Our study confirmed the presence of high oxidative stress in active IBD. More importantly, we have demonstrated a lower antioxidant capacity of patients in remission versus control group. This may represent a risk factor for the disease and can be an additional argument for the direct implication of oxidative stress in the pathogenesis of IBD.

Background and objectives: Oxidative stress and inflammation have been implicated in the etiology of irritable bowel syndrome (IBS), a common gastrointestinal functional disease. This study aimed to further characterize the contention-stress rat model by exploring a possible correlation between oxidative stress markers measured in brain tissues with behavioral components of the aforementioned model. Thus, it is hereby proposed a possible IBS animal model relevant to pharmacological and complementary medicine studies. Materials and Methods: Wild-type male Wistar rats (n = 5/group) were chronically exposed to 6-hour/day contention, consisting of isolating the animals in small, vital space-granting plastic devices, for seven consecutive days. Following contention exposure, temporal lobes were extracted and subjected to biochemical analyses to assess oxidative stress-status parameters. Results: Our results show increased brain oxidative stress in contention-stress rat model: decreased superoxide dismutase and glutathione peroxidase activities and increased malondialdehyde production in the IBS group, as compared to the control group. Furthermore, the biochemical ratios which are used to evaluate the effectiveness of an antioxidant system on oxidative stress could be described in this model. Conclusions: The correlations between the behavioral patterns and biochemical oxidative stress features could suggest that this may be a complex model, which can successfully mimic IBS symptomatology further providing evidence of a strong connection between the digestive system, enteric nervous system, and the central nervous system.

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Among bacterial infections associated with hepatic cirrhosis, the most common is spontaneous bacterial peritonitis (SBP). Despite different protective measures, such as early diagnosis, therapy with albumin and the introduction of new antibiotics, the prognosis of these patients remains poor, with a mortality rate of 20-40%. In this context, the identification of patients with increased risk of death is extremely important for improving the prognosis. Thus, there is growing interest for studying the effects and mechanisms of oxidative stress, considering the requirements for identifying new substances with hepatoprotective functions and reducing various adverse effects. In this study, we assessed oxidative stress markers, the antioxidant enzyme superoxide dismutase (SOD) and the marker of lipid peroxidation, malondialdehyde (MDA), in the serum and ascitic fluid in patients with decompensated cirrhosis and SBP, in patients diagnosed with decompensated liver cirrhosis with ascites and in patients with compensated liver cirrhosis. Increased oxidative stress, demonstrated by a significant decrease of SOD and increase in MDA levels, was observed in patients with decompensated cirrhosis and SBP, compared with those without SBS, as well as those with compensated liver cirrhosis. Measuring these oxidative stress markers could have a fundamental importance in the diagnosis, treatment and follow-up of this liver pathology.