“…We also observed the same effects, although the differences were not significant. In a study of attention deficit-hyperactivity disorder, patients’ mean serum native and total thiol levels were higher than those of the controls (21). In a study evaluating thiol-disulphide homeostasis in acute brucellosis, the authors observed lower native and total thiol levels in an acute brucellosis group than in a healthy group.…”
Summary
Background
The purpose of the study was to determine oxidative stress-related plasma thiol/disulphide, ischemia-modified albumin (IMA) levels and ferroxidase activity among women with obesity in insulin-resistant and non-insulin-resistant groups in comparison with an overweight group.
Methods
We compared plasma thiol/disulphide, IMA levels, and ferroxidase activity between the study groups. We analyzed plasma thiol/disulphide homeostasis with a newly developed automated measurement method; IMA with Albumin Cobalt Binding Test and ferroxidase (ceruloplasmin) levels with an automated, colourimetric method.
Results
There were no significant differences between insulin-resistant and non-insulin-resistant women with obesity in terms of plasma native thiol, total thiol, disulphide, disulphide/native thiol ratio, disulphide/total thiol or native thiol/total thiol values. Ferroxidase activity was higher in insulin-resistant than in non-insulin-resistant women with obesity and higher in the total women with obesity group than in the overweight subjects (p<0.001, and p=0.014, respectively). IMA was lower in the insulin-resistant group than in the non-insulin-resistant group and overweight groups (p=0.011, and p=0.042, respectively).
Conclusions
The significantly greater increase in ferroxidase activity in insulin-resistant subjects with obesity may reflect its role as a positive acute phase protein. These findings may be related to the pathogenesis of the disease. Changes in oxidative status occur in women with obesity, and partially in overweight subjects. The ferroxidase activity of ceruloplasmin plays a crucial role in iron homeostasis and lowers oxidative stress by reducing the detrimental effects of iron.
“…We also observed the same effects, although the differences were not significant. In a study of attention deficit-hyperactivity disorder, patients’ mean serum native and total thiol levels were higher than those of the controls (21). In a study evaluating thiol-disulphide homeostasis in acute brucellosis, the authors observed lower native and total thiol levels in an acute brucellosis group than in a healthy group.…”
Summary
Background
The purpose of the study was to determine oxidative stress-related plasma thiol/disulphide, ischemia-modified albumin (IMA) levels and ferroxidase activity among women with obesity in insulin-resistant and non-insulin-resistant groups in comparison with an overweight group.
Methods
We compared plasma thiol/disulphide, IMA levels, and ferroxidase activity between the study groups. We analyzed plasma thiol/disulphide homeostasis with a newly developed automated measurement method; IMA with Albumin Cobalt Binding Test and ferroxidase (ceruloplasmin) levels with an automated, colourimetric method.
Results
There were no significant differences between insulin-resistant and non-insulin-resistant women with obesity in terms of plasma native thiol, total thiol, disulphide, disulphide/native thiol ratio, disulphide/total thiol or native thiol/total thiol values. Ferroxidase activity was higher in insulin-resistant than in non-insulin-resistant women with obesity and higher in the total women with obesity group than in the overweight subjects (p<0.001, and p=0.014, respectively). IMA was lower in the insulin-resistant group than in the non-insulin-resistant group and overweight groups (p=0.011, and p=0.042, respectively).
Conclusions
The significantly greater increase in ferroxidase activity in insulin-resistant subjects with obesity may reflect its role as a positive acute phase protein. These findings may be related to the pathogenesis of the disease. Changes in oxidative status occur in women with obesity, and partially in overweight subjects. The ferroxidase activity of ceruloplasmin plays a crucial role in iron homeostasis and lowers oxidative stress by reducing the detrimental effects of iron.
“…This unchanged homeostasis may result in both selecting patients taking mono or poly antiepileptic medication and preferring seizure-free period in collection of patient samples [37]. It has been demonstrated increased NT and TT levels in the attention deficit hyperactivity disorder and migraine patients [38,39].…”
Dynamic thiol-disulfide homeostasis (TDH) is a new area has begun to attract more scrutiny. Dynamic TDH is reversal of thiol oxidation in proteins and represents the status of thiols (-SH) and disulfides (-S-S-). Organic compounds containing the sulfhydryl group is called thiol, composed of sulfur and hydrogen atoms. Disulfides are the most important class of dynamic, redox responsive covalent bonds build in between two thiol groups. For many years, thiol levels were analyzed by several methods. During last years, measurements of disulfide levels have been analyzed by a novel automated method, developed by Erel and Neselioglu. In this method, addition to thiol-termed as native thiol-levels, disulfide levels were also measured and sum of native thiol and disulfide levels were termed as total thiol. Therefore, TDH was begun to be understood in organism. In healthy humans, TDH is maintained within a certain range. Dysregulated dynamic TDH has been implicated several disorders with unknown etiology. A growing body of evidence has demonstrated that the thiol-disulfide homeostasis is involved in variety diseases, such as diabetes mellitus, hypertension, non-small cell lung cancer, Familial Mediterranean fever, inflammatory bowel diseases, occupational diseases, gestational diabetes mellitus and preeclampsia. These results may elucidate some pathogenic mechanism or may be a predictor indicating diagnostic clue, prognostic marker or therapeutic sign. In conclusion, protection of the thiol disulfide homeostasis is of great importance for the human being. Evidence achieved so far has proposed that thiol-disulfide homeostasis is an important issue needs to elucidate wholly.
“…A growing body of evidence has shown that an impaired DTDH state can contribute to the pathogenesis of a variety of disorders including diabetes, cardiovascular diseases, malignant tumors; rheumatoid arthritis, Parkinson's disease, Alzheimer's disease; Friedreich's ataxia, multiple sclerosis, and amyotrophic lateral sclerosis [Erel & Neselioglu, 2014]. Additionally, there are various studies investigating plasma DTDH levels on child samples with ADHD [Avcil, Uysal, Avcil, Alışık, & Biçer, 2017; Görmez, Örengül, Özer, Uzuner, & Selek, 2016; Guney et al, 2015]. The present study aimed to assess the role of the redox imbalance on the etiopathogenesis of autism with a novel oxidative stress marker, dynamic thiol/disulfide homeostasis, and the relationship between the symptom severities of autism, problem behaviors, and these plasma biomarkers.…”
We aimed to investigate the role of impaired oxidant‐antioxidant homeostasis on the etiopathogenesis of autism with a novel oxidative stress (OS) marker, dynamic thiol/disulfide homeostasis (DTDH), and relationship between the symptom severity and markers. A total of 60 children with ASD aged 3–10 years and 54 unaffected children were investigated for the plasma DTDH parameters. A sociodemographic‐data form, K‐SADS‐PL, Childhood Autism Rating Scale, Abnormal Behavior Checklist, Autism Behavior Checklist, and a developmentally appropriate IQ test were administered to all participants. Distortion of DTDH to the OS‐side in the autism group was determined with lower plasma levels of native and total thiol, in contrast to a higher disulfide and thiol oxidation–reduction ratio. However, biomarkers had no correlation with the symptom severity of autism. Cutoff values for each parameter on the ROC curve might be useful to predict ASD and each DTDH biomarker was detected as an independent predictor of ASD. The present study demonstrated a disturbed redox status and absence of an expected compensatory increase in antioxidant response in a pediatric sample of ASD by measuring dynamic oxidation/reduction shifts with a novel, practical and reproducible analytical technique, and contributes to data