Obesity on Cholinergic and Noncholinergic Endpoints of Organophosphate Toxicity Following Chlorpyrifos Exposure in Standard and High Fat Diet Fed Animals.

Record Type:	Electronic resources : Monograph/item
Title/Author:	Effects of Obesity on Cholinergic and Noncholinergic Endpoints of Organophosphate Toxicity Following Chlorpyrifos Exposure in Standard and High Fat Diet Fed Animals./
Author:	Kondakala, Sandeep Reddy.
Published:	Ann Arbor : ProQuest Dissertations & Theses, : 2020,
Description:	157 p.
Notes:	Source: Dissertations Abstracts International, Volume: 82-06, Section: B.
Contained By:	Dissertations Abstracts International82-06B.
Subject:	Environmental science. -
Online resource:	https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=28158099
ISBN:	9798698593362

Effects of Obesity on Cholinergic and Noncholinergic Endpoints of Organophosphate Toxicity Following Chlorpyrifos Exposure in Standard and High Fat Diet Fed Animals.
Kondakala, Sandeep Reddy.

Effects of Obesity on Cholinergic and Noncholinergic Endpoints of Organophosphate Toxicity Following Chlorpyrifos Exposure in Standard and High Fat Diet Fed Animals. - Ann Arbor : ProQuest Dissertations & Theses, 2020 - 157 p.

Source: Dissertations Abstracts International, Volume: 82-06, Section: B.

Thesis (Ph.D.)--Mississippi State University, 2020.

This item must not be sold to any third party vendors.

Obesity is a prevalent disease in which, when compared to individuals of normal weight, obese individuals have noted pathophysiological alterations including increased adiposity and fat mass which may alter toxicokinetics of xenobiotics and therefore alter their toxicities. However, the effects of obesity and the altered pathophysiology accompanying this condition on the toxicity of many widely utilized pesticides have not been established. Organophosphate (OP) pesiticides, including chlorpyrifos (CPS), have historically been widely used for agricultural purposes. CPS and several other notable OPs are no longer registered for household use but still used mainly in agriculture by registered users. CPS is bioactivated to form chlorpyrifos-oxon (CPO) in liver by cytochrome P450 isozymes. Acute toxicity of CPS exposure is inhibition of acetylcholinesterase (AChE) in the central and peripheral nervous systems. The other targets following CPS exposure are the noncholinergic serine hydrolase enzymes: carboxylesterase (CES), fatty acid amide hydrolase (FAAH), and monoacylglycerol lipase (MAGL). Therefore the current study was designed to: 1) determine the time and concentration-dependent effects of CPS on noncholinergic endpoints of OP toxicity utilizing hepatoma cells under normal and steatotic conditions 2) determine if obese phenotype altered the toxicity of CPS, including both cholinergic and non-cholinergic endpoints and 3) determine the effects of high fat diet on CPS bioaccumulation and detoxication by determining CPS and 3,5,6-trichloro-2-pyridinol (TCP) levels at different time points. The current in vitro studies determined that CES is more sensitive to CPS mediated inhibition in normal and steatotic conditions compared to FAAH and MAGL. The in vivo studies determined that CPS (2 mg/kg) exposure produced a greater inhibitory effect on hepatic CES and FAAH in obese animals compared to lean animals which indicates that the obese animals may be at greater risk for CPS mediated alterations in hepatic lipid metabolism upon chronic exposure. Our toxicokinetic studies using a higher dose of CPS (25 mg/kg) did not inhibit AChE in CNS and did not alter the overall CPS levels between normal and obese animals. Peak levels of TCP were decreased in liver of obese animals at 3 hours and overall hepatic TCP levels were significantly decreased in obese animals.

ISBN: 9798698593362Subjects--Topical Terms:

677245
Environmental science.
Subjects--Index Terms:

Chlorpyrifos

Effects of Obesity on Cholinergic and Noncholinergic Endpoints of Organophosphate Toxicity Following Chlorpyrifos Exposure in Standard and High Fat Diet Fed Animals.
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520 $a Obesity is a prevalent disease in which, when compared to individuals of normal weight, obese individuals have noted pathophysiological alterations including increased adiposity and fat mass which may alter toxicokinetics of xenobiotics and therefore alter their toxicities. However, the effects of obesity and the altered pathophysiology accompanying this condition on the toxicity of many widely utilized pesticides have not been established. Organophosphate (OP) pesiticides, including chlorpyrifos (CPS), have historically been widely used for agricultural purposes. CPS and several other notable OPs are no longer registered for household use but still used mainly in agriculture by registered users. CPS is bioactivated to form chlorpyrifos-oxon (CPO) in liver by cytochrome P450 isozymes. Acute toxicity of CPS exposure is inhibition of acetylcholinesterase (AChE) in the central and peripheral nervous systems. The other targets following CPS exposure are the noncholinergic serine hydrolase enzymes: carboxylesterase (CES), fatty acid amide hydrolase (FAAH), and monoacylglycerol lipase (MAGL). Therefore the current study was designed to: 1) determine the time and concentration-dependent effects of CPS on noncholinergic endpoints of OP toxicity utilizing hepatoma cells under normal and steatotic conditions 2) determine if obese phenotype altered the toxicity of CPS, including both cholinergic and non-cholinergic endpoints and 3) determine the effects of high fat diet on CPS bioaccumulation and detoxication by determining CPS and 3,5,6-trichloro-2-pyridinol (TCP) levels at different time points. The current in vitro studies determined that CES is more sensitive to CPS mediated inhibition in normal and steatotic conditions compared to FAAH and MAGL. The in vivo studies determined that CPS (2 mg/kg) exposure produced a greater inhibitory effect on hepatic CES and FAAH in obese animals compared to lean animals which indicates that the obese animals may be at greater risk for CPS mediated alterations in hepatic lipid metabolism upon chronic exposure. Our toxicokinetic studies using a higher dose of CPS (25 mg/kg) did not inhibit AChE in CNS and did not alter the overall CPS levels between normal and obese animals. Peak levels of TCP were decreased in liver of obese animals at 3 hours and overall hepatic TCP levels were significantly decreased in obese animals.
590 $a School code: 0132.
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650 4 $a Veterinary services. $3 3433982
653 $a Chlorpyrifos
653 $a NAFLD
653 $a Obesity
653 $a Organophosphates
653 $a Toxicodynamics
653 $a Toxicokinetics
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690 $a 0778
710 2 $a Mississippi State University. $b Veterinary Medicine. $3 1263176
773 0 $t Dissertations Abstracts International $g 82-06B.
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