Impairment of Hepatic and Renal Functions by 2,5-Hexanedione Is Accompanied by Oxidative Stress in Rats
2,5-Hexanedione (2,5-HD) is the toxic metabolite of n-hexane which is widely used as solvent in numerous industries. The present study elucidated the precise mechanism of 2,5-HD in hepatorenal toxicity by determining the involvement of oxidative stress in rats. Adult male Wistar rats were exposed to...
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| Language: | English |
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Wiley
2014-01-01
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| Series: | Journal of Toxicology |
| Online Access: | http://dx.doi.org/10.1155/2014/239240 |
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| author | Isaac A. Adedara Amos O. Abolaji Blessing E. Odion Isioma J. Okwudi Abiola A. Omoloja Ebenezer O. Farombi |
| author_facet | Isaac A. Adedara Amos O. Abolaji Blessing E. Odion Isioma J. Okwudi Abiola A. Omoloja Ebenezer O. Farombi |
| author_sort | Isaac A. Adedara |
| collection | DOAJ |
| description | 2,5-Hexanedione (2,5-HD) is the toxic metabolite of n-hexane which is widely used as solvent in numerous industries. The present study elucidated the precise mechanism of 2,5-HD in hepatorenal toxicity by determining the involvement of oxidative stress in rats. Adult male Wistar rats were exposed to 0, 0.25, 0.5, and 1% 2,5-HD in drinking water for 21 days. Exposure to 2,5-HD caused liver and kidney atrophy evidenced by significant elevation in serum aminotransferases, alkaline phosphatase, albumin, bilirubin, urea, creatinine, and electrolytes levels compared with control. The marked dose-dependent increase in total cholesterol (TC), triglyceride (TG), and low-density lipoprotein (LDL) was accompanied with significant decrease in high-density lipoprotein (HDL) levels in 2,5-HD-exposed animals when compared with the control. Administration of 2,5-HD significantly diminished glutathione (GSH) level but increased the activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glutathione-S-transferase (GST) concomitantly with marked elevation in hydrogen peroxide (H2O2) and malondialdehyde (MDA) levels in liver and kidney of the treated groups compared with control. These findings suggest that undue exposure to 2,5-HD at environmentally relevant levels may impair liver and kidney functions through induction of oxidative stress. |
| format | Article |
| id | doaj-art-2c112dd53f4c436b909f80472ccacbce |
| institution | Kabale University |
| issn | 1687-8191 1687-8205 |
| language | English |
| publishDate | 2014-01-01 |
| publisher | Wiley |
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| series | Journal of Toxicology |
| spelling | doaj-art-2c112dd53f4c436b909f80472ccacbce2025-02-03T01:26:22ZengWileyJournal of Toxicology1687-81911687-82052014-01-01201410.1155/2014/239240239240Impairment of Hepatic and Renal Functions by 2,5-Hexanedione Is Accompanied by Oxidative Stress in RatsIsaac A. Adedara0Amos O. Abolaji1Blessing E. Odion2Isioma J. Okwudi3Abiola A. Omoloja4Ebenezer O. Farombi5Drug Metabolism & Toxicology Research Laboratories, Department of Biochemistry, College of Medicine, University of Ibadan, Ibadan 20005, NigeriaDrug Metabolism & Toxicology Research Laboratories, Department of Biochemistry, College of Medicine, University of Ibadan, Ibadan 20005, NigeriaDrug Metabolism & Toxicology Research Laboratories, Department of Biochemistry, College of Medicine, University of Ibadan, Ibadan 20005, NigeriaDrug Metabolism & Toxicology Research Laboratories, Department of Biochemistry, College of Medicine, University of Ibadan, Ibadan 20005, NigeriaDrug Metabolism & Toxicology Research Laboratories, Department of Biochemistry, College of Medicine, University of Ibadan, Ibadan 20005, NigeriaDrug Metabolism & Toxicology Research Laboratories, Department of Biochemistry, College of Medicine, University of Ibadan, Ibadan 20005, Nigeria2,5-Hexanedione (2,5-HD) is the toxic metabolite of n-hexane which is widely used as solvent in numerous industries. The present study elucidated the precise mechanism of 2,5-HD in hepatorenal toxicity by determining the involvement of oxidative stress in rats. Adult male Wistar rats were exposed to 0, 0.25, 0.5, and 1% 2,5-HD in drinking water for 21 days. Exposure to 2,5-HD caused liver and kidney atrophy evidenced by significant elevation in serum aminotransferases, alkaline phosphatase, albumin, bilirubin, urea, creatinine, and electrolytes levels compared with control. The marked dose-dependent increase in total cholesterol (TC), triglyceride (TG), and low-density lipoprotein (LDL) was accompanied with significant decrease in high-density lipoprotein (HDL) levels in 2,5-HD-exposed animals when compared with the control. Administration of 2,5-HD significantly diminished glutathione (GSH) level but increased the activities of superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glutathione-S-transferase (GST) concomitantly with marked elevation in hydrogen peroxide (H2O2) and malondialdehyde (MDA) levels in liver and kidney of the treated groups compared with control. These findings suggest that undue exposure to 2,5-HD at environmentally relevant levels may impair liver and kidney functions through induction of oxidative stress.http://dx.doi.org/10.1155/2014/239240 |
| spellingShingle | Isaac A. Adedara Amos O. Abolaji Blessing E. Odion Isioma J. Okwudi Abiola A. Omoloja Ebenezer O. Farombi Impairment of Hepatic and Renal Functions by 2,5-Hexanedione Is Accompanied by Oxidative Stress in Rats Journal of Toxicology |
| title | Impairment of Hepatic and Renal Functions by 2,5-Hexanedione Is Accompanied by Oxidative Stress in Rats |
| title_full | Impairment of Hepatic and Renal Functions by 2,5-Hexanedione Is Accompanied by Oxidative Stress in Rats |
| title_fullStr | Impairment of Hepatic and Renal Functions by 2,5-Hexanedione Is Accompanied by Oxidative Stress in Rats |
| title_full_unstemmed | Impairment of Hepatic and Renal Functions by 2,5-Hexanedione Is Accompanied by Oxidative Stress in Rats |
| title_short | Impairment of Hepatic and Renal Functions by 2,5-Hexanedione Is Accompanied by Oxidative Stress in Rats |
| title_sort | impairment of hepatic and renal functions by 2 5 hexanedione is accompanied by oxidative stress in rats |
| url | http://dx.doi.org/10.1155/2014/239240 |
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