Descartes 466 Int. A, Col. Villa Universidad, C.P. 80010 Culiacán, Sinaloa, México
+52 (667) 753-1584


Culiacán, Sin. México, DF.

Effects of ozone oxidative preconditioning on nitric oxide generation and cellular redox balance in a rat model of hepatic ischaemia–reperfusion

Título
Effects of ozone oxidative preconditioning on nitric oxide generation and cellular redox balance in a rat model of hepatic ischaemia–reperfusion
Autores

Ajamieh HH, Mene´ndez S, Martı´nez-Sa´ nchez G, Candelario-Jalil E, Re L, Giuliani A, Ferna´ ndez OSL. Effects of ozone oxidative preconditioning on nitric oxide generation and cellular redox balance in a rat model of hepatic ischaemia–reperfusion.

1, S. Mene´ndez2, G. Martı´nez-Sa´nchez1, E. Candelario-Jalil1, L. Re3, A. Giuliani4 and Olga Sonia Leo´n Ferna´ndez1 1 Center of Studies for Research and Biological Evaluation (CEIEB-IFAL-UH), University of Havana, Havana City, Cuba, 2 Ozone Research Center, Havana City, Cuba, 3 University of Ancona, Ancona, Italy and 4 Department of Chemistry and Medical Biochemistry, University of Milan, Milan, Italy

Revista o sitio electrónico (URL) donde se publicó

Liver International 2004, 24, 55–62

Ischaemia–reperfusion – liver damage – nitric oxide – ozone – ozone preconditioning

Abstract

Background

Many studies indicate that oxygen free-radical formation after reoxygenation of liver may initiate the cascade of hepatocellular injury. It has been demonstrated that controlled ozone administration may promote an oxidative preconditioning or adaptation to oxidative stress, preventing the damage induced by reactive oxygen species and protecting against liver ischaemia–reperfusion (I/R) injury. Aims: In the present study, the effects of ozone oxidative preconditioning (OzoneOP) on nitric oxide (NO) generation and the cellular redox balance have been studied.

Methods

Six groups of rats were classified as follows: (1) sham-operated; (2) sham-operated1L-NAME (No-nitro-L-arginine methyl ester);(3) I/R (ischaemia 90 min–reperfusion 90 min); (4) OzoneOP1I/R; (5) OzoneOP1L-NAME1I/R; and (6) L-NAME1I/R. The following parameters were measured: plasma transaminases (aspartateaminotransferase, alanine aminotransferase) as an index of hepatocellularinjury; in homogenates of hepatic tissue: nitrate/nitrite as an index of NO production; superoxide dismutase (SOD), catalase (CAT) and glutathione levels as markers of endogenous antioxidant system; and finally malondialdehyde14-hydroxyalkenals (MDA14-HDA) and total hydroperoxides (TH) as indicators of oxidative stress.

Results

A correspondence between liver damage and the increase of NO, CAT, TH, glutathione and MDA14-HDA concentrations were observed just as a decrease of SOD activity. OzoneOP prevented and attenuated hepatic damage in I/R and OzoneOP1L-NAME1I/R, respectively, in close relation with the above-mentioned parameters.

Conclusions

These results show that OzoneOP protected against liver I/R injury through mechanisms that promote a regulation of endogenous NO concentrations and maintenance of cellular redox balance. Ozone treatment may have important clinical implications, particularly in view of the increasing hepatic transplantation programs.

Regresar

Leave a reply