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ABSTRACT Objective Thyroid hormones are known to affect the biosynthesis and degradation of antioxidant compounds, suggesting a possible link between hypothyroidism and oxidative stress. However, there is no clear consensus in the literature regarding this association. The aim of this study was to evaluate oxidative stress markers (extracellular thiol-disulfide homeostasis and intracellular glutathione homeostasis) in patients with hypothyroidism due to autoimmune (Hashimoto’s thyroiditis) or nonautoimmune thyroid disease rendered euthyroid after levothyroxine replacement. Subjects and methods The study included 116 patients admitted to the Taksim Training and Research Hospital (Istanbul, Türkiye). Of these, 50 had hypothyroidism due to Hashimoto’s thyroiditis (HT group), 30 had nonautoimmune hypothyroidism (NAIH group), and 36 were healthy controls (control group). All participants were women. Extracellular thiol-disulfide homeostasis and intracellular glutathione homeostasis tests were assessed as oxidative stress markers. Results Thiol-disulfide homeostasis in both HT and NAIH groups was shifted toward the oxidative spectrum. Compared with the control group, the HT and NAIH groups had lower levels of native (p < 0.001 and p = 0.001, respectively) and total (p = 0.002 and p = 0.012, respectively) thiol, as well as a lower native thiol/total thiol ratio (p < 0.001 for both). The HT group also had higher disulfide levels than the control group (p = 0.027). Reduced glutathione (GSH) and oxidized glutathione (GSSG) values were comparable across all three groups, but the HT and NAIH groups had higher GSSG/GSH (p < 0.001 for both) and GSSG/(GSH+GSSG) ratios (p = 0.003 and p = 0.005, respectively), along with lower GSH/(GSH+GSSG) ratio (p = 0.001 and p = 0.002, respectively) than the control group. Conclusion Levothyroxine replacement was ineffective in ameliorating oxidative stress in patients with hypothyroidism due to Hashimoto’s thyroiditis or nonautoimmune causes, as extracellular thiol-disulfide homeostasis was notably altered in these patients compared with healthy controls. The findings of this study suggest that oxidative stress remains a prevailing issue in patients with autoimmune or nonautoimmune hypothyroidism even after euthyroidism is restored.

(1) Reduced glutathione (GSH) is considered the first line of antioxidant defense. During oxidative stress, it is oxidized to glutathione disulphide (GSSG). (2) A simple and quick spectrophotometric method based on sodium borohydride (NaBH4) as a reductant to measure the total and reduced GSH in porcine saliva was analytically validated and evaluated in two situations in this species: (a) in a physiological situation, involving sows during the late lactation and post-weaning periods, and (b) in a situation of sepsis in pigs experimentally induced by LPS administration. (3) The results of the analytical validation showed that the assay was precise and accurate in the porcine saliva samples. Higher total GSH and GSSG and lower reduced GSH were observed in the saliva of sows during the post-weaning period, as well as in pigs with experimentally induced sepsis. (4) In conclusion, the validated assay showed adequate analytical results and could be used to evaluate the GSH system of porcine saliva, as demonstrated during the clinical performance.

Aim. We aimed to examine the thiol-disulfide (SS) balance, a recognized marker of oxidative stress, in fibromyalgia syndrome (FMS). Methods. The study comprised 98 female participants (61 newly diagnosed patients and 37 patients under treatment) with FMS, along with 82 apparently healthy female volunteers. In both groups, assessments were conducted using the Fibromyalgia Impact Questionnaire (FIQ), Visual Analogue Scale (VAS), Pittsburgh Sleep Quality Index (PSQI), Fatigue Severity Scale (FSS), Short Form-36 (SF-36), Tender Point Count, Beck Depression Inventory (BDI), and Beck Anxiety Inventory (BAI). Native thiol (NT) and total thiol (TT) levels were measured, SS levels and SS/NT ratio were calculated. Results. FMS patients demonstrated significantly lower NT levels, higher SS levels, and an elevated SS/NT ratio compared to the control group (p< 0.05 for all groups). In FMS patients, a statistically significant correlation was found between SS level and the SS/NT ratio, as well as the number of tender points (r=-0.24, p=0.02; r=-0.21, p=0.04), SF-36 pain subscales (r=0.22, p=0.032; r=0.21, p=0.04), and BAI scores (r=-0.22, p=0.01; r=-0.23 p=0.03). In the subgroup analysis, all health assessment scales were observed to exhibit statistically significant differences between the under-treatment group and newly-diagnosed group when compared to the control group (p< 0.05 for all groups). The FIQ, VAS, FSS, and BAI scores were found to be significantly lower in the under-treatment group as compared to the newly-diagnosed group (p< 0.05 for all groups). In the newly-diagnosed group, NT was significantly lower and the SS/NT ratio was significantly higher than those in the control group (p< 0.05). In the under-treatment group, SS levels and SS/NT ratio were significantly higher as compared to the control group (p< 0.05). In the multivariate regression analysis, which incorporated age, health assessment scales, patient subgroups, tender points, and duration of symptoms to predict the SS/NT ratio, variabes such as being in the under-treatment group, tender points, and BAI score were identified as significant predictors (p< 0.05). Conclusions. The thiol-SS balance was observed to shift in the oxidative direction, and oxidative stress was higher in the FMS group. The absence of a significant difference between the under-treatment group and the newly-diagnosed group in terms of thiol-SS balance parameters suggests a shift to oxidative stress in patients, independent of the treatment status.

Abstract Background Thiol-disulfide homeostasis (TDH) plays a pivotal role in various physiological mechanisms, including antioxidant defence, detoxification, apoptosis, regulation of enzyme activities and cellular signal transduction. TDH can be used as a biomarker to detect oxidative stress (OS) levels and ischemia status in the tissues. Coronary artery bypass grafting (CABG) surgery is a procedure associated with high oxidative stress. Dexmedetomidine, an alpha-2 agonist anaesthetic agent, has antioxidant effects. In this study, the effects of dexmedetomidine on oxidative stress in CABG surgery were investigated. Methods Patients who underwent on-pump CABG surgery were divided into two groups: those receiving dexmedetomidine (Group D) and those not receiving dexmedetomidine (Group C). From anesthesia induction to the end of surgery, patients in Group D received intravenous infusions of 0.05–0.2 mcg/kg/min remifentanil and 0.2–0.7 mcg/kg/h dexmedetomidine. Patients in Group C received intravenous infusion of 0.05–0.2 mcg/kg/min remifentanil. Blood samples were collected from the patients 30 min before induction of anesthesia (T1), 30 min after removal of the aortic cross-clamp (T2), and at the end of the surgery (T3). Thiol-disulfide homeostasis (TDH) was assessed using a novel method. A novel automated method enables the determination of native thiols, total thiols and disulfides levels in plasma, allowing the calculation of their respective ratios. Results In patients receiving dexmedetomidine, lower postoperative levels of disulfide, disulfide/native thiol, and disulfide/total thiol, along with higher native thiol/total thiol, were observed compared to the control group. (p 0.05) Conclusions In our study, through dynamic thiol-disulfide measurements, we found that levels of oxidative stress (OS) were lower in patients who received dexmedetomidine. We believe that the positive effects of dexmedetomidine on OS could be beneficial in CABG surgery. Furthermore, we anticipate that with further studies conducted in larger patient cohorts, the clinical utilization of dexmedetomidine will become more widespread. Trial registration number NCT05895331 / 06.07.2023.

Objective: Patients with rheumatoid arthritis (RA) are generally seropositive, but 15-20% of patients with RA may be seronegative. Diagnosing patients with RA sometimes requires long and challenging research, and new diagnostic biomarkers are needed. This study aimed to investigate the use of netrin-1 as a biomarker in the differential diagnosis of RA from healthy controls and the relationships between netrin-1 and RA’s disease activity scores and joint erosions. Methods: The study group included 60 RA patients, and the control group included 41 healthy volunteers. Serum netrin-1 was measured using an ELISA kit with the quantitative sandwich enzyme immunoassay method. The RA Disease Impact (RAID) score was used to determine changes in quality of life, and the disease activity score-28 (DAS-28) and Clinical Disease Activity Index (CDAI) were used to assess disease activity. Results: In the comparison of netrin-1 serum levels, netrin-1 levels were found to be similar between RA and healthy controls [64.4 (35.8-551.4) and 65 (35.8-436.6), p=0.786, respectively]. No significant correlation was found between netrin-1 levels and disease indices (CDAI, DAS-28 ESR, RAID, and DAS-28 CRP) (p>0.05). Conclusion: Netrin-1 is not higher in the serum of RA patients compared to healthy controls, and its levels have no correlation with disease indices of RA.

Background: Prolidase is a manganese (Mn)-dependent cytosolic exopeptidase that degrades imidodipeptides with C-terminal proline or hydroxyproline. Prolidase recycling from imidodipeptides plays a critical role in collagen resynthesis and extracellular matrix (ECM) remodelling. Following an increase in gonadotropins, ovarian and follicular collagen undergo substantial degradation. Abnormal ovarian ECM composition is associated with polycystic ovary syndrome (PCOS). This study aimed to examine prolidase activity in the serum and follicular fluid (FF) of women undergoing in vitro fertilisation/intracytoplasmic sperm injection (IVF/ICSI) treatment, comparing those with PCOS to those with normal ovarian function.Methods: This prospective study enrolled 50 participants, of whom 44 were included. PCOS diagnosis followed the Rotterdam consensus criteria, with 20 patients constituting the study group. The control group comprised 24 individuals with mild-to-moderate male infertility. Prolidase enzyme activity in serum and FF was measured using the Chinard reagent via spectrophotometric analysis and compared between the groups.Results: Serum and FF prolidase levels were significantly lower in patients with PCOS (p 0.05). A negative correlation existed between serum prolidase levels and total antral follicle (AF) count (p

Objective: We investigated oxidative status in patients with rotator cuff tendinopathy (RCT) and evaluated their relationship with radiological and clinical parameters. Methods: In this cross-section study, 88 patients with RCT (59 males and 29 females) and 86 healthy controls (66 males, 20 females) were enrolled. The sample consisted of nontraumatic patients who are suffering from shoulder pain because of rotator cuff disease, which was established by clinical tests and MRI scanning. Oxidative stress in patients with RCT was analyzed via the dynamic thiol/disulfide homeostasis (TDH). Thiol/disulfide homeostasis was measured by a new colorimetric method. Furthermore, oxidative stress was indirectly measured by serum total oxidant status (TOS), oxidative stress index (OSI), and total antioxidant capacity (TAC). Results: Serum disulfide levels and the other oxidative stress parameters of the RCT group were significantly greater than those of the control group (P < .001 for all), whereas the anti-oxidative stress parameters remained unchanged (P > .05 for all). The lowest and highest serum disulfide levels were detected in patients with grades 1 and 3, respectively (P < .001). Furthermore, in a multiple regression analysis, the disulfide/natural thiol ratio (β=–4.886, P = .004) and the MRI grading (β=0.314, P=.001) were independently associated with the Western Ontario Rotator Cuff Index WORC score. Conclusion: We found an association between the levels of various serum markers of oxidative injury, especially serum disulfide levels, and the increasing severity of RCT. Thiol/disulfide homeostasis seems to play a critical role in RCT, both in the beginning and during the progression of disease. Level of Evidence: Level III, Diagnostic study.

INTRODUCTION: Ischemia-modified albumin (IMA) formation is associated with increased reactive oxygen species (ROS) production, while increased cortisol leads to decreased ROS levels. We aimed to evaluate the effect of adrenocorticotropic hormone (ACTH) stimulation on IMA levels and whether the effect was dose-dependent or not. METHODS: A total of 99 subjects with normal ACTH test results were included in the study. Of these, 80 had standard-dose ACTH test while 19 had low-dose ACTH test. Blood samples were collected to determine cortisol and IMA levels; at minutes 0, 30, and 60 following the standard-dose ACTH test and at minutes 0 and 30 following the low-dose ACTH test. RESULTS: IMA levels decreased significantly within 30 minutes and the decrease continued up to the sixtieth minute (p=0.002) after standard-dose ACTH stimulation. After ACTH stimulation, a weak negative correlation was found between peak cortisol and IMA levels at the thirtieth minute (r=0.233, p=0.02). There was no significant difference in IMA levels after low-dose ACTH stimulation, despite an increase in cortisol (p=0.161). DISCUSSION AND CONCLUSION: IMA levels decreased rapidly after standard-dose ACTH stimulation, while a decrease in IMA levels was not observed after low-dose ACTH stimulation. The lack of decrease in IMA levels after low-dose ACTH stimulation suggests a possible dose-dependent relationship between ACTH and IMA. The moderate increase in cortisol with no reduction in IMA levels after low-dose ACTH stimulation and the weak correlation between peak cortisol and 30-minute IMA levels after standard-dose ACTH stimulation suggest that ACTH may have a direct effect on IMA.