Toxicity and detoxification of imidacloprid in mouse ovarian follicles
type: CreativeWork
description: Neonicotinoids are synthetic nicotine derivates synthesized with high affinity for invertebrate nicotinic acetylcholine receptors (nAChRs) and comparatively low affinity for mammalian nAChRs. They are used in diverse industries ranging from commercial agriculture to veterinary pharmaceuticals, resulting in chronic exposure of nontarget species such as humans, birds, fish, and insect pollinators. Although neonicotinoids are considered insect selective, they can be activated in the environment and within mammals into more toxic metabolites. Imidacloprid (IMI) was the first neonicotinoid synthesized and continues to be the most popular member of the neonicotinoid family today. Mammals are exposed to IMI primarily through ingestion of contaminated food and water as well as through interactions with companion animals. IMI is readily absorbed in the gastrointestinal tract and undergoes phase I and phase II biotransformation in the liver prior to excretion primarily in the urine. In the liver, IMI is subjected to oxidations and reductions by cytochrome P450s (CYPs) and aldehyde oxidases (AOXs). Notably, IMI can be reduced to desnitro-imidacloprid (DNI), a protonated metabolite that binds mammalian nAChRs with much higher affinity than IMI. DNI as well as other redox intermediates are further modified to 6-hydroxynicotinic acid (6HNA) and 6-chloronicotinic acid (6CNA), which are the terminal phase I metabolites. IMI, 6HNA, and 6CNA have been detected in the ovaries of female animals within hours of exposure, verifying that the ovaries are exposed to IMI and IMI metabolites. Although some evidence exists that IMI is a reproductive toxicant, there are many unanswered questions regarding the effects of IMI on the ovaries. Thus, the studies described in my dissertation were designed to test the hypothesis that IMI causes ovarian follicle toxicity via acetylcholine pathways and the ovary itself contributes to this ovotoxicity using its metabolic machinery. In Chapter 3, I compar…
abstract: Neonicotinoids are synthetic nicotine derivates synthesized with high affinity for invertebrate nicotinic acetylcholine receptors (nAChRs) and comparatively low affinity for mammalian nAChRs. They are used in diverse industries ranging from commercial agriculture to veterinary pharmaceuticals, resulting in chronic exposure of nontarget species such as humans, birds, fish, and insect pollinators. Although neonicotinoids are considered insect selective, they can be activated in the environment and within mammals into more toxic metabolites. Imidacloprid (IMI) was the first neonicotinoid synthesized and continues to be the most popular member of the neonicotinoid family today. Mammals are exposed to IMI primarily through ingestion of contaminated food and water as well as through interactions with companion animals. IMI is readily absorbed in the gastrointestinal tract and undergoes phase I and phase II biotransformation in the liver prior to excretion primarily in the urine. In the liver, IMI is subjected to oxidations and reductions by cytochrome P450s (CYPs) and aldehyde oxidases (AOXs). Notably, IMI can be reduced to desnitro-imidacloprid (DNI), a protonated metabolite that binds mammalian nAChRs with much higher affinity than IMI. DNI as well as other redox intermediates are further modified to 6-hydroxynicotinic acid (6HNA) and 6-chloronicotinic acid (6CNA), which are the terminal phase I metabolites. IMI, 6HNA, and 6CNA have been detected in the ovaries of female animals within hours of exposure, verifying that the ovaries are exposed to IMI and IMI metabolites. Although some evidence exists that IMI is a reproductive toxicant, there are many unanswered questions regarding the effects of IMI on the ovaries. Thus, the studies described in my dissertation were designed to test the hypothesis that IMI causes ovarian follicle toxicity via acetylcholine pathways and the ovary itself contributes to this ovotoxicity using its metabolic machinery. In Chapter 3, I compar…
author: Mourikes, Vasiliki E
language: en
keywords: ovary, follicles, ovarian follicles, antral follicles, pesticide, pesticide toxicology, neonicotinoid, insecticide, imidacloprid, reproductive toxicology, toxicology
date published: 2024-12
date modified: 2026-07-22T22:25:03Z
provider: University of Illinois - Urbana-Champaign
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: University of Illinois at Urbana-Champaign

PropertyValue
property ID: Handle
value: https://hdl.handle.net/2142/127305