title: Involvement of galectin-3 in cadmium-induced cardiac toxicity.
abstract: OBJECTIVE
  Accumulation of the wide spread environmental toxin cadmium (Cd) in tissues results in toxicity. Heart is one of the most effected tissues. Cd exposure induces inflammation in effected tissues. The present study was focused to evaluate roles of tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6) in Cd toxicity and their relationships with galectin-3 levels.
  
  
  METHODS
  In this experimental study, male Wistar rats were divided randomly to control and experimental groups. Experimental group was exposed to Cd at the dose of 15 ppm for 8 weeks (n=10/group). Inflammatory status in hearts was evaluated with measurement of tissue TNF-α and IL-6 levels. Histopathological examination of heart was carried out by light microscopy. Heart tissue caspase-3 level was used to identify apoptosis. Tissue galectin-3 level was evaluated by ELISA. Statistical difference between groups was evaluated by unpaired Student t-test, correlation was analyzed by Pearson's test.
  
  
  RESULTS
  Heart sizes were increased after Cd toxicity. A significant increase in galectin-3 tissue levels was seen after Cd toxicity, this was accompanied with a significant increase in the TNF-α (control: 402±39, Cd: 793±26 pg/g tissue, p<0.001) and IL-6 (control: 150±78, Cd: 325±65 pg/g tissue, p<0.001) levels. Histopathological examination under light microscope suggested a combination of ongoing necrosis and apoptosis. Increased caspase-3 levels were measured after Cd toxicity (control: 12±2, Cd: 18±3 pmol/µg/min, p<0.001).
  
  
  CONCLUSIONS
  Chronic Cd administration induces inflammation and apoptosis in rat hearts. Cadmium causes increased galectin-3 production from heart tissue. The formation of TNF-α due to Cd exposure may likely trigger this mechanism.
authors.affiliation: Department of Pathophysiology, Faculty of Medicine, Ankara University, Turkey. nurayyazihan@yahoo.com
authors.forename: Nuray
authors.initials: N
authors.lastname: Yazıhan
authors.forename: Mehtap Kaçar
authors.initials: MK
authors.lastname: Koçak
authors.forename: Ethem
authors.initials: E
authors.lastname: Akçıl
authors.forename: Onur
authors.initials: O
authors.lastname: Erdem
authors.forename: Ahmet
authors.initials: A
authors.lastname: Sayal
authors.forename: Cengiz
authors.initials: C
authors.lastname: Güven
authors.forename: Nalan
authors.initials: N
authors.lastname: Akyürek
mesh_terms: D000818:Animals; D017209:Apoptosis; D002104:Cadmium / Q000494:pharmacology* / Q000633:toxicity; D053148:Caspase 3 / Q000187:drug effects / Q000378:metabolism; D064420:Drug-Related Side Effects and Adverse Reactions / Q000378:metabolism / Q000473:pathology; D037502:Galectin 3 / Q000187:drug effects* / Q000378:metabolism; D006331:Heart Diseases / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology; D015850:Interleukin-6 / Q000378:metabolism; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D037502:Galectin 3; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D002104:Cadmium; D053148:Caspase 3