3 edition of Selectivity and Molecular Mechanisms of Toxicity found in the catalog.
by Macmillan Pub Co
Written in English
|Contributions||E. A. Lock (Editor)|
|The Physical Object|
These chemicals destroy the outer coating of cells (such as sperm) and pathogens (such as enveloped viruses), which renders the latter non-infectious. While very effective at killing HIV and other sexually-transmitted pathogens in vitro, the selectivity index (i.e. the ratio of HIV inhibition to host cell toxicity). Toxicology and its types by Kashikant Yadav 1. • Industrial toxicology: • It is the study of selective and specific area of environmental toxicology. and molecular mechanisms of chemicals exert toxic effects on living organisms and how the biological system protects themselves against these adverse effects. • It aims at.
derstanding the mechanisms underlying chemically induced developmental defects. Perhaps the most influential review and assessment of the state of knowledge published in that expansionary phase of teratology was J.G. Wilson’s landmark book Environment and Birth Defects (). To this day, Wilson’s book is useful as a summary of the principles of teratogenesis (described . Mechanisms of antifungal action Griseofulvin The earliest inhibitory agent speciﬁc to fungal species was griseofulvin (Fig. 2). The precise mechanism of action of this compound is still unknown , but the favoured explanation is that it interferes with microtubule assem-bly. The selective toxicity of griseofulvin for fungi is onlyFile Size: 2MB.
Toxicity is the degree to which a chemical substance or a particular mixture of substances can damage an organism. Toxicity can refer to the effect on a whole organism, such as an animal, bacterium, or plant, as well as the effect on a substructure of the organism, such as a cell (cytotoxicity) or an organ such as the liver (hepatotoxicity).By extension, the word may be . Incorporation of nucleoside analogues by the mitochondrial DNA polymerase has been implicated as the primary cause underlying many of the toxic side effects of these drugs in HIV therapy. Recent success in reconstituting recombinant human enzyme has afforded a detailed mechanistic analysis of the reactions governing nucleotide selectivity of the polymerase and the Cited by:
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Toxicology of Impurities in Malathion: Potentiation of Malathion Toxicity and Lung Toxicity Caused by Trialkyl Phosphorothioates W. Aldridge, D. Dinsdale, B. Selectivity and Molecular Mechanisms of Toxicity.
Authors: Matteis, Francesco De, Lock, Edward A. Free Preview. The first section considers selected aspects of molecular mechanisms, including selectivity of toxic agents and repair processes in the nervous system, toxicity of oxygen, fibers and aflatoxins.
The second section discusses the interactions of carcinogens with DNA, and other targets, and their relevance to both molecular dosimetry of exposure and development of.
ISBN: OCLC Number: Notes: Based on a symposium held in Sept. at the University of Kent to mark the retirement of W. Norman Aldridge. Selectivity and molecular mechanisms of toxicity. New York: Macmillan, © (OCoLC) Online version: Selectivity and molecular mechanisms of toxicity.
New York: Macmillan, © (OCoLC) Document Type: Book: All Authors / Contributors: Francesco De Matteis; E A Lock. Essentially, this book is a discussion of the physical and chemical means which contribute to selectivity, and this is the basis of molecular pharmacology.
_Selective Toxicity began as a course of lectures that Professor F. Young encouraged me to give in University College London, in and again in 19 Molecular Mechanisms of Respiratory Toxicity James C. Bonner. Introduction Anatomy and Function of the Respiratory Tract Toxicant ]Induced Lung Injury, Remodeling, and Repair Occupational and Environmental Lung Diseases Suggested.
Reading 20 Molecular Mechanisms of Hepatotoxicity This chapter is focused on the fundamental principles of toxic mechanisms of injury. Toxicity is influenced by the amount of toxicant that reaches the target organ, the reactivity of the compound itself or metabolites that are formed by major biotransformation systems.
Mechanisms of Necrosis • Cells must synthesize endogenous molecules, assemble macromolecular complexes, membranes, and cell organelles, maintain intracellular environment, and produce energy for operation.
• Agents that disrupt these functions (especially energy-producing function of the mitochondria and protein synthesis) will cause cell death. An understanding of the mechanisms of toxicity provides a rational basis for interpreting descriptive toxicity data. The cellular mechanisms that contribute to the manifestation of toxicities are overviewed by relating a series of events that begins with exposure, involves a multitude of interactions between the invading toxicant and the organism, and culminates in a toxic effect.
Purchase Mechanisms of Cell Toxicity, Volume 20 - 1st Edition. Print Book & E-Book. ISBN Purchase Mechanisms of Toxicity and Metabolism - 1st Edition. Print Book & E-Book. ISBNBook Edition: 1. This module is focussed on understanding mechanisms of toxicity at the molecular level.
In a number of lectures and case-studies, molecular mechanisms underlying (organ-selective) toxicity and carcinogenicity will be discussed. Special emphasis will be on the role of drug metabolism and bio(in)activation in toxicology. In the following sections, the various direct mechanisms of acrolein toxicity such as protein and DNA adduction, and indirect mechanisms including induction of oxidative, mitochondrial, and ER stress, are critically discussed with possible connection to affected organs and pathological by: Extensively illustrated, this book forms a conceptual bridge between multiple events at the molecular level and the determinants of toxicity at the physiological and cellular level.
Specific examples of drugs, environmental pollutants. The neonicotinoids, the newest major class of insecticides, have outstanding potency and systemic action for crop protection against piercing-sucking pests, and they are highly effective for flea control on cats and dogs.
Their common names are acetamiprid, clothianidin, dinotefuran, imidacloprid, nitenpyram, thiacloprid, and thiamethoxam. They generally have low toxicity to Cited by: This volume provides an up-to-date review of the molecular mechanisms of toxicity.
Individual chapters deal with specific aspects of toxicity problems associated with selected organs. Contains a review of contemporary knowledge of the molecular mechanisms of toxicity as applied to various organsContrasts with other volumes in dealing with the mechanistic.
This review provides a basis for understanding aldehyde mechanisms and environmental toxicity through the context of electronic structure, electrophilicity, and nucleophile target selectivity. The common mechanism of toxicity for the different aldehyde subgroups suggests a significant potential for interaction among respective by: Molecular Mechanisms of Pesticide Toxicity.
DOI: / In book: Pesticides in the Modern World - Pests Control and Pesticides Exposure and Toxicity Assessment. This edited book is a compilation of findings on the molecular and cellular toxicity of nanoparticles (NPs) in animal cell, human cells, invertebrates.
The varied selection of test models will provide better understanding about the horizon of NPs toxicity. Such events involve many molecular, biochemical, and cellular processes that may act in isolation or in a complex combination to produce a given response.
Given the multitude of cells, organs, and pathways that underlie toxic mechanisms, it is unrealistic to discuss every possible mechanism of toxicity in this chapter.Molecular mechanisms of fluoride toxicity Article Literature Review (PDF Available) in Chemico-biological interactions (2) November.
Aluminum (Al) toxicity is one of the major constraints to agricultural production in acid soils. Molecular mechanisms of coping with Al toxicity have now been investigated in a range of plant species. Two main mechanisms of Al tolerance in plants are Al exclusion from the roots and the ability to tolerate Al in the by: 6.