Published December 1977
by Academic Press Inc.,U.S. .
Written in English
|The Physical Object|
|Number of Pages||250|
Compare book prices from over , booksellers. Find Biochemical Mechanisms of Paraquat Toxicity () by Autor, Anne P. Primary events in lung following exposure to toxic chemicals / Hanspeter Witschi, Kei-Ichi Hirai, and Michel G. Coté --Electron transfer reactions of paraquat / Anthony Ledwith --The pathology of the lung in paraquat poisoning / Donald Heath and Paul Smith --Importance of oxygen and of pulmonary alveolar surfactant in lung injury by paraquat. Electronic books Conference papers and proceedings Congresses: Additional Physical Format: Print version: Iowa Symposium on Toxic Mechanisms (1st: Iowa City). Biochemical mechanisms of paraquat toxicity. New York: Academic Press, (DLC) (OCoLC) Material Type: Conference publication, Document, Internet resource. As discussed later, the biochemical mechanism of paraquat toxicity is due to the cyclic oxidation and reduction that occurs in various tissues, especially lung, leading to production of superoxide anion and other free radicals; these chemical species react with polyunsaturated free radicals, eventually forming the highly destructive hydrogen peroxide.
The acute toxicity profile toxicity of paraquat demonstrates that in laboratory animals, paraquat is of moderate to high acute oral toxicity and high acute inhalational toxicity, but low dermal toxicity. Paraquat is a severe eye irritant, moderate skin irritantbut, not a skin sensitiser. Paraquat is moderately to highly acutely toxic. Paraquat is highly toxic and there is no antidote. One small accidental sip can be fatal. Paraquat is about 28 times more acutely toxic than glyphosate. Acute poisoning may occur through contact with skin, eyes, or via inhalation. There is now also increasing evidence that chronic exposure to paraquat is linked with adverse effects, for example. Paraquat causes direct damage when it comes into contact with the lining of the mouth, stomach, or intestines. After paraquat enters the body, it is distributed to all areas of the body. Paraquat causes toxic chemical reactions to occur throughout many parts of the body, primarily the lungs, liver, and kidneys. In contrast, paraquat toxicity in mice was increased by exposure to % oxygen and by deficiencies of the antioxidants selenium, vitamin E, or reduced glutahione (GSH). Paraquat, given IP to mice, at 30 mg/kg, decreased concentrations of the water-soluble antioxidant GSH in liver and lipid soluble antioxidants in lung.
Paraquat is moderately to highly toxic to many species of aquatic life including rainbow trout, bluegill, and channel catfish. At high levels, paraquat inhibits the photosynthesis of some algae in stream waters. Paraquat is rapidly excreted by animals, so tissue accumulation is unlikely. Paraquat is broken down and excreted via the kidneys. Very low steady exposure doesn’t cause poisoning because it’s being excreted all the time—there is no tissue accumulation in animals. You have to ingest or absorb a threshold amount over a couple days to become seriously ill from poisoning. This chapter focuses on the primary biochemical pathways altered in cyanide toxicity and the biological manifestations attributed to their inhibition. The rapidity of action and multiple toxic pathways contribute to the extreme lethality of cyanide and the complexities of effectively reversing or treating the toxicity. oxygen toxicity Irwin Fridovich and H. Moustafa Hassan Paraquat subverts electron flow from the normal cytochrome pathway and increases intracellular production of superoxide radical. This radical, which is the cause of paraquat toxicity, elicits increased synthesis of the .