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Nitrite-derived nitric oxide by xanthine oxidoreductase protects the liver against ischemia-reperfusion injury.
Hepatobiliary Pancreat Dis Int. 2005 Aug; 4(3):350-5.HP

Abstract

BACKGROUND

It was demonstrated that xanthine oxidoreductase (XOR), during ischemia, catalyzes the formation of nitric oxide (NO) from nitrite (NO2-) and this NO2- -derived NO protects the isolated perfused rat heart against the damaging effects of ischemia-reperfusion (I/R) when conventional nitric oxide synthase (NOS)-dependent NO production is impaired. Liver is one of the organs with the highest XOR concentration. This study was designed to determine whether NO2- -derived NO by XOR protects liver against I/R injury in vivo. For its minute amounts and active reactivity, NO can not be detected directly in real time in vivo by this time. We have to prove the above hypothesis indirectly.

METHODS

Wistar rats were pretreated with saline, NOS inhibitor L-NAME (10 mg/kg intravenously), XOR inhibitor allopurinol (1.5 mg/kg orally), L-NAME +allopurinol and NO scavenger carboxy-PTIO (0.6 mg/kg intravenously) respectively (12 animals per group). And then, they were subjected to total liver ischemia for 40 minutes followed by reperfusion. Blood samples and liver tissues were obtained for analysis after 3 hours of reperfusion. Survival was also investigated.

RESULTS

Allopurinol-treated animals exhibited further increased serum alanine aminotransferase(ALT) levels and liver myeloperoxidase(MPO) activities, but further decreased liver adenosine triphosphate(ATP) stores after I/R compared to saline-treated counterparts (830.5+/-108.3 U/L, 56.5+/-11.0 U/mg protein and 1.93+/-0.47 mumol/g vs. 505.8+/-184.2 U/L, 41.5+/-10.2 U/mg protein and 3.05+/-0.55 micromol/g respectively, P < 0.01, P < 0.05 and P < 0.01 respectively). The hepatocyte injury was further exacerbated and the overall survival rate was significantly decreased after I/R in animals given by allopurinol compared to those pretreated by saline (P < 0.05). L-NAME and allopurinol co-treated animals exhibited more severe liver injury (P < 0.05 and P<0.01)and a further decreased overall survival rate (P < 0.05)compared to L-NAME or allopurinol alone-treated counterparts, but they were not different from carboxy-PTIO treated animals (P > 0.05).

CONCLUSION

NO2- -derived NO by XOR in the hypoxic and acidic environment induced by hepatic I/R protects the liver against I/R injury in vivo.

Authors+Show Affiliations

Department of General Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022, China. luliu@public.wh.hb.cnNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

16109514

Citation

Lu, Ping, et al. "Nitrite-derived Nitric Oxide By Xanthine Oxidoreductase Protects the Liver Against Ischemia-reperfusion Injury." Hepatobiliary & Pancreatic Diseases International : HBPD INT, vol. 4, no. 3, 2005, pp. 350-5.
Lu P, Liu F, Yao Z, et al. Nitrite-derived nitric oxide by xanthine oxidoreductase protects the liver against ischemia-reperfusion injury. Hepatobiliary Pancreat Dis Int. 2005;4(3):350-5.
Lu, P., Liu, F., Yao, Z., Wang, C. Y., Chen, D. D., Tian, Y., Zhang, J. H., & Wu, Y. H. (2005). Nitrite-derived nitric oxide by xanthine oxidoreductase protects the liver against ischemia-reperfusion injury. Hepatobiliary & Pancreatic Diseases International : HBPD INT, 4(3), 350-5.
Lu P, et al. Nitrite-derived Nitric Oxide By Xanthine Oxidoreductase Protects the Liver Against Ischemia-reperfusion Injury. Hepatobiliary Pancreat Dis Int. 2005;4(3):350-5. PubMed PMID: 16109514.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nitrite-derived nitric oxide by xanthine oxidoreductase protects the liver against ischemia-reperfusion injury. AU - Lu,Ping, AU - Liu,Fang, AU - Yao,Zhong, AU - Wang,Chun-You, AU - Chen,Dao-Da, AU - Tian,Yuan, AU - Zhang,Jing-Hui, AU - Wu,Yi-Hua, PY - 2005/8/20/pubmed PY - 2005/10/19/medline PY - 2005/8/20/entrez SP - 350 EP - 5 JF - Hepatobiliary & pancreatic diseases international : HBPD INT JO - Hepatobiliary Pancreat Dis Int VL - 4 IS - 3 N2 - BACKGROUND: It was demonstrated that xanthine oxidoreductase (XOR), during ischemia, catalyzes the formation of nitric oxide (NO) from nitrite (NO2-) and this NO2- -derived NO protects the isolated perfused rat heart against the damaging effects of ischemia-reperfusion (I/R) when conventional nitric oxide synthase (NOS)-dependent NO production is impaired. Liver is one of the organs with the highest XOR concentration. This study was designed to determine whether NO2- -derived NO by XOR protects liver against I/R injury in vivo. For its minute amounts and active reactivity, NO can not be detected directly in real time in vivo by this time. We have to prove the above hypothesis indirectly. METHODS: Wistar rats were pretreated with saline, NOS inhibitor L-NAME (10 mg/kg intravenously), XOR inhibitor allopurinol (1.5 mg/kg orally), L-NAME +allopurinol and NO scavenger carboxy-PTIO (0.6 mg/kg intravenously) respectively (12 animals per group). And then, they were subjected to total liver ischemia for 40 minutes followed by reperfusion. Blood samples and liver tissues were obtained for analysis after 3 hours of reperfusion. Survival was also investigated. RESULTS: Allopurinol-treated animals exhibited further increased serum alanine aminotransferase(ALT) levels and liver myeloperoxidase(MPO) activities, but further decreased liver adenosine triphosphate(ATP) stores after I/R compared to saline-treated counterparts (830.5+/-108.3 U/L, 56.5+/-11.0 U/mg protein and 1.93+/-0.47 mumol/g vs. 505.8+/-184.2 U/L, 41.5+/-10.2 U/mg protein and 3.05+/-0.55 micromol/g respectively, P < 0.01, P < 0.05 and P < 0.01 respectively). The hepatocyte injury was further exacerbated and the overall survival rate was significantly decreased after I/R in animals given by allopurinol compared to those pretreated by saline (P < 0.05). L-NAME and allopurinol co-treated animals exhibited more severe liver injury (P < 0.05 and P<0.01)and a further decreased overall survival rate (P < 0.05)compared to L-NAME or allopurinol alone-treated counterparts, but they were not different from carboxy-PTIO treated animals (P > 0.05). CONCLUSION: NO2- -derived NO by XOR in the hypoxic and acidic environment induced by hepatic I/R protects the liver against I/R injury in vivo. SN - 1499-3872 UR - https://www.unboundmedicine.com/medline/citation/16109514/Nitrite_derived_nitric_oxide_by_xanthine_oxidoreductase_protects_the_liver_against_ischemia_reperfusion_injury_ DB - PRIME DP - Unbound Medicine ER -