title: HO-1 induction attenuates renal damage and oxidative stress induced by K2Cr2O7.
abstract: Heme oxygenase (HO) is the rate-limiting enzyme in the degradation of heme; its inducible isozyme HO-1 protects against some types of acute tissue injury. The expression and functional role of HO-1 in rats with renal injury induced by potassium dichromate (K(2)Cr(2)O(7)) was investigated in this work. Rats were studied 24 h after a single injection of K(2)Cr(2)O(7). To address the possible protective effect of HO-1 in this experimental model, this enzyme was induced by an injection of stannous chloride (SnCl(2)) 12 h before K(2)Cr(2)O(7) administration. The functional role of HO-1 in K(2)Cr(2)O(7) + SnCl(2)-treated animals was tested by inhibiting HO activity with an injection of zinc (II) protoporphyrin IX (ZnPP) 18 h before K(2)Cr(2)O(7). In K(2)Cr(2)O(7)-treated rats: (i) renal HO-1 content, measured by Western blot, increased 2.6-fold; and, (ii) renal nitrotyrosine and protein carbonyl content, markers of oxidative stress, increased 3.5- and 1.36-fold, respectively. Renal damage and oxidative stress were ameliorated and HO-1 content was increased in the K(2)Cr(2)O(7) + SnCl(2) group. The attenuation of renal injury and oxidative stress was lost by the inhibition of HO activity in K(2)Cr(2)O(7) + SnCl(2) + ZnPP-treated animals. Our data suggest that HO-1 overexpression induced by SnCl(2) is responsible for the attenuation of renal damage and oxidative stress induced by K(2)Cr(2)O(7).
authors.affiliation: Department of Biology, School of Chemistry, Universidad Nacional Autónoma de México, Ciudad Universitaria, 04510 Mexico City, Mexico.
authors.forename: Diana
authors.initials: D
authors.lastname: Barrera
authors.forename: Perla D
authors.initials: PD
authors.lastname: Maldonado
authors.forename: Omar N
authors.initials: ON
authors.lastname: Medina-Campos
authors.forename: Rogelio
authors.initials: R
authors.lastname: Hernández-Pando
authors.forename: María E
authors.initials: ME
authors.lastname: Ibarra-Rubio
authors.forename: José
authors.initials: J
authors.lastname: Pedraza-Chaverrí
authors.forename: José
authors.initials: J
authors.lastname: Pedraza-Chaverrrí
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002424:Caustics / Q000633:toxicity*; D003404:Creatinine / Q000378:metabolism; D004790:Enzyme Induction; D006419:Heme Oxygenase (Decyclizing) / Q000037:antagonists & inhibitors / Q000096:biosynthesis*; D051547:Heme Oxygenase-1; D007668:Kidney / Q000187:drug effects* / Q000201:enzymology; D007674:Kidney Diseases / Q000139:chemically induced / Q000201:enzymology / Q000517:prevention & control*; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D011192:Potassium Dichromate / Q000633:toxicity*; D011524:Protoporphyrins / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D017971:Tin Compounds / Q000494:pharmacology; D014443:Tyrosine / Q000031:analogs & derivatives* / Q000378:metabolism
chemical_list: D002424:Caustics; D011524:Protoporphyrins; D017971:Tin Compounds; C017803:zinc protoporphyrin; C023599:stannous chloride; C002744:3-nitrotyrosine; D014443:Tyrosine; D003404:Creatinine; D006419:Heme Oxygenase (Decyclizing); D051547:Heme Oxygenase-1; D011192:Potassium Dichromate