Protective effect of L-carnitine on experimental lead toxicity in rats: a clinical, histopathological and immunohistochemical study

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dc.authoridAytekin, Ismail/0000-0001-6794-5453
dc.contributor.authorOzsoy, S. Y.
dc.contributor.authorOzsoy, B.
dc.contributor.authorOzyildiz, Z.
dc.contributor.authorAytekin, I.
dc.date.accessioned2024-09-18T20:26:39Z
dc.date.available2024-09-18T20:26:39Z
dc.date.issued2011
dc.departmentHatay Mustafa Kemal Üniversitesien_US
dc.description.abstractFemale Wistar-albino rats were given lead acetate (PbAc) for 60 days to investigate the protective effects of L-carnitine (CA) clinically and histopathologically on PbAc-induced tissue damage. Blood samples were obtained from the jugular vein for hemoglobin (HB), hematocrit (HCT), red blood cells (RBC), white blood cells (WBC), platelets (PLT), aspartate aminotransferase (AST), alanine aminotransferase (ALT) and creatinine. PbAc treatment caused a significant decrease in HB, HCT and RBC, a significant increase in WBC, AST, ALT and creatinine compared to controls. Although administration of CA did not reverse HB and HCT values, it reversed both the decrease in RBC and the increase in WBC, AST, ALT and creatinine. After the experimental period, all rats were weighed, then decapitated for pathological examination. Control rat liver, kidney and brain showed normal histological architecture. Lead-induced nephropathic kidneys; degenerative changes, inflammation and portal edema of the liver; and brain neuropil vacuolation, neuronal vacuolation, satellitosis and neuronophagia were observed in experimental groups. All changes were reduced in the PbAc group treated with CA (PbAc + CA). PbAc caused copper/zinc superoxide dismutase (Cu/Zn-SOD) expression in both the hepatocytes and tubular epithelium of the kidney. PbAc + CA exposure caused moderate Cu/Zn-SOD immunoreactivity. While in the brain sections of the PbAc group the degenerative neurons were stained intensely with anti-ubiquitin antibody, PbAc + CA rats showed moderate staining in neurons with anti-ubiquitin antibody. These results show that CA as a food additive reduced the severity of tissue damage caused by PbAc.en_US
dc.identifier.doi10.3109/10520295.2010.529825
dc.identifier.endpage443en_US
dc.identifier.issn1052-0295
dc.identifier.issn1473-7760
dc.identifier.issue6en_US
dc.identifier.pmid21039307en_US
dc.identifier.scopus2-s2.0-81255205048en_US
dc.identifier.scopusqualityQ2en_US
dc.identifier.startpage436en_US
dc.identifier.urihttps://doi.org/10.3109/10520295.2010.529825
dc.identifier.urihttps://hdl.handle.net/20.500.12483/10458
dc.identifier.volume86en_US
dc.identifier.wosWOS:000297022600008en_US
dc.identifier.wosqualityQ4en_US
dc.indekslendigikaynakWeb of Scienceen_US
dc.indekslendigikaynakScopusen_US
dc.indekslendigikaynakPubMeden_US
dc.language.isoenen_US
dc.publisherTaylor & Francis Ltden_US
dc.relation.ispartofBiotechnic & Histochemistryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjecthematologyen_US
dc.subjecthistopathologyen_US
dc.subjectimmunohistochemistryen_US
dc.subjectL-carnitineen_US
dc.subjectlead-toxicityen_US
dc.subjectraten_US
dc.titleProtective effect of L-carnitine on experimental lead toxicity in rats: a clinical, histopathological and immunohistochemical studyen_US
dc.typeArticleen_US

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