Background/Objectives: Inflammatory bowel diseases primarily encompass Crohn’s disease and ulcerative colitis. Insufficient levels of tryptophan cause an imbalance in the gut microbiota, leading to inflammation in the gastrointestinal tract. The main catabolic pathway of tryptophan is the kynurenine pathway. Our study aims to evaluate serum tryptophan, the kynurenine pathway, and oxidative stress parameters, including total oxidant status and total antioxidant capacity, in patients with Crohn’s disease and ulcerative colitis. Methods: The study included 80 follow-up patients in remission diagnosed with Crohn’s disease and ulcerative colitis who attended the Gastroenterology Outpatient Clinic, as well as 78 healthy controls. Serum tryptophan, kynurenine, 3-hydroxykynurenine, 3-hydroxyanthranilic acid, and kynurenic acid levels were measured with liquid chromatography and tandem mass spectrometry (LC-MS/MS). All statistical analysis was performed using R version 4.2.1. Statistical Language. Results: Serum tryptophan, 3-hydroxyanthranilic acid, and total antioxidant capacity were lower in patients with ulcerative colitis and Crohn’s disease compared to those in the control group. The serum total oxidant status in the control group was significantly lower than in patients with Crohn’s disease and ulcerative colitis. Conclusions: The results of our research indicate that tryptophan and kynurenine pathway metabolites could potentially contribute to the pathogenesis of inflammatory bowel diseases.

Background/aim: This experimental study aimed to define a biochemical marker that will enable early diagnosis of acute compartment syndrome (ACS) of extremities, a mortal condition that occurs due to trauma. Materials and methods: A total of 15 Wistar rats were included in the study in which saline infusion technique, a clinically compatible ACS model, was applied. After the rats were anesthetized with ketamine-xylazine, the in-compartment pressure of the hind limb was slowly increased with saline delivered through the angiocatheter, and after reaching the target compartment pressure, the pressure level was kept with a rubber tourniquet. The in-compartment pressure level was continuously monitored with a pressure transducer. The rats were divided into three groups. No intervention was applied to the control group (CG) (n = 3). In study group 1 (SG1) (n = 6), ACS was created using the saline infusion technique, keeping the in-compartment pressure between 30 and 40 mmHg for 45 min. In study group 2 (SG2) (n = 6), ACS was created using the saline infusion technique, keeping the in-compartment pressure between 30 and 40 mmHg for 90 min. Fasciotomy was performed on all rats. Tissue samples were obtained for histopathological examination and blood samples for biochemical analysis. Results: Total oxidant status (TOS) (p = 0.004), ischemia-modified albumin (IMA) (p = 0.030), aspartate transferase (AST) (p = 0.003) and neopterin (p = 0.012) levels differed significantly between groups in the early period of muscle ischemia. In fact, TOS levels differed significantly between the groups even in the cellular phase where signs of ischemia were not observed (p = 0.048, p = 0.024). According to histopathological evaluation, there was no significant difference between the groups. Conclusion: TOS can be detected in the early reversible stage of ischemia, when the histopathological findings of ACS do not occur.

Objectives: Dental caries is a multifactorial infectious disease caused by the colonization and proliferation of bacteria in the mouth. Recently, it has been reported that local antioxidant and oxidant status may play an important role in the pathogenesis of dental caries. Visfatin is an adipocytokine that enhances leukocyte activation and release of proinflammatory cytokines. In this study, our aim was to investigate the salivary visfatin levels, total antioxidant capacity (TAC), and total oxidant status (TOS) in patients with and without dental caries. Methods: Saliva samples were collected from 50 caries-free individuals and 115 patients with dental caries who were admitted to Selcuk University Restorative Dentistry Clinics. Saliva samples were collected based on the stimulated saliva collection procedure. Visfatin levels were measured using enzyme-linked immunosorbent assay. Spectrophotometric methods were used to determine salivary TAC and TOS. Results: Salivary TAC, TOS, and visfatin levels were statistically higher in patients with dental caries compared to caries-free group (p=0.035; p=0.003; p<0.001 respectively). There was a positive correlation between caries number and salivary TOS and visfatin levels. Conclusions: Findings of this prospective study demonstrated that oxidative stress may be involved in the pathogenesis of dental caries. Salivary visfatin, TAC, and TOS may be novel markers to evaluate dental caries.