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TOX 4100 (1)
Lecture

TOX4100_GITract.pdf (1).pdf

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Department
Toxicology
Course
TOX 4100
Professor
Patricia Turner
Semester
Winter

Description
TOX*4100. Written by Garry Go Gastro-Intestinal Toxicity Some of the major functions of the alimentary tract include digestion, absorption, elimination, and defence. Characteristic of the upper alimentary tract is a stratified squamous epithelium (flattened epithelial cells) variable in terms of thickness and permeability. Upper GI tract includes: - Mouth - Pharynx - Esophagus - Stomach A chaotropic agent denatures macromolecules such as proteins and nucleic acids. Some notable agents that can affect the alimentary tract include acids, formaldehyde, glutaraldehyde, heavy metals (lead, mercury, etc.), and detergents. Trichothecene mycotoxins (a toxic secondary metabolite produced by the organisms of the fungi kingdom – like molds) are powerful inhibitors of protein synthesis. This is done by interaction with the ribosomes – structures within the cell responsible for protein synthesis. These mycotoxins can cause rapid irritation to the skin or the intestinal mucosa upon contact. They can cause lesions in the digestive tract. T-2 toxin is known as the most toxic trichothecene. T-2 toxins have the capability to inhibit eukaryotic protein synthesis as well as induce apoptosis. It has been shown that T-2 toxins can inhibit proliferation and Ig production in human lymphocytes. T-2 toxins can upregulate procaspase 3 and caspase 3 – apoptotic factors. Mild GI mucosal injury can manifest itself in pain, increased motility (vomiting, diarrhea), increased secretion (mucous, water, protein), and reduced digestion and absorption capabilities. Drugs such as NSAIDs, ibuprofen, and aspirin can cause ulcers as well as worsen their condition. NSAIDs inhibit two enzymes: COX-1 and COX-2. Both of these enzymes are responsible for the production of prostaglandins. Prostaglandins promote pain, fever, and inflammation. COX-1 is responsible for the production of the prostaglandin responsible for protecting the stomach’s lining. Inhibition of cyclooxygenase-1 (COX-1) increases the risk of ulcer development. Platelet and neutrophilic effects can b
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