Effects of the Antifungal Agent Itraconazole on Proliferative Changes of the Forestomach Mucosa in Alloxan-induced Diabetic Rats
Alloxan-induced diabetic rats frequently exhibit proliferative lesions of squamous hyperplasia accompanied by chronic inflammation and Candida albicans infection in the forestomach, and some lesions progress to squamous cell carcinoma (SCC). Candida infection causes not only hyperplastic changes wit...
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| Veröffentlicht in: | Toxicologic pathology 2009-10, Vol.37 (6), p.790-798 |
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| creator | Sano, Tomoya Ozaki, Kiyokazu Kodama, Yasushi Matsuura, Tetsuro Narama, Isao |
| description | Alloxan-induced diabetic rats frequently exhibit proliferative lesions of squamous hyperplasia accompanied by chronic inflammation and Candida albicans infection in the forestomach, and some lesions progress to squamous cell carcinoma (SCC). Candida infection causes not only hyperplastic changes with inflammation but might also lead to SCC in human oral mucosa. Thus, the present study was conducted to examine the effects of the antifungal agent itraconazole (ITCZ) on proliferative and inflammatory changes of the forestomach in alloxan-induced diabetic WBN/Kob rats. Diabetes was induced by alloxan at fifteen weeks of age. Rats were allocated to three groups at forty-five weeks of age and were given ITCZ by gavage 0 (vehicle control), 5, and 10 mg/kg/day for four weeks, and they were sacrificed at the sixty-fifth week of age. Mucosal hyperplastic changes were consistently accompanied by inflammation and Candida infections in the 0 mg/kg group. These lesions were reduced by ITCZ (0 mg/kg; 100%, 5 mg/kg; 53.5%, 10 mg/kg; 61.5%). Squamous cell carcinoma was detected in three rats from the 0 mg/kg, but only one rat from the 10 mg/kg dose groups in this study. Itraconazole reduced the degree of mucosal hyperplasia, inflammatory changes, and Candida infection. Therefore, C. albicans infection was an important factor in pathogenesis of mucosal proliferation and inflammation. |
| doi_str_mv | 10.1177/0192623309344204 |
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Candida infection causes not only hyperplastic changes with inflammation but might also lead to SCC in human oral mucosa. Thus, the present study was conducted to examine the effects of the antifungal agent itraconazole (ITCZ) on proliferative and inflammatory changes of the forestomach in alloxan-induced diabetic WBN/Kob rats. Diabetes was induced by alloxan at fifteen weeks of age. Rats were allocated to three groups at forty-five weeks of age and were given ITCZ by gavage 0 (vehicle control), 5, and 10 mg/kg/day for four weeks, and they were sacrificed at the sixty-fifth week of age. Mucosal hyperplastic changes were consistently accompanied by inflammation and Candida infections in the 0 mg/kg group. These lesions were reduced by ITCZ (0 mg/kg; 100%, 5 mg/kg; 53.5%, 10 mg/kg; 61.5%). Squamous cell carcinoma was detected in three rats from the 0 mg/kg, but only one rat from the 10 mg/kg dose groups in this study. Itraconazole reduced the degree of mucosal hyperplasia, inflammatory changes, and Candida infection. Therefore, C. albicans infection was an important factor in pathogenesis of mucosal proliferation and inflammation.</description><identifier>ISSN: 0192-6233</identifier><identifier>EISSN: 1533-1601</identifier><identifier>DOI: 10.1177/0192623309344204</identifier><identifier>PMID: 19700660</identifier><language>eng</language><publisher>Los Angeles, CA: SAGE Publications</publisher><subject>Animals ; Antifungal Agents - pharmacology ; Biological and medical sciences ; Candida albicans ; Candidiasis - drug therapy ; Candidiasis - metabolism ; Candidiasis - pathology ; Cell Growth Processes - drug effects ; Cyclooxygenase 2 - metabolism ; Dermatology ; Diabetes Mellitus, Experimental - drug therapy ; Diabetes Mellitus, Experimental - metabolism ; Diabetes Mellitus, Experimental - microbiology ; Diabetes Mellitus, Experimental - pathology ; Diabetes. Impaired glucose tolerance ; Endocrine pancreas. Apud cells (diseases) ; Endocrinopathies ; Etiopathogenesis. Screening. Investigations. Target tissue resistance ; Female ; Gastric Mucosa - drug effects ; Gastric Mucosa - metabolism ; Gastric Mucosa - microbiology ; Gastric Mucosa - pathology ; Glycosuria - drug therapy ; Glycosuria - metabolism ; Glycosuria - microbiology ; Glycosuria - pathology ; Histocytochemistry ; Hyperglycemia - drug therapy ; Hyperglycemia - metabolism ; Hyperglycemia - microbiology ; Hyperglycemia - pathology ; Hyperplasia ; Itraconazole - pharmacology ; Medical sciences ; Proliferating Cell Nuclear Antigen - metabolism ; Rats ; Toxicology ; Tumors of the skin and soft tissue. 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Candida infection causes not only hyperplastic changes with inflammation but might also lead to SCC in human oral mucosa. Thus, the present study was conducted to examine the effects of the antifungal agent itraconazole (ITCZ) on proliferative and inflammatory changes of the forestomach in alloxan-induced diabetic WBN/Kob rats. Diabetes was induced by alloxan at fifteen weeks of age. Rats were allocated to three groups at forty-five weeks of age and were given ITCZ by gavage 0 (vehicle control), 5, and 10 mg/kg/day for four weeks, and they were sacrificed at the sixty-fifth week of age. Mucosal hyperplastic changes were consistently accompanied by inflammation and Candida infections in the 0 mg/kg group. These lesions were reduced by ITCZ (0 mg/kg; 100%, 5 mg/kg; 53.5%, 10 mg/kg; 61.5%). Squamous cell carcinoma was detected in three rats from the 0 mg/kg, but only one rat from the 10 mg/kg dose groups in this study. Itraconazole reduced the degree of mucosal hyperplasia, inflammatory changes, and Candida infection. Therefore, C. albicans infection was an important factor in pathogenesis of mucosal proliferation and inflammation.</description><subject>Animals</subject><subject>Antifungal Agents - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Candida albicans</subject><subject>Candidiasis - drug therapy</subject><subject>Candidiasis - metabolism</subject><subject>Candidiasis - pathology</subject><subject>Cell Growth Processes - drug effects</subject><subject>Cyclooxygenase 2 - metabolism</subject><subject>Dermatology</subject><subject>Diabetes Mellitus, Experimental - drug therapy</subject><subject>Diabetes Mellitus, Experimental - metabolism</subject><subject>Diabetes Mellitus, Experimental - microbiology</subject><subject>Diabetes Mellitus, Experimental - pathology</subject><subject>Diabetes. Impaired glucose tolerance</subject><subject>Endocrine pancreas. Apud cells (diseases)</subject><subject>Endocrinopathies</subject><subject>Etiopathogenesis. Screening. Investigations. Target tissue resistance</subject><subject>Female</subject><subject>Gastric Mucosa - drug effects</subject><subject>Gastric Mucosa - metabolism</subject><subject>Gastric Mucosa - microbiology</subject><subject>Gastric Mucosa - pathology</subject><subject>Glycosuria - drug therapy</subject><subject>Glycosuria - metabolism</subject><subject>Glycosuria - microbiology</subject><subject>Glycosuria - pathology</subject><subject>Histocytochemistry</subject><subject>Hyperglycemia - drug therapy</subject><subject>Hyperglycemia - metabolism</subject><subject>Hyperglycemia - microbiology</subject><subject>Hyperglycemia - pathology</subject><subject>Hyperplasia</subject><subject>Itraconazole - pharmacology</subject><subject>Medical sciences</subject><subject>Proliferating Cell Nuclear Antigen - metabolism</subject><subject>Rats</subject><subject>Toxicology</subject><subject>Tumors of the skin and soft tissue. Premalignant lesions</subject><issn>0192-6233</issn><issn>1533-1601</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkU1rVDEUhoModqzuXUk24urafF-zHMZWCy2K6PpyJvdkJiWT1CRX1FV_uneYoYJQXJ0D53nP10vIS87ect73Z4xbYYSUzEqlBFOPyIJrKTtuGH9MFvtyt6-fkGe13jDG33HFnpITbnvGjGELcnfuPbpWafa0bZEuUwt-ShuIdLnB1OhlK-Bygt85Is2Jfi45Bo8FWviBdLWFtMF79UUuWFvegdvS68nlCjQkuowx_4TUhTRODkf6PsAaW3D0C7T6nDzxECu-OMZT8u3i_OvqY3f16cPlannVOaVY65xcgx6NsesetNRaoOAarHFCOSsFQ69xVGDY6LiYMw7SqflKgVJxAU6ekjeHvrclf5_mLYddqA5jhIR5qkOvtLFCKP1_UiqmeynMTLID6UqutaAfbkvYQfk1cDbsDRr-NWiWvDo2n9Y7HP8Kjo7MwOsjANVB9AWSC_WeE9xqa-1-dnfgKmxwuMlTSfP7Hh78B4K3pO0</recordid><startdate>20091001</startdate><enddate>20091001</enddate><creator>Sano, Tomoya</creator><creator>Ozaki, Kiyokazu</creator><creator>Kodama, Yasushi</creator><creator>Matsuura, Tetsuro</creator><creator>Narama, Isao</creator><general>SAGE Publications</general><general>Sage Publications</general><scope>IQODW</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><scope>7T7</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>M7N</scope><scope>P64</scope></search><sort><creationdate>20091001</creationdate><title>Effects of the Antifungal Agent Itraconazole on Proliferative Changes of the Forestomach Mucosa in Alloxan-induced Diabetic Rats</title><author>Sano, Tomoya ; Ozaki, Kiyokazu ; Kodama, Yasushi ; Matsuura, Tetsuro ; Narama, Isao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c440t-c3ba5d669b7a53552e215a96c24c9320ef5ed4a60dc12ed41a3c49702e3412ac3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Animals</topic><topic>Antifungal Agents - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Candida albicans</topic><topic>Candidiasis - drug therapy</topic><topic>Candidiasis - metabolism</topic><topic>Candidiasis - pathology</topic><topic>Cell Growth Processes - drug effects</topic><topic>Cyclooxygenase 2 - metabolism</topic><topic>Dermatology</topic><topic>Diabetes Mellitus, Experimental - drug therapy</topic><topic>Diabetes Mellitus, Experimental - metabolism</topic><topic>Diabetes Mellitus, Experimental - microbiology</topic><topic>Diabetes Mellitus, Experimental - pathology</topic><topic>Diabetes. Impaired glucose tolerance</topic><topic>Endocrine pancreas. Apud cells (diseases)</topic><topic>Endocrinopathies</topic><topic>Etiopathogenesis. Screening. Investigations. Target tissue resistance</topic><topic>Female</topic><topic>Gastric Mucosa - drug effects</topic><topic>Gastric Mucosa - metabolism</topic><topic>Gastric Mucosa - microbiology</topic><topic>Gastric Mucosa - pathology</topic><topic>Glycosuria - drug therapy</topic><topic>Glycosuria - metabolism</topic><topic>Glycosuria - microbiology</topic><topic>Glycosuria - pathology</topic><topic>Histocytochemistry</topic><topic>Hyperglycemia - drug therapy</topic><topic>Hyperglycemia - metabolism</topic><topic>Hyperglycemia - microbiology</topic><topic>Hyperglycemia - pathology</topic><topic>Hyperplasia</topic><topic>Itraconazole - pharmacology</topic><topic>Medical sciences</topic><topic>Proliferating Cell Nuclear Antigen - metabolism</topic><topic>Rats</topic><topic>Toxicology</topic><topic>Tumors of the skin and soft tissue. Premalignant lesions</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sano, Tomoya</creatorcontrib><creatorcontrib>Ozaki, Kiyokazu</creatorcontrib><creatorcontrib>Kodama, Yasushi</creatorcontrib><creatorcontrib>Matsuura, Tetsuro</creatorcontrib><creatorcontrib>Narama, Isao</creatorcontrib><collection>Pascal-Francis</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><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Toxicologic pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sano, Tomoya</au><au>Ozaki, Kiyokazu</au><au>Kodama, Yasushi</au><au>Matsuura, Tetsuro</au><au>Narama, Isao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of the Antifungal Agent Itraconazole on Proliferative Changes of the Forestomach Mucosa in Alloxan-induced Diabetic Rats</atitle><jtitle>Toxicologic pathology</jtitle><addtitle>Toxicol Pathol</addtitle><date>2009-10-01</date><risdate>2009</risdate><volume>37</volume><issue>6</issue><spage>790</spage><epage>798</epage><pages>790-798</pages><issn>0192-6233</issn><eissn>1533-1601</eissn><abstract>Alloxan-induced diabetic rats frequently exhibit proliferative lesions of squamous hyperplasia accompanied by chronic inflammation and Candida albicans infection in the forestomach, and some lesions progress to squamous cell carcinoma (SCC). Candida infection causes not only hyperplastic changes with inflammation but might also lead to SCC in human oral mucosa. Thus, the present study was conducted to examine the effects of the antifungal agent itraconazole (ITCZ) on proliferative and inflammatory changes of the forestomach in alloxan-induced diabetic WBN/Kob rats. Diabetes was induced by alloxan at fifteen weeks of age. Rats were allocated to three groups at forty-five weeks of age and were given ITCZ by gavage 0 (vehicle control), 5, and 10 mg/kg/day for four weeks, and they were sacrificed at the sixty-fifth week of age. Mucosal hyperplastic changes were consistently accompanied by inflammation and Candida infections in the 0 mg/kg group. These lesions were reduced by ITCZ (0 mg/kg; 100%, 5 mg/kg; 53.5%, 10 mg/kg; 61.5%). Squamous cell carcinoma was detected in three rats from the 0 mg/kg, but only one rat from the 10 mg/kg dose groups in this study. Itraconazole reduced the degree of mucosal hyperplasia, inflammatory changes, and Candida infection. Therefore, C. albicans infection was an important factor in pathogenesis of mucosal proliferation and inflammation.</abstract><cop>Los Angeles, CA</cop><pub>SAGE Publications</pub><pmid>19700660</pmid><doi>10.1177/0192623309344204</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Antifungal Agents - pharmacology Biological and medical sciences Candida albicans Candidiasis - drug therapy Candidiasis - metabolism Candidiasis - pathology Cell Growth Processes - drug effects Cyclooxygenase 2 - metabolism Dermatology Diabetes Mellitus, Experimental - drug therapy Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Experimental - microbiology Diabetes Mellitus, Experimental - pathology Diabetes. Impaired glucose tolerance Endocrine pancreas. Apud cells (diseases) Endocrinopathies Etiopathogenesis. Screening. Investigations. Target tissue resistance Female Gastric Mucosa - drug effects Gastric Mucosa - metabolism Gastric Mucosa - microbiology Gastric Mucosa - pathology Glycosuria - drug therapy Glycosuria - metabolism Glycosuria - microbiology Glycosuria - pathology Histocytochemistry Hyperglycemia - drug therapy Hyperglycemia - metabolism Hyperglycemia - microbiology Hyperglycemia - pathology Hyperplasia Itraconazole - pharmacology Medical sciences Proliferating Cell Nuclear Antigen - metabolism Rats Toxicology Tumors of the skin and soft tissue. Premalignant lesions |
| title | Effects of the Antifungal Agent Itraconazole on Proliferative Changes of the Forestomach Mucosa in Alloxan-induced Diabetic Rats |
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