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Final Edit - "Xenobiotic"
[edit]The body removes xenobiotics by xenobiotic metabolism. This consists of the deactivation and the excretion of xenobiotics, and happens mostly in the liver. Excretion routes are urine, faeces, breath, and sweat. Hepatic enzymes are responsible for the metabolism of xenobiotics by first activating them (oxidation, reduction, hydrolysis and/or hydration of the xenobiotic), and then conjugating the active secondary metabolite with glucuronic acid, sulphuric acid, or glutathione, followed by excretion in bile or urine. An example of a group of enzymes involved in xenobiotic metabolism is hepatic microsomal cytochrome P450. These enzymes that metabolize xenobiotics are very important for the pharmaceutical industry, because they are responsible for the breakdown of medications.
Although the body is able to remove xenobiotics by reducing it to a less toxic form through xenobiotic metabolism then excreting it, it is also possible for it to be converted into a more toxic form in some cases. This process is referred to as bioactivation and can result in structural and functional changes to the microbiota.[1] Exposure to xenobiotics can disrupt the microbiome community structure, either by increasing or decreasing the size of certain bacterial populations depending on the substance. Functional changes that result vary depending on the substance and can include increased expression in genes involved in stress response and antibiotic resistance, changes in the levels of metabolites produced, etc.[2]
Organisms can also evolve to tolerate xenobiotics. An example is the co-evolution of the production of tetrodotoxin in the rough-skinned newt and the evolution of tetrodotoxin resistance in its predator, the Common Garter Snake. In this predator–prey pair, an evolutionary arms race has produced high levels of toxin in the newt and correspondingly high levels of resistance in the snake.[3] This evolutionary response is based on the snake evolving modified forms of the ion channels that the toxin acts upon, so becoming resistant to its effects.[4] Another example of a xenobiotic tolerance mechanism is the use of ATP-binding cassette (ABC) transporters, which is largely exhibited in insects.[5] Such transporters contribute to resistance by enabling the transport of toxins across the cell membrane, thus preventing accumulation of these substances within cells.
Theottlo (talk) 05:00, 20 November 2017 (UTC)
Original - "Xenobiotic"
[edit]Xenobiotic Metabolism The body removes xenobiotics by xenobiotic metabolism. This consists of the deactivation and the excretion of xenobiotics, and happens mostly in the liver. Excretion routes are urine, faeces, breath, and sweat. Hepatic enzymes are responsible for the metabolism of xenobiotics by first activating them (oxidation, reduction, hydrolysis and/or hydration of the xenobiotic), and then conjugating the active secondary metabolite with glucuronic acid, sulphuric acid, or glutathione, followed by excretion in bile or urine. An example of a group of enzymes involved in xenobiotic metabolism is hepatic microsomal cytochrome P450. These enzymes that metabolize xenobiotics are very important for the pharmaceutical industry, because they are responsible for the breakdown of medications.
Organisms can also evolve to tolerate xenobiotics. An example is the co-evolution of the production of tetrodotoxin in the rough-skinned newt and the evolution of tetrodotoxin resistance in its predator, the Common Garter Snake. In this predator–prey pair, an evolutionary arms race has produced high levels of toxin in the newt and correspondingly high levels of resistance in the snake. This evolutionary response is based on the snake evolving modified forms of the ion channels that the toxin acts upon, so becoming resistant to its effects.
--Theottlo (talk) 03:30, 9 October 2017 (UTC)
Edit - "Xenobiotic"
[edit]Xenobiotic Metabolism The body removes xenobiotics by xenobiotic metabolism. This consists of the deactivation and the excretion of xenobiotics, and happens mostly in the liver. Excretion routes are urine, faeces, breath, and sweat. Hepatic enzymes are responsible for the metabolism of xenobiotics by first activating them (oxidation, reduction, hydrolysis and/or hydration of the xenobiotic), and then conjugating the active secondary metabolite with glucuronic acid, sulphuric acid, or glutathione, followed by excretion in bile or urine. An example of a group of enzymes involved in xenobiotic metabolism is hepatic microsomal cytochrome P450. These enzymes that metabolize xenobiotics are very important for the pharmaceutical industry, because they are responsible for the breakdown of medications.
Although the body is able to remove xenobiotics by reducing it to a less toxic form through xenobiotic metabolism then excreting it, it is also possible for it to be converted into a more toxic form in some cases. This process is referred to as bioactivation.[1] Various studies have analyzed the effects of this on the gut microbiota—particularly the structural and functional effects. Studies performed on typical substances such as antibiotics, pesticides, air pollutants, polychlorinated biphenyls (PCBs), and heavy metals show that exposure can disrupt the gut microbiome community structure, either by increasing or decreasing the size of certain bacterial populations depending on the substance. Building on this research, other studies observed the functional effects of these changes in the gut microbiome community structure upon exposure to antibiotics and arsenic. In the case of antibiotics, increased expression in genes involved in stress response and antibiotic resistance was observed, creating an environment that selects for antibiotic resistant bacteria. As for exposure to arsenic, there were changes in the levels of metabolites produced—either increased or decreased depending on the particular metabolite.[2]
Organisms can also evolve to tolerate xenobiotics. An example is the co-evolution of the production of tetrodotoxin in the rough-skinned newt and the evolution of tetrodotoxin resistance in its predator, the Common Garter Snake. In this predator–prey pair, an evolutionary arms race has produced high levels of toxin in the newt and correspondingly high levels of resistance in the snake.[3] This evolutionary response is based on the snake evolving modified forms of the ion channels that the toxin acts upon, so becoming resistant to its effects.[4] Various studies have shown that ATP-binding cassette (ABC) transporters play an important role in xenobiotic tolerance as they enable the transport of toxins across the cell membrane. This is particularly true with insects, as exhibited in Tribolium castaneum[5], and it is also involved in the fungus Clonostachys rosea.[6]
--Theottlo (talk) 03:30, 9 October 2017 (UTC)
- ^ a b Park, B.K.; Laverty, H.; Srivastava, A.; Antoine, D.J.; Naisbitt, D.; Williams, D.P. "Drug bioactivation and protein adduct formation in the pathogenesis of drug-induced toxicity". Chemico-Biological Interactions. 192 (1–2): 30–36. doi:10.1016/j.cbi.2010.09.011.
- ^ a b Lu, Kun; Mahbub, Ridwan; Fox, James G. (2015-08-31). "Xenobiotics: Interaction with the Intestinal Microflora". ILAR Journal. 56 (2): 218–227. doi:10.1093/ilar/ilv018. ISSN 1084-2020.
- ^ a b Brodie ED, Ridenhour BJ, Brodie ED (2002). "The evolutionary response of predators to dangerous prey: hotspots and coldspots in the geographic mosaic of coevolution between garter snakes and newts". Evolution. 56 (10): 2067–82. doi:10.1554/0014-3820(2002)056[2067:teropt]2.0.co;2. PMID 12449493.
- ^ a b Geffeney S, Brodie ED, Ruben PC, Brodie ED (2002). "Mechanisms of adaptation in a predator–prey arms race: TTX-resistant sodium channels". Science. 297 (5585): 1336–9. doi:10.1126/science.1074310. PMID 12193784.
- ^ a b Broehan, Gunnar; Kroeger, Tobias; Lorenzen, Marcé; Merzendorfer, Hans (2013-01-16). "Functional analysis of the ATP-binding cassette (ABC) transporter gene family of Tribolium castaneum". BMC Genomics. 14: 6. doi:10.1186/1471-2164-14-6. ISSN 1471-2164.
{{cite journal}}: CS1 maint: unflagged free DOI (link) - ^ Dubey, Mukesh K.; Jensen, Dan Funck; Karlsson, Magnus (2014-03-21). "An ATP-Binding Cassette Pleiotropic Drug Transporter Protein Is Required for Xenobiotic Tolerance and Antagonism in the Fungal Biocontrol Agent Clonostachys rosea". Molecular Plant-Microbe Interactions. 27 (7): 725–732. doi:10.1094/mpmi-12-13-0365-r. ISSN 0894-0282.