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Effect of vitamin C on oxidative liver injury due to isoniazid in rats
Background: The aim of the present study was to investigate the effect of different doses of vitamin C on oxidative liver injury due to isoniazid (INH) in rats. Methods: Rats were divided into four subgroups, each containing 10 rats. Group 1 was the control group; group 2, INH 50 mg/kg per day; gr...
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Published in: | Pediatrics international 2010-02, Vol.52 (1), p.69-74 |
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description | Background: The aim of the present study was to investigate the effect of different doses of vitamin C on oxidative liver injury due to isoniazid (INH) in rats.
Methods: Rats were divided into four subgroups, each containing 10 rats. Group 1 was the control group; group 2, INH 50 mg/kg per day; group 3, INH 50 mg/kg per day + low‐dose vitamin C (100 mg/kg per day); group 4, INH 50 mg/kg per day + high‐dose vitamin C (1000 mg/kg per day). INH and vitamin C were administered into their stomachs through an oral tube. After 21 days, measurements were made in both serum and homogenized liver tissues. The levels of glutathione (GSH), superoxide dismutase (SOD) and other biochemical variables were measured. Malondialdehyde (MDA), glutathione peroxidase (GSH‐px) and vitamin C were measured using commercial kits.
Results: Aspartate amino transferase and alanine aminotransferase in group 2 were higher than those in groups 1, 3 and 4 (P < 0.008 for both). Serum and tissue levels of MDA in group 2 were higher than that in groups 1 and 3 (P < 0.008 for both). There was no difference in the SOD levels between the four groups (P= 0.095). Erythrocyte and tissue GSH in group 2 were higher than that in groups 1 and 3 (P < 0.008 for both). Interestingly, erythrocyte and tissue GSH in group 4 were lower than those in group 1 (P < 0.008 for both). Erythrocyte level of GSH‐px in group 2 was higher than that in groups 1 and 3 (P < 0.008 for both).
Conclusions: INH‐induced liver injury is associated with oxidative stress, and co‐administration of low‐dose vitamin C may reduce this damage effectively in a rat model. The antioxidant effect of high‐dose vitamin C does not seem more potent compared to the low dose. |
doi_str_mv | 10.1111/j.1442-200X.2009.02891.x |
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Methods: Rats were divided into four subgroups, each containing 10 rats. Group 1 was the control group; group 2, INH 50 mg/kg per day; group 3, INH 50 mg/kg per day + low‐dose vitamin C (100 mg/kg per day); group 4, INH 50 mg/kg per day + high‐dose vitamin C (1000 mg/kg per day). INH and vitamin C were administered into their stomachs through an oral tube. After 21 days, measurements were made in both serum and homogenized liver tissues. The levels of glutathione (GSH), superoxide dismutase (SOD) and other biochemical variables were measured. Malondialdehyde (MDA), glutathione peroxidase (GSH‐px) and vitamin C were measured using commercial kits.
Results: Aspartate amino transferase and alanine aminotransferase in group 2 were higher than those in groups 1, 3 and 4 (P < 0.008 for both). Serum and tissue levels of MDA in group 2 were higher than that in groups 1 and 3 (P < 0.008 for both). There was no difference in the SOD levels between the four groups (P= 0.095). Erythrocyte and tissue GSH in group 2 were higher than that in groups 1 and 3 (P < 0.008 for both). Interestingly, erythrocyte and tissue GSH in group 4 were lower than those in group 1 (P < 0.008 for both). Erythrocyte level of GSH‐px in group 2 was higher than that in groups 1 and 3 (P < 0.008 for both).
Conclusions: INH‐induced liver injury is associated with oxidative stress, and co‐administration of low‐dose vitamin C may reduce this damage effectively in a rat model. The antioxidant effect of high‐dose vitamin C does not seem more potent compared to the low dose.</description><identifier>ISSN: 1328-8067</identifier><identifier>EISSN: 1442-200X</identifier><identifier>DOI: 10.1111/j.1442-200X.2009.02891.x</identifier><identifier>PMID: 19496975</identifier><language>eng</language><publisher>Melbourne, Australia: Blackwell Publishing Asia</publisher><subject>Animals ; Antioxidants - pharmacology ; Antitubercular Agents - toxicity ; Ascorbic Acid - blood ; Ascorbic Acid - pharmacology ; Chemical and Drug Induced Liver Injury - physiopathology ; Disease Models, Animal ; Dose-Response Relationship, Drug ; glutathione ; Glutathione - blood ; Glutathione Peroxidase - blood ; hepatotoxicity ; isoniazid ; Isoniazid - toxicity ; Liver diseases ; Liver Function Tests ; Male ; Malondialdehyde - blood ; oxidative stress ; Oxidative Stress - drug effects ; Oxidative Stress - physiology ; Rats ; Rats, Wistar ; Rodents ; Superoxide Dismutase - blood ; Vitamin C</subject><ispartof>Pediatrics international, 2010-02, Vol.52 (1), p.69-74</ispartof><rights>2010 Japan Pediatric Society</rights><rights>Journal compilation © 2010 Japan Pediatric Society</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4861-bbb55e2e8d2f0888f448f8d59ebe9cc484919011bda53014cd3da6481d6ffe8c3</citedby><cites>FETCH-LOGICAL-c4861-bbb55e2e8d2f0888f448f8d59ebe9cc484919011bda53014cd3da6481d6ffe8c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19496975$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ergul, Yakup</creatorcontrib><creatorcontrib>Erkan, Tulay</creatorcontrib><creatorcontrib>Uzun, Hafize</creatorcontrib><creatorcontrib>Genc, Habibe</creatorcontrib><creatorcontrib>Altug, Tuncay</creatorcontrib><creatorcontrib>Erginoz, Ethem</creatorcontrib><title>Effect of vitamin C on oxidative liver injury due to isoniazid in rats</title><title>Pediatrics international</title><addtitle>Pediatr Int</addtitle><description>Background: The aim of the present study was to investigate the effect of different doses of vitamin C on oxidative liver injury due to isoniazid (INH) in rats.
