Role of Cytochrome P450-Dependent Monooxygenases and Polymorphic Variants of GSTT1 and GSTM1 Genes in the Formation of Brain Lesions in Individuals Chronically Exposed to Mercury
The metabolic test with antipyrine was performed, the relationship between genotypes of GSTT1 and GSTM1 polymorphisms were studied, and cotinine level was measured in 116 men chronically exposed to mercury. The individuals were divided in 4 groups depending on the diagnosis of chronic mercury intoxi...
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Veröffentlicht in: | Bulletin of experimental biology and medicine 2013-11, Vol.156 (1), p.15-18 |
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creator | Chernyak, Yu. I. Itskovich, V. B. D’yakovich, O. A. Kolesnikov, S. I. |
description | The metabolic test with antipyrine was performed, the relationship between genotypes of
GSTT1
and
GSTM1
polymorphisms were studied, and cotinine level was measured in 116 men chronically exposed to mercury. The individuals were divided in 4 groups depending on the diagnosis of chronic mercury intoxication. The changes in the parameters of antipyrine test were studied in linked samples (
N
= 62, 4 year interval); in patients with chronic mercury intoxication, the disease stage was taken into account. Inhibition of antipyrine metabolism, increased frequency of combination of GSTT1(0/0)/GSTM1(+) genotypes in patients with chronic mercury intoxication, and the specificity of cytochrome P450 inhibition with mercury suggest that disease progression is related to inhibition of cytochrome P450 isoforms in the brain that catalyze regulation of endogenous substrates. |
doi_str_mv | 10.1007/s10517-013-2266-2 |
format | Article |
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GSTT1
and
GSTM1
polymorphisms were studied, and cotinine level was measured in 116 men chronically exposed to mercury. The individuals were divided in 4 groups depending on the diagnosis of chronic mercury intoxication. The changes in the parameters of antipyrine test were studied in linked samples (
N
= 62, 4 year interval); in patients with chronic mercury intoxication, the disease stage was taken into account. Inhibition of antipyrine metabolism, increased frequency of combination of GSTT1(0/0)/GSTM1(+) genotypes in patients with chronic mercury intoxication, and the specificity of cytochrome P450 inhibition with mercury suggest that disease progression is related to inhibition of cytochrome P450 isoforms in the brain that catalyze regulation of endogenous substrates.</description><identifier>ISSN: 0007-4888</identifier><identifier>EISSN: 1573-8221</identifier><identifier>DOI: 10.1007/s10517-013-2266-2</identifier><identifier>PMID: 24319713</identifier><identifier>CODEN: BEXBAN</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Antipyrine - metabolism ; Biomedical and Life Sciences ; Biomedicine ; Brain damage ; Brain Diseases - chemically induced ; Brain Diseases - enzymology ; Cell Biology ; Cytochrome P-450 Enzyme System - metabolism ; Development and progression ; Genes ; Genetic Association Studies ; Genotype ; Glutathione transferase ; Glutathione Transferase - genetics ; Glutathione Transferase - metabolism ; Humans ; Internal Medicine ; Laboratory Medicine ; Male ; Mercury - toxicity ; Mercury Poisoning, Nervous System - enzymology ; Occupational Diseases - chemically induced ; Occupational Diseases - enzymology ; Occupational Exposure ; Pathology ; Physiological aspects ; Polymorphism, Genetic</subject><ispartof>Bulletin of experimental biology and medicine, 2013-11, Vol.156 (1), p.15-18</ispartof><rights>Springer Science+Business Media New York 2013</rights><rights>COPYRIGHT 2013 Springer</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c503t-8967b60f52c757324069ab3fc31556226eead918482658619bd5a2e5d37ebc053</citedby><cites>FETCH-LOGICAL-c503t-8967b60f52c757324069ab3fc31556226eead918482658619bd5a2e5d37ebc053</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10517-013-2266-2$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10517-013-2266-2$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,777,781,27906,27907,41470,42539,51301</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24319713$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chernyak, Yu. I.</creatorcontrib><creatorcontrib>Itskovich, V. B.</creatorcontrib><creatorcontrib>D’yakovich, O. A.</creatorcontrib><creatorcontrib>Kolesnikov, S. I.</creatorcontrib><title>Role of Cytochrome P450-Dependent Monooxygenases and Polymorphic Variants of GSTT1 and GSTM1 Genes in the Formation of Brain Lesions in Individuals Chronically Exposed to Mercury</title><title>Bulletin of experimental biology and medicine</title><addtitle>Bull Exp Biol Med</addtitle><addtitle>Bull Exp Biol Med</addtitle><description>The metabolic test with antipyrine was performed, the relationship between genotypes of
GSTT1
and
GSTM1
polymorphisms were studied, and cotinine level was measured in 116 men chronically exposed to mercury. The individuals were divided in 4 groups depending on the diagnosis of chronic mercury intoxication. The changes in the parameters of antipyrine test were studied in linked samples (
N
= 62, 4 year interval); in patients with chronic mercury intoxication, the disease stage was taken into account. Inhibition of antipyrine metabolism, increased frequency of combination of GSTT1(0/0)/GSTM1(+) genotypes in patients with chronic mercury intoxication, and the specificity of cytochrome P450 inhibition with mercury suggest that disease progression is related to inhibition of cytochrome P450 isoforms in the brain that catalyze regulation of endogenous substrates.</description><subject>Antipyrine - metabolism</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain damage</subject><subject>Brain Diseases - chemically induced</subject><subject>Brain Diseases - enzymology</subject><subject>Cell Biology</subject><subject>Cytochrome P-450 Enzyme System - metabolism</subject><subject>Development and progression</subject><subject>Genes</subject><subject>Genetic Association Studies</subject><subject>Genotype</subject><subject>Glutathione transferase</subject><subject>Glutathione Transferase - genetics</subject><subject>Glutathione Transferase - metabolism</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Laboratory Medicine</subject><subject>Male</subject><subject>Mercury - toxicity</subject><subject>Mercury Poisoning, Nervous System - enzymology</subject><subject>Occupational Diseases - chemically induced</subject><subject>Occupational Diseases - enzymology</subject><subject>Occupational Exposure</subject><subject>Pathology</subject><subject>Physiological aspects</subject><subject>Polymorphism, Genetic</subject><issn>0007-4888</issn><issn>1573-8221</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqFks1u1DAUhSMEokPhAdggS0iITYp_YjtZlqEdKs2ICga2lse5mXGV2IOdoOa1eEKcToEWgZAX_vvOke_1ybLnBJ8QjOWbSDAnMseE5ZQKkdMH2YxwyfKSUvIwm-EE5UVZlkfZkxivpi0W5HF2RAtGKknYLPv-0beAfIPmY-_NLvgO0GXBcf4O9uBqcD1aeef99bgFpyNEpF2NLn07dj7sd9agLzpY7fo4mSw-rdfkhkirFUELcElhHep3gM596HRvvZvIt0Gn4yXEtL8hLlxtv9l60G1E8_QOZ41u2xGdXe99hBr1Hq0gmCGMT7NHTaLg2e18nH0-P1vP3-fLD4uL-ekyNxyzPi8rITcCN5wamXpCCywqvWGNYYRzkfoFoOuKlEVJBS8FqTY11xR4zSRsDObsOHt98N0H_3WA2KvORgNtqx34ISoiy9T-qsL4_2ghBJO85CyhL_9Ar_wQXCokGaZnEso4_01tdQvKusb3QZvJVJ2meyl5VZFEnfyFSqOGzhrvoLHp_J7g1R3BDnTb76Jvh-lX4n2QHEATfIwBGrUPttNhVASrKXvqkD2Vsqem7CmaNC9uKxs2HdS_FD_DlgB6AGK6clsId0r_p-sPrpDgpw</recordid><startdate>20131101</startdate><enddate>20131101</enddate><creator>Chernyak, Yu. 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I. ; Itskovich, V. B. ; D’yakovich, O. A. ; Kolesnikov, S. I.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c503t-8967b60f52c757324069ab3fc31556226eead918482658619bd5a2e5d37ebc053</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Antipyrine - metabolism</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain damage</topic><topic>Brain Diseases - chemically induced</topic><topic>Brain Diseases - enzymology</topic><topic>Cell Biology</topic><topic>Cytochrome P-450 Enzyme System - metabolism</topic><topic>Development and progression</topic><topic>Genes</topic><topic>Genetic Association Studies</topic><topic>Genotype</topic><topic>Glutathione transferase</topic><topic>Glutathione Transferase - genetics</topic><topic>Glutathione Transferase - metabolism</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Laboratory Medicine</topic><topic>Male</topic><topic>Mercury - toxicity</topic><topic>Mercury Poisoning, Nervous System - enzymology</topic><topic>Occupational Diseases - chemically induced</topic><topic>Occupational Diseases - enzymology</topic><topic>Occupational Exposure</topic><topic>Pathology</topic><topic>Physiological aspects</topic><topic>Polymorphism, Genetic</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chernyak, Yu. 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GSTT1
and
GSTM1
polymorphisms were studied, and cotinine level was measured in 116 men chronically exposed to mercury. The individuals were divided in 4 groups depending on the diagnosis of chronic mercury intoxication. The changes in the parameters of antipyrine test were studied in linked samples (
N
= 62, 4 year interval); in patients with chronic mercury intoxication, the disease stage was taken into account. Inhibition of antipyrine metabolism, increased frequency of combination of GSTT1(0/0)/GSTM1(+) genotypes in patients with chronic mercury intoxication, and the specificity of cytochrome P450 inhibition with mercury suggest that disease progression is related to inhibition of cytochrome P450 isoforms in the brain that catalyze regulation of endogenous substrates.</abstract><cop>Boston</cop><pub>Springer US</pub><pmid>24319713</pmid><doi>10.1007/s10517-013-2266-2</doi><tpages>4</tpages></addata></record> |
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source | MEDLINE; SpringerLink Journals |
subjects | Antipyrine - metabolism Biomedical and Life Sciences Biomedicine Brain damage Brain Diseases - chemically induced Brain Diseases - enzymology Cell Biology Cytochrome P-450 Enzyme System - metabolism Development and progression Genes Genetic Association Studies Genotype Glutathione transferase Glutathione Transferase - genetics Glutathione Transferase - metabolism Humans Internal Medicine Laboratory Medicine Male Mercury - toxicity Mercury Poisoning, Nervous System - enzymology Occupational Diseases - chemically induced Occupational Diseases - enzymology Occupational Exposure Pathology Physiological aspects Polymorphism, Genetic |
title | Role of Cytochrome P450-Dependent Monooxygenases and Polymorphic Variants of GSTT1 and GSTM1 Genes in the Formation of Brain Lesions in Individuals Chronically Exposed to Mercury |
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