RESUMO
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). CONCLUSIONS: 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.