Methods: Rats were divided into four subgroups, each containing 10 rats. Group 1 was the control group; group 2, INH 50 mg/kg per day; group 3, INH 50 mg/kg per day + low‐dose vitamin C (100 mg/kg per day); group 4, INH 50 mg/kg per day + high‐dose vitamin C (1000 mg/kg per day). INH and vitamin C were administered into their stomachs through an oral tube. After 21 days, measurements were made in both serum and homogenized liver tissues. The levels of glutathione (GSH), superoxide dismutase (SOD) and other biochemical variables were measured. Malondialdehyde (MDA), glutathione peroxidase (GSH‐px) and vitamin C were measured using commercial kits.
Results: Aspartate amino transferase and alanine aminotransferase in group 2 were higher than those in groups 1, 3 and 4 (P < 0.008 for both). Serum and tissue levels of MDA in group 2 were higher than that in groups 1 and 3 (P < 0.008 for both). There was no difference in the SOD levels between the four groups (P= 0.095). Erythrocyte and tissue GSH in group 2 were higher than that in groups 1 and 3 (P < 0.008 for both). Interestingly, erythrocyte and tissue GSH in group 4 were lower than those in group 1 (P < 0.008 for both). Erythrocyte level of GSH‐px in group 2 was higher than that in groups 1 and 3 (P < 0.008 for both).
Conclusions: INH‐induced liver injury is associated with oxidative stress, and co‐administration of low‐dose vitamin C may reduce this damage effectively in a rat model. The antioxidant effect of high‐dose vitamin C does not seem more potent compared to the low dose.</description><subject>Animals</subject><subject>Antioxidants - pharmacology</subject><subject>Antitubercular Agents - toxicity</subject><subject>Ascorbic Acid - blood</subject><subject>Ascorbic Acid - pharmacology</subject><subject>Chemical and Drug Induced Liver Injury - physiopathology</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Drug</subject><subject>glutathione</subject><subject>Glutathione - blood</subject><subject>Glutathione Peroxidase - blood</subject><subject>hepatotoxicity</subject><subject>isoniazid</subject><subject>Isoniazid - toxicity</subject><subject>Liver diseases</subject><subject>Liver Function Tests</subject><subject>Male</subject><subject>Malondialdehyde - blood</subject><subject>oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Oxidative Stress - physiology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Rodents</subject><subject>Superoxide Dismutase - blood</subject><subject>Vitamin C</subject><issn>1328-8067</issn><issn>1442-200X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><recordid>eNqNkE9P2zAYxq1p02CFrzBZu-yUzH8T-7ADKm1BqqAH0LhZTuxIztIY7ARaPv2ctWISp_nw-JX9ex69egCAGOU4nR9tjhkjGUHoIU8ic0SExPnuAzh9-_iYZkpEJlBRnoAvMbYIIVEK9hmcYMlkIUt-CpaLprH1AH0Dn92gt66Hc-h76HfO6ME9W9glCdD17Rj20IwWDh666HunX51J7zDoIZ6BT43uoj0_3jNwv1zcza-y9e3qen6xzmomCpxVVcW5JVYY0iAhRMOYaITh0lZW1olhEkuEcWU0pwiz2lCjCyawKdKaoqYz8P2Q-xj802jjoLYu1rbrdG_9GFVJKSeMcpHIb-_I1o-hT8spggkniFCeIHGA6uBjDLZRj8FtddgrjNTUtGrVVKiaCp1Eqr9Nq12yfj3mj9XWmn_GY7UJ-HkAXlxn9_8drDaLy2lK_uzgd3Gwuze_Dr9VUdKSq183K1Ws2OZSbrha0j-plZrA</recordid><startdate>201002</startdate><enddate>201002</enddate><creator>Ergul, Yakup</creator><creator>Erkan, Tulay</creator><creator>Uzun, Hafize</creator><creator>Genc, Habibe</creator><creator>Altug, Tuncay</creator><creator>Erginoz, Ethem</creator><general>Blackwell Publishing Asia</general><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7TK</scope><scope>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>201002</creationdate><title>Effect of vitamin C on oxidative liver injury due to isoniazid in rats</title><author>Ergul, Yakup ; Erkan, Tulay ; Uzun, Hafize ; Genc, Habibe ; Altug, Tuncay ; Erginoz, Ethem</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4861-bbb55e2e8d2f0888f448f8d59ebe9cc484919011bda53014cd3da6481d6ffe8c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animals</topic><topic>Antioxidants - pharmacology</topic><topic>Antitubercular Agents - toxicity</topic><topic>Ascorbic Acid - blood</topic><topic>Ascorbic Acid - pharmacology</topic><topic>Chemical and Drug Induced Liver Injury - physiopathology</topic><topic>Disease Models, Animal</topic><topic>Dose-Response Relationship, Drug</topic><topic>glutathione</topic><topic>Glutathione - blood</topic><topic>Glutathione Peroxidase - blood</topic><topic>hepatotoxicity</topic><topic>isoniazid</topic><topic>Isoniazid - toxicity</topic><topic>Liver diseases</topic><topic>Liver Function Tests</topic><topic>Male</topic><topic>Malondialdehyde - blood</topic><topic>oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Oxidative Stress - physiology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Rodents</topic><topic>Superoxide Dismutase - blood</topic><topic>Vitamin C</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ergul, Yakup</creatorcontrib><creatorcontrib>Erkan, Tulay</creatorcontrib><creatorcontrib>Uzun, Hafize</creatorcontrib><creatorcontrib>Genc, Habibe</creatorcontrib><creatorcontrib>Altug, Tuncay</creatorcontrib><creatorcontrib>Erginoz, Ethem</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Neurosciences Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Pediatrics international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ergul, Yakup</au><au>Erkan, Tulay</au><au>Uzun, Hafize</au><au>Genc, Habibe</au><au>Altug, Tuncay</au><au>Erginoz, Ethem</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of vitamin C on oxidative liver injury due to isoniazid in rats</atitle><jtitle>Pediatrics international</jtitle><addtitle>Pediatr Int</addtitle><date>2010-02</date><risdate>2010</risdate><volume>52</volume><issue>1</issue><spage>69</spage><epage>74</epage><pages>69-74</pages><issn>1328-8067</issn><eissn>1442-200X</eissn><abstract>Background: The aim of the present study was to investigate the effect of different doses of vitamin C on oxidative liver injury due to isoniazid (INH) in rats.
Methods: Rats were divided into four subgroups, each containing 10 rats. Group 1 was the control group; group 2, INH 50 mg/kg per day; group 3, INH 50 mg/kg per day + low‐dose vitamin C (100 mg/kg per day); group 4, INH 50 mg/kg per day + high‐dose vitamin C (1000 mg/kg per day). INH and vitamin C were administered into their stomachs through an oral tube. After 21 days, measurements were made in both serum and homogenized liver tissues. The levels of glutathione (GSH), superoxide dismutase (SOD) and other biochemical variables were measured. Malondialdehyde (MDA), glutathione peroxidase (GSH‐px) and vitamin C were measured using commercial kits.
Results: Aspartate amino transferase and alanine aminotransferase in group 2 were higher than those in groups 1, 3 and 4 (P < 0.008 for both). Serum and tissue levels of MDA in group 2 were higher than that in groups 1 and 3 (P < 0.008 for both). There was no difference in the SOD levels between the four groups (P= 0.095). Erythrocyte and tissue GSH in group 2 were higher than that in groups 1 and 3 (P < 0.008 for both). Interestingly, erythrocyte and tissue GSH in group 4 were lower than those in group 1 (P < 0.008 for both). Erythrocyte level of GSH‐px in group 2 was higher than that in groups 1 and 3 (P < 0.008 for both).
Conclusions: INH‐induced liver injury is associated with oxidative stress, and co‐administration of low‐dose vitamin C may reduce this damage effectively in a rat model. The antioxidant effect of high‐dose vitamin C does not seem more potent compared to the low dose.</abstract><cop>Melbourne, Australia</cop><pub>Blackwell Publishing Asia</pub><pmid>19496975</pmid><doi>10.1111/j.1442-200X.2009.02891.x</doi><tpages>6</tpages></addata></record> |
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subjects | Animals Antioxidants - pharmacology Antitubercular Agents - toxicity Ascorbic Acid - blood Ascorbic Acid - pharmacology Chemical and Drug Induced Liver Injury - physiopathology Disease Models, Animal Dose-Response Relationship, Drug glutathione Glutathione - blood Glutathione Peroxidase - blood hepatotoxicity isoniazid Isoniazid - toxicity Liver diseases Liver Function Tests Male Malondialdehyde - blood oxidative stress Oxidative Stress - drug effects Oxidative Stress - physiology Rats Rats, Wistar Rodents Superoxide Dismutase - blood Vitamin C |
title | Effect of vitamin C on oxidative liver injury due to isoniazid in rats |
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