The effect of isoniazide on myocardial tissue: protective role of cape

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dc.contributor.authorCil, Habib
dc.contributor.authorYavuz, Celal
dc.contributor.authorAtilgan, Zuhal Ariturk
dc.contributor.authorDemirtas, Sinan
dc.contributor.authorCaliskan, Ahmet
dc.contributor.authorGunduz, Ercan
dc.date.accessioned2024-04-24T17:38:19Z
dc.date.available2024-04-24T17:38:19Z
dc.date.issued2012
dc.departmentDicle Üniversitesien_US
dc.description.abstractAim: To investigate a toxic effect of Isoniazide on the myocardial tissue and protective role of the caffeic acid phenyl ester (CAPE). Material and methods: Animals: Male Sprague-Dawley rats were divided into four experimental groups, with ten animals in each group; Control, INH-treated group, CAPE treated group and INH plus CAPE-treated group. Biochemical analyses: Superoxide dismutase activity was measured according to the method described by Fridovich. Lipid peroxidation level in the myocardium was expressed as malondy-aldehyde (MDA). It was measured according to procedure of Ohkawa et al. The total antioxidant capacity of supernatant fractions was evaluated by using a novel automated and colorimetric measurement method developed by Erel (13). Histopathological analyses: Myocardial tissue specimens were fixed in 10% formaldehyde, dehydrated in alcohol solution and were embedded in paraffin for 24 hours and used for histopathological examination. Four micrometer (mu m) thick sections were cut, deparaffinized, hydrated and stained with hematoxyline and eosin (H&E) under a light microscope (Nikon Eclipse 80i, JAPAN). Results: In the INH group, malondialdehyde and total oxidant status levels were significantly higher than those of the control group in the myocardial tissues (p<0.05). In the INH group myocardial TAC levels, activities of SOD and PON-1 decreased compared with control group (p<0.05). CAPE plus INH treatment caused a significant decrease in MDA and TOS generation in the myocardium (p<0.05). Also, CAPE plus INH caused a significant an increase in TAC levels, SOD and PON-1 activities (p<0.05). Conclusion: We have shown that experimental administration of INH is accompanied by in-creased lipid peroxidation and oxidants in myocardial tissues of rats. Therefore, we suggest that oxidative stress is a cause of INH induced cardiotoxicity. Simultaneously, CAPE is a protective agent in this toxicity by overcoming the inactivation of antioxidant enzyme systems by INH. Thereby CAPE may play a role in preventing INH induced cardiotoxicity.en_US
dc.identifier.endpage3100en_US
dc.identifier.issn1840-2291
dc.identifier.issn1986-8103
dc.identifier.issue9en_US
dc.identifier.scopus2-s2.0-84869763884
dc.identifier.scopusqualityN/A
dc.identifier.startpage3095en_US
dc.identifier.urihttps://hdl.handle.net/11468/21405
dc.identifier.volume6en_US
dc.identifier.wosWOS:000311487500027
dc.identifier.wosqualityN/A
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.language.isoenen_US
dc.publisherDrunpp-Sarajevoen_US
dc.relation.ispartofHealthmed
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectIsoniazideen_US
dc.subjectMyocardial Toxicityen_US
dc.subjectCapeen_US
dc.titleThe effect of isoniazide on myocardial tissue: protective role of capeen_US
dc.titleThe effect of isoniazide on myocardial tissue: protective role of cape
dc.typeArticleen_US

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