NDLI: Role of midkine in cadmium-induced liver, heart and kidney damage.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Yazihan, Nuray Kocak, Mehtap Kacar Akcil, Ethem Erdem, Onur Sayal, Ahmet
Description	Country affiliation: Turkey Author Affiliation: Yazihan N ( Pathophysiology Department, Faculty of Medicine, Ankara University, Ankara, Turkey. nurayyazihan@yahoo.com)
Abstract	Accumulation of the widespread environmental toxin cadmium (Cd) in tissues results in toxicity. Cd, which can induce a broad spectrum of biological effects, is a toxic substance and is associated with inflammation and apoptosis. Midkine (MK) has fibrinolytic, antiapoptotic, transforming, angiogenetic and chemotactic activities. After Cd toxicity, we found increased MK expression in liver cells in an in vitro cell culture model. The aim of this study was to determine the possibility of relationship between tissue MK expression levels, tumor necrosis factor (TNF- ) levels and apoptosis in a chronic Cd toxicity model in rats. Male Wistar rats were exposed to Cd at the dose of 15 parts per million (ppm) for 8 weeks. MK levels were measured in kidney, heart and liver tissue by enzyme-linked-immunosorbent assay (ELISA). MK messenger RNA (mRNA) expression was evaluated by RT-PCR. Tissue apoptosis level was evaluated with tissue caspase-3 activity levels. Accumulation of Cd in liver is higher than the kidney and heart. Cd-treated rats had significantly higher tissue TNF- and caspase-3 levels when compared with the control rats (p < 0.001). MK mRNA and protein levels were also significantly upregulated in the Cd-treated group (p < 0.05, p < 0.001, respectively). When compared with apoptosis in tissues, it was more prominent in the liver than kidney and heart. MK level is found increased 3, 1.7 and 1.3× folds in liver, kidney and heart, respectively. Our results showed that chronic Cd administration induces inflammation and apoptosis in rat liver, kidney and heart. MK involved in damage mechanisms of Cd-induced tissues. Further studies will show the underlying mechanism of increased MK expression in Cd toxicity.
File Format	HTM / HTML
ISSN	09603271
Issue Number	5
Volume Number	30
e-ISSN	14770903
Journal	Human & Experimental Toxicology
Language	English
Publisher	Sage Publication
Publisher Date	2011-05-01
Publisher Place	Great Britain (UK)
Access Restriction	Subscribed
Subject Keyword	Discipline Toxicology Cadmium Chloride Toxicity Cytokines Physiology Environmental Pollutants Heart Drug Effects Kidney Liver Animals Apoptosis Immunology Pharmacokinetics Biosynthesis Pathology Male Myocardium Rats Rats, Wistar Tissue Distribution Up-regulation Journal Article
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Medicine Toxicology

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