title: Sulforaphane decreases kidney injury after transplantation in rats: role of mitochondrial damage.
abstract: BACKGROUND
  Sulforaphane is a naturally occuring antioxidative and anti-inflammatory isothiocyanat. In this study, its impact on experimental kidney transplantation was evaluated.
  
  
  METHODS
  Male Brown Norway rats (n=112) were used as experimental animals. Donor kidneys were harvested and stored for 12 hours in HTK-solution at 4°C. D,L-Sulforaphane (4.4 mg/kg BW; 0.2ml) or normal saline (0.2 ml) was given i.v. to the recipients 24 and 1 hour before, and 6 hours after transplantation. Recipients were nephrectomized bilaterally and subsequently transplantation was performed. After 6 and 48 hours, biopsies were taken and processed for light and electron microscopy. Graft function was monitored using serum values of creatinine and BUN after 6 and 24 hours. Quantitative real-time PCR was used to detect differences in SOD2-gene expression after 6 hours and apoptotic activity was detected after 6 hours using propidium iodide flow cytometry.
  
  
  RESULTS
  Recipient preconditioning improved reperfusion damage index from 12.8±1.6 in controls to 8.8±1.8 (p<0.001). Serum levels of creatinine and BUN decreased from 4.29±0.25 mg/dl and 119±23 mg/dl in controls to 3.65±0.7 mg/dl and 81±19 mg/dl (p<0.05). The number of severely injured tubules decreased (p<0.05). Apoptotic activity was increased in SFN-treated rats. Mitochondrial microstructure was better preserved after SFN, while SOD 2 gene expression increased (p<0.05).
  
  
  CONCLUSIONS
  SFN ameliorates ischemia/reperfusion injury after KTx, most likely through anti-oxidative effects.
authors.affiliation: Department of General and Transplant Surgery, Ruprecht-Karls-University Heidelberg, Germany.
authors.forename: Albertas
authors.initials: A
authors.lastname: Cekauskas
authors.forename: Helge
authors.initials: H
authors.lastname: Bruns
authors.forename: Martynas
authors.initials: M
authors.lastname: Manikas
authors.forename: Ingrid
authors.initials: I
authors.lastname: Herr
authors.forename: Marie-Luise
authors.initials: ML
authors.lastname: Gross
authors.forename: Markus
authors.initials: M
authors.lastname: Zorn
authors.forename: Feliksas
authors.initials: F
authors.lastname: Jankevicius
authors.forename: Kestutis
authors.initials: K
authors.lastname: Strupas
authors.forename: Peter
authors.initials: P
authors.lastname: Schemmer
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology / Q000627:therapeutic use*; D017209:Apoptosis / Q000187:drug effects; D017879:Isothiocyanates / Q000494:pharmacology / Q000627:therapeutic use*; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D016030:Kidney Transplantation / Q000379:methods*; D008297:Male; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D051381:Rats; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D013454:Sulfoxides; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism; D000099156:Superoxide Dismutase 2
chemical_list: D000975:Antioxidants; D017879:Isothiocyanates; D013454:Sulfoxides; D013482:Superoxide Dismutase; D000099156:Superoxide Dismutase 2; C016766:sulforaphane