Advances in Clinical and Experimental Medicine

Title abbreviation: Adv Clin Exp Med
JCR Impact Factor (IF) – 2.1 (5-Year IF – 2.0)
Journal Citation Indicator (JCI) (2023) – 0.4
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Index Copernicus  – 171.00; MNiSW – 70 pts

ISSN 1899–5276 (print)
ISSN 2451-2680 (online)
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Advances in Clinical and Experimental Medicine

2020, vol. 29, nr 10, October, p. 1175–1180

doi: 10.17219/acem/126294

Publication type: original article

Language: English

License: Creative Commons Attribution 3.0 Unported (CC BY 3.0)

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The role of N-acetylcysteine in preventing hepatic injury associated with systemic oxidative stress after extracorporeal shock wave treatment

Sebahat Cam1,A,B,C,D,E,F, Dursun Baba2,A,B,D,F, Yusuf Senoğlu2,B,C, Alpaslan Yuksel2,C,D, Havva Erdem3,C,D,E,F

1 Department of Pediatric Gastroenterology, Istanbul Medeniyet University, Turkey

2 Department of Urology, Duzce University, Turkey

3 Department of Pathology, Ordu University, Turkey

Abstract

Background. Systemic oxidative stress may cause detrimental consequences for the liver, leading to hepatic fibrogenesis.
Objectives. To investigate histopathological changes in liver tissues due to the increased systemic oxidative stress associated with rat extracorporeal shock wave lithotripsy (SWL) model and to document the consequences of N-acetylcysteine (NAC) administration.
Material and Methods. In this experimental SWL model, 18 Wistar albino rats were randomly assigned into 3 groups. The control group (group I) had no intervention. Group II underwent SWL treatment with intraperitoneal saline injection. Group III also had SWL with intraperitoneal NAC and was divided into short-term (group III-14 days) and long-term (group III-28 days) subgroup. Hepatectomy was performed for histopathological examinations. Histopathological alterations were evaluated with light microscopy. Immunohistological staining for p53 and myeloperoxidase was also performed.
Results. Blood samples revealed a significant increase in plasma oxidative stress index (OSI) after plasma total antioxidant status (TAS) and total oxidant status (TOS) had been measured. It was shown that this increased systemic oxidative stress adversely affected liver tissues. Predominantly, sinusoidal dilatation was remarkably observed in rats with significantly high OSI values (p = 0.043). Similarly, periportal necrosis significantly increased in rats with high OSI values (p = 0.033). p53 positivity was also remarkable in rats with systemic oxidative stress (p = 0.049). N-acetylcysteine administration provided a significant decrease in OSI. N-acetylcysteine also improved all these alterations, including p53 staining. Particularly, sinusoidal dilatation was significantly protected in the long-term NAC group (group III-28 days).
Conclusion. We demonstrated that SWL-induced systemic oxidative stress causes histological alterations in liver tissues. Increased p53 and myeloperoxidase staining as markers of oxidative damage were also detected. N-acetylcysteine may protect from these histological and ultra-structural alterations related to oxidative stress.

Key words

liver, oxidative stress, N-acetylcysteine, sinusoidal dilatation, p53

References (24)

  1. Lisboa QC, Costa SM, Couto CA. Current management of non-alcoholic fatty liver disease. Rev Assoc Med Bras (1992). 2016;62(9):872–878.
  2. Kim M, Yoo G, Randy A, Kim HS, Nho CW. Chicoric acid attenuate a nonalcoholic steatohepatitis by inhibiting key regulators of lipid metabolism, fibrosis, oxidation and inflammation in mice with methionine and choline deficiency. Mol Nutr Food Res. 2017;61(5). doi:10.1002/mnfr.201600632
  3. Elswefy SE, Abdallah FR, Atteia HH, Wahba AS, Hasan RA. Inflammation, oxidative stress and apoptosis cascade implication in bisphenol A-induced liver fibrosis in male rats. Int J Exp Pathol. 2016;97(5):369–379.
  4. Yin R, Guo D, Zhang S, Zhang X. miR-706 inhibits the oxidative stress-induced activation of PKCα/TAOK1 in liver fibrogenesis. Sci Rep. 2016;6:37509.
  5. Li X, He D, Zhang L, Cheng X, Sheng B, Luo Y. A novel antioxidant agent, astragalosides, prevents shock wave-induced renal oxidative injury in rabbits. Urol Res. 2006;34(4):277–282.
  6. Baba D, Cam K, Senoglu Y, Yuksel A, Erdem H, Basaran E. The efficacy of N-acetylcysteine against renal oxidative stress after extracorporeal shock wave treatment: An experimental rat model. J Urol Surg. 2020;7(1):8–15.
  7. Zafarullah M, Li WQ, Sylvester J, Ahmad M. Molecular mechanisms of N-acetylcysteine actions. Cell Mol Life Sci. 2003;60(1):6–20.
  8. Erel O. A new automated colorimetric method for measuring total oxidant status. Clin Biochem. 2005;38(12):1103–1111.
  9. Chatterjee R, Mitra A. An overview of effective therapies and recent advances in biomarkers for chronic liver diseases and associated liver cancer. Int Immunopharmacol. 2015;24(2):335–345.
  10. Turk C, Petřík A, Sarica K, et al. EAU guidelines on interventional treatment for urolithiasis. Eur Urol. 2016;69(3):475–482.
  11. Al-Awadi KA, Kehinde EO, Loutfi I, et al. Treatment of renal ­calculi by lithotripsy: Minimizing short-term shock wave induced renal damage by using antioxidants. Urol Res. 2008;36(1):51–60.
  12. Ozguner F, Armagan A, Koyu A, Calıskan S, Koylu H. A novel antioxidant agent caffeic acid phenethyl ester prevents shock wave-induced renal tubular oxidative stress. Urol Res. 2005;33(3):239–243.
  13. Aksoy H, Aksoy Y, Turhan H, Keles S, Ziypak T, Ozbey I. The effect of shock wave lithotripsy on nitric oxide and malondialdehyde levels in plasma and urine samples. Cell Biochem Function. 2007;25(5):533–536.
  14. Aksoy Y, Malkoc I, Atmaca AF, Aksoy H, Altinkaynak K, Akcay F. The effects of extracorporeal shock wave lithotripsy on antioxidant enzymes in erythrocytes. Cell Biochem Funct. 2006;24(5):467–469.
  15. Greuter T, Shah VH. Hepatic sinusoids in liver injury, inflammation, and fibrosis: New pathophysiological insights. J Gastroenterol. 2016;51(6):511–519.
  16. Iwakiri Y, Shah V, Rockey DC. Vascular pathobiology in chronic liver disease and cirrhosis: Current status and future directions. J Hepatol. 2014;61(4):912–924.
  17. Bosch J, Groszmann RJ, Shah VH. Evolution in the understanding of the pathophysiological basis of portal hypertension: How changes in paradigm are leading to successful new treatments. J Hepatol. 2015;62(1):S121–S130.
  18. Thong-Ngam D, Samuhasaneeto S, Kulaputana O, Klaikeaw N. N-acetylcysteine attenuates oxidative stress and liver pathology in rats with non-alcoholic steatohepatitis. World J Gastroenterol. 2007;13(38):5127–5132.
  19. Brunt EM. Histological assessment of nonalcoholic fatty liver disease in adults and children. Clin Liver Dis (Hoboken). 2012;1(4):108–111.
  20. Kanwar P, Nelson JE, Yates K, Kleiner DE, Unalp-Arida A, Kowdley KV. Association between metabolic syndrome and liver histology among NAFLD patients without diabetes. BMJ Open Gastroenterol. 2016;3(1):e000114.
  21. Choi JE, Kim S, Ahn JH, et al. Induction of oxidative stress and apoptosis by silver nanoparticles in the liver of adult zebrafish. Aquat Toxicol. 2010;100(2):151–159.
  22. Xu J, Lian LJ, Wu C, Wang XF, Fu WY, Xu LH. Lead induces oxidative stress, DNA damage and alteration of p53, Bax and Bcl-2 expressions in mice. Food Chem Toxicol. 2008;46(5):1488–1494.
  23. Cichoż-Lach H, Michalak A. Oxidative stress as a crucial factor in liver diseases. World J Gastroenterol. 2014;20(25):8082–8091.
  24. de Andrade KQ, Moura FA, dos Santos JM, de Araújo ORP, de Farias Santos JC, Goulart MOF. Oxidative stress and inflammation in hepatic diseases: Therapeutic possibilities of N-acetylcysteine. Int J Mol Sci. 2015;16(12):30269–30308.
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