Augmentation of hepatic and renal oxidative stress and disrupted glucose homeostasis by monocrotophos in streptozotocin-induced diabetic rats
► Monocrotophos significantly elevated the blood glucose levels in diabetic rats. ► Monocrotophos depleted liver glycogen content in diabetic rats. ► Monocrotophos increased gluconeogenetic enzyme activities in diabetic rats. ► Monocrotophos enhanced lipid peroxidation in kidney. ► Monocrotophos alt...
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| Veröffentlicht in: | Chemico-biological interactions 2011-09, Vol.193 (3), p.240-245 |
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| description | ► Monocrotophos significantly elevated the blood glucose levels in diabetic rats. ► Monocrotophos depleted liver glycogen content in diabetic rats. ► Monocrotophos increased gluconeogenetic enzyme activities in diabetic rats. ► Monocrotophos enhanced lipid peroxidation in kidney. ► Monocrotophos altered enzymatic antioxidants in liver and kidney of diabetic rats.
Several recent studies have demonstrated that organophosphorus insecticides (OPI) possess the potential to disrupt glucose homeostasis leading to hyperglycemia in experimental animals. The propensity of OPI to induce hyperglycemia along with oxidative stress may have far-reaching consequences on diabetic outcomes and associated complications. The primary objective of this study was to assess the potential of monocrotophos (MCP), an extensively used OPI, on hepatic and renal oxidative stress markers and dysregulation of hepatic glucose homeostasis in experimentally induced diabetic rats. Rats rendered diabetic by a single dose of streptozotocin (60
mg/kg b.w) were orally administered MCP (0.9
mg/kg b.w/d for 5
d). Monocrotophos
per se caused only a marginal increase in blood glucose levels but significantly elevated the blood glucose levels and also disrupted glucose homeostasis by depleting liver glycogen content and increasing the gluconeogenetic enzyme activities in diabetic rats. Experimentally induced diabetes was also associated with alterations in antioxidant enzymes in liver and kidney. MCP markedly enhanced lipid peroxidation in kidney and altered the enzymatic antioxidant defense mechanisms in both liver and kidney of diabetic rats. Collectively our data provides evidence that MCP has the propensity to augment the oxidative stress and further disrupt glucose homeostasis in diabetic rats. |
| doi_str_mv | 10.1016/j.cbi.2011.07.003 |
| format | Article |
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Several recent studies have demonstrated that organophosphorus insecticides (OPI) possess the potential to disrupt glucose homeostasis leading to hyperglycemia in experimental animals. The propensity of OPI to induce hyperglycemia along with oxidative stress may have far-reaching consequences on diabetic outcomes and associated complications. The primary objective of this study was to assess the potential of monocrotophos (MCP), an extensively used OPI, on hepatic and renal oxidative stress markers and dysregulation of hepatic glucose homeostasis in experimentally induced diabetic rats. Rats rendered diabetic by a single dose of streptozotocin (60
mg/kg b.w) were orally administered MCP (0.9
mg/kg b.w/d for 5
d). Monocrotophos
per se caused only a marginal increase in blood glucose levels but significantly elevated the blood glucose levels and also disrupted glucose homeostasis by depleting liver glycogen content and increasing the gluconeogenetic enzyme activities in diabetic rats. Experimentally induced diabetes was also associated with alterations in antioxidant enzymes in liver and kidney. MCP markedly enhanced lipid peroxidation in kidney and altered the enzymatic antioxidant defense mechanisms in both liver and kidney of diabetic rats. Collectively our data provides evidence that MCP has the propensity to augment the oxidative stress and further disrupt glucose homeostasis in diabetic rats.</description><identifier>ISSN: 0009-2797</identifier><identifier>EISSN: 1872-7786</identifier><identifier>DOI: 10.1016/j.cbi.2011.07.003</identifier><identifier>PMID: 21821013</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>Animals ; antioxidants ; blood glucose ; Blood Glucose - metabolism ; Catalase - metabolism ; defense mechanisms ; Diabetes ; Diabetes Mellitus, Experimental - metabolism ; Diabetes Mellitus, Experimental - pathology ; enzyme activity ; enzymes ; glucose ; Glucose homeostasis ; Glutathione - metabolism ; glycogen ; Glycogen - analysis ; homeostasis ; hyperglycemia ; Insecticides - toxicity ; Kidney - drug effects ; Kidney - enzymology ; Kidney - metabolism ; kidneys ; laboratory animals ; Lipid Peroxidation ; liver ; Liver - drug effects ; Liver - enzymology ; Liver - metabolism ; Male ; Monocrotophos ; Monocrotophos - toxicity ; oral administration ; Oxidative stress ; Oxidative Stress - drug effects ; Rats ; Rats, Wistar ; Streptozocin - toxicity ; streptozotocin ; Superoxide Dismutase - metabolism ; Tyrosine Transaminase - metabolism</subject><ispartof>Chemico-biological interactions, 2011-09, Vol.193 (3), p.240-245</ispartof><rights>2011 Elsevier Ireland Ltd</rights><rights>Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c376t-64df66d61edede990785f6b3af5864e93c5fb1cd687e2725d3d72205258ee04a3</citedby><cites>FETCH-LOGICAL-c376t-64df66d61edede990785f6b3af5864e93c5fb1cd687e2725d3d72205258ee04a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0009279711002444$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21821013$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Begum, Khamrunissa</creatorcontrib><creatorcontrib>Rajini, P.S.</creatorcontrib><title>Augmentation of hepatic and renal oxidative stress and disrupted glucose homeostasis by monocrotophos in streptozotocin-induced diabetic rats</title><title>Chemico-biological interactions</title><addtitle>Chem Biol Interact</addtitle><description>► Monocrotophos significantly elevated the blood glucose levels in diabetic rats. ► Monocrotophos depleted liver glycogen content in diabetic rats. ► Monocrotophos increased gluconeogenetic enzyme activities in diabetic rats. ► Monocrotophos enhanced lipid peroxidation in kidney. ► Monocrotophos altered enzymatic antioxidants in liver and kidney of diabetic rats.
Several recent studies have demonstrated that organophosphorus insecticides (OPI) possess the potential to disrupt glucose homeostasis leading to hyperglycemia in experimental animals. The propensity of OPI to induce hyperglycemia along with oxidative stress may have far-reaching consequences on diabetic outcomes and associated complications. The primary objective of this study was to assess the potential of monocrotophos (MCP), an extensively used OPI, on hepatic and renal oxidative stress markers and dysregulation of hepatic glucose homeostasis in experimentally induced diabetic rats. Rats rendered diabetic by a single dose of streptozotocin (60
mg/kg b.w) were orally administered MCP (0.9
mg/kg b.w/d for 5
d). Monocrotophos
per se caused only a marginal increase in blood glucose levels but significantly elevated the blood glucose levels and also disrupted glucose homeostasis by depleting liver glycogen content and increasing the gluconeogenetic enzyme activities in diabetic rats. Experimentally induced diabetes was also associated with alterations in antioxidant enzymes in liver and kidney. MCP markedly enhanced lipid peroxidation in kidney and altered the enzymatic antioxidant defense mechanisms in both liver and kidney of diabetic rats. Collectively our data provides evidence that MCP has the propensity to augment the oxidative stress and further disrupt glucose homeostasis in diabetic rats.</description><subject>Animals</subject><subject>antioxidants</subject><subject>blood glucose</subject><subject>Blood Glucose - metabolism</subject><subject>Catalase - metabolism</subject><subject>defense mechanisms</subject><subject>Diabetes</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetes Mellitus, Experimental - pathology</subject><subject>enzyme activity</subject><subject>enzymes</subject><subject>glucose</subject><subject>Glucose homeostasis</subject><subject>Glutathione - metabolism</subject><subject>glycogen</subject><subject>Glycogen - analysis</subject><subject>homeostasis</subject><subject>hyperglycemia</subject><subject>Insecticides - toxicity</subject><subject>Kidney - drug effects</subject><subject>Kidney - enzymology</subject><subject>Kidney - metabolism</subject><subject>kidneys</subject><subject>laboratory animals</subject><subject>Lipid Peroxidation</subject><subject>liver</subject><subject>Liver - drug effects</subject><subject>Liver - enzymology</subject><subject>Liver - metabolism</subject><subject>Male</subject><subject>Monocrotophos</subject><subject>Monocrotophos - toxicity</subject><subject>oral administration</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Streptozocin - toxicity</subject><subject>streptozotocin</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Tyrosine Transaminase - metabolism</subject><issn>0009-2797</issn><issn>1872-7786</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kcFuFSEUhonR2NvqA7hRdq5mBGYGZuKqadSaNHGhXRMGztzLzR0YOUzT-g6-s9ze6tKwAA7f_wPnJ-QNZzVnXH7Y13b0tWCc10zVjDXPyIb3SlRK9fI52TDGhkqoQZ2Rc8R92TLRspfkTPBeFIdmQ35frtsZQjbZx0DjRHewlLWlJjiaIJgDjffeldIdUMwJEB-PnMe0Lhkc3R5WGxHoLs4QMRv0SMcHOscQbYo5LruI1IdH8ZLjr1KyPlQ-uNXC0ciMcLwwmYyvyIvJHBBeP80X5Pbzpx9X19XNty9fry5vKtsomSvZuklKJzm4MoaBqb6b5NiYqetlC0Nju2nk1slegVCic41TQrBOdD0Aa01zQd6ffJcUf66AWc8eLRwOJkBcUff9wJUUnSwkP5HlL4gJJr0kP5v0oDnTxxD0XpcQ9DEEzZQuIRTN2yf3dZzB_VP87XoB3p2AyURttsmjvv1eHLoSkOzbThXi44mA0oU7D0mj9RBKw3wCm7WL_j8P-APtZqSs</recordid><startdate>20110930</startdate><enddate>20110930</enddate><creator>Begum, Khamrunissa</creator><creator>Rajini, P.S.</creator><general>Elsevier Ireland Ltd</general><scope>FBQ</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>7X8</scope></search><sort><creationdate>20110930</creationdate><title>Augmentation of hepatic and renal oxidative stress and disrupted glucose homeostasis by monocrotophos in streptozotocin-induced diabetic rats</title><author>Begum, Khamrunissa ; Rajini, P.S.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c376t-64df66d61edede990785f6b3af5864e93c5fb1cd687e2725d3d72205258ee04a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Animals</topic><topic>antioxidants</topic><topic>blood glucose</topic><topic>Blood Glucose - metabolism</topic><topic>Catalase - metabolism</topic><topic>defense mechanisms</topic><topic>Diabetes</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diabetes Mellitus, Experimental - pathology</topic><topic>enzyme activity</topic><topic>enzymes</topic><topic>glucose</topic><topic>Glucose homeostasis</topic><topic>Glutathione - metabolism</topic><topic>glycogen</topic><topic>Glycogen - analysis</topic><topic>homeostasis</topic><topic>hyperglycemia</topic><topic>Insecticides - toxicity</topic><topic>Kidney - drug effects</topic><topic>Kidney - enzymology</topic><topic>Kidney - metabolism</topic><topic>kidneys</topic><topic>laboratory animals</topic><topic>Lipid Peroxidation</topic><topic>liver</topic><topic>Liver - drug effects</topic><topic>Liver - enzymology</topic><topic>Liver - metabolism</topic><topic>Male</topic><topic>Monocrotophos</topic><topic>Monocrotophos - toxicity</topic><topic>oral administration</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Streptozocin - toxicity</topic><topic>streptozotocin</topic><topic>Superoxide Dismutase - metabolism</topic><topic>Tyrosine Transaminase - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Begum, Khamrunissa</creatorcontrib><creatorcontrib>Rajini, P.S.</creatorcontrib><collection>AGRIS</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Chemico-biological interactions</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Begum, Khamrunissa</au><au>Rajini, P.S.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Augmentation of hepatic and renal oxidative stress and disrupted glucose homeostasis by monocrotophos in streptozotocin-induced diabetic rats</atitle><jtitle>Chemico-biological interactions</jtitle><addtitle>Chem Biol Interact</addtitle><date>2011-09-30</date><risdate>2011</risdate><volume>193</volume><issue>3</issue><spage>240</spage><epage>245</epage><pages>240-245</pages><issn>0009-2797</issn><eissn>1872-7786</eissn><abstract>► Monocrotophos significantly elevated the blood glucose levels in diabetic rats. ► Monocrotophos depleted liver glycogen content in diabetic rats. ► Monocrotophos increased gluconeogenetic enzyme activities in diabetic rats. ► Monocrotophos enhanced lipid peroxidation in kidney. ► Monocrotophos altered enzymatic antioxidants in liver and kidney of diabetic rats.
Several recent studies have demonstrated that organophosphorus insecticides (OPI) possess the potential to disrupt glucose homeostasis leading to hyperglycemia in experimental animals. The propensity of OPI to induce hyperglycemia along with oxidative stress may have far-reaching consequences on diabetic outcomes and associated complications. The primary objective of this study was to assess the potential of monocrotophos (MCP), an extensively used OPI, on hepatic and renal oxidative stress markers and dysregulation of hepatic glucose homeostasis in experimentally induced diabetic rats. Rats rendered diabetic by a single dose of streptozotocin (60
mg/kg b.w) were orally administered MCP (0.9
mg/kg b.w/d for 5
d). Monocrotophos
per se caused only a marginal increase in blood glucose levels but significantly elevated the blood glucose levels and also disrupted glucose homeostasis by depleting liver glycogen content and increasing the gluconeogenetic enzyme activities in diabetic rats. Experimentally induced diabetes was also associated with alterations in antioxidant enzymes in liver and kidney. MCP markedly enhanced lipid peroxidation in kidney and altered the enzymatic antioxidant defense mechanisms in both liver and kidney of diabetic rats. Collectively our data provides evidence that MCP has the propensity to augment the oxidative stress and further disrupt glucose homeostasis in diabetic rats.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>21821013</pmid><doi>10.1016/j.cbi.2011.07.003</doi><tpages>6</tpages></addata></record> |
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| issn | 0009-2797 1872-7786 |
| language | eng |
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| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Animals antioxidants blood glucose Blood Glucose - metabolism Catalase - metabolism defense mechanisms Diabetes Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Experimental - pathology enzyme activity enzymes glucose Glucose homeostasis Glutathione - metabolism glycogen Glycogen - analysis homeostasis hyperglycemia Insecticides - toxicity Kidney - drug effects Kidney - enzymology Kidney - metabolism kidneys laboratory animals Lipid Peroxidation liver Liver - drug effects Liver - enzymology Liver - metabolism Male Monocrotophos Monocrotophos - toxicity oral administration Oxidative stress Oxidative Stress - drug effects Rats Rats, Wistar Streptozocin - toxicity streptozotocin Superoxide Dismutase - metabolism Tyrosine Transaminase - metabolism |
| title | Augmentation of hepatic and renal oxidative stress and disrupted glucose homeostasis by monocrotophos in streptozotocin-induced diabetic rats |
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