ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Abstract: SA-PO593

Coenzyme Q-10 Protects Against Radiocontrast-Induced AKI by Regulating Heme Oxygenase-1 (HO-1) and Inducible Nitric Oxide Synthase (iNOS)

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Fernandes, Sheila Marques, Universidade de São Paulo (USP), São Paulo, Brazil
  • Vattimo, Maria De Fatima, Universidade de São Paulo (USP), São Paulo, Brazil
  • da Fonseca, Cassiane Dezoti, Universidade de São Paulo (USP), São Paulo, Brazil
  • Watanabe, Mirian, Universidade de São Paulo (USP), São Paulo, Brazil
  • Peres, Karina Batista, Universidade de São Paulo (USP), São Paulo, Brazil
  • Vasco, Carolina Ferreira, Universidade de São Paulo, São Paulo, Brazil
Background

Radiocontrast agents are thought to induce acute kidney injury in part through increased production of reactive oxygen species. Recently, we reported that IC reduced inulin clearance and increased urinary peroxides, nitric oxide and TBARS with consumption of antioxidant reserve, that were significantly attenuated by COQ-10 (Vattimo MFF, JASN 2016).The aim of this study is to examine if the renoprotective effect of COQ-10 is mediated by heme oxygenase-1 (HO-1) and inducible nitric oxide synthase (iNOS) in diabetic rats.

Methods

Adult male Wistar rats, randomized into 4 groups: Citrate - citrate buffer (streptozotocin vehicle); DM (streptozotocin, 65 mg/kg, iv).; DM+IC - DM animals that after 4 weeks received iodinated contrast (IC, 6 ml/kg, ip); DM+IC+CO-Q10 - DM preconditioned animals (COQ-10, (10 mg/kg, ip). Were evaluated gene expression and protein syntesis of heme oxygenase-1 (HO-1) and inducible nitric oxide synthase (iNOS) in CI-AKI in diabetic rats treated with COQ-10.

Results

Treatment with IC significantly incresed gene expression and reduced protein syntesis of HO-1 in diabetic rats compared the DM group. COQ-10 induced an elevation in gene expression and in the protein syntesis of HO-1. IC led to a increasing the levels of gene expression and protein syntesis of iNOS in the kidney rats diabetic. Treatment with COQ-10 was able to attenuate the increase in iNOS protein levels observed in DM+CI group.

Conclusion

The data highlighted that the regulation of HO-1 and iNOS can be point out as the mechanism involved in the renal protective effect of the COQ10 in the CI-AKI in diabetic rats, probably due to its anti-oxidative and anti-nitrosative effective.

Funding

  • Government Support - Non-U.S.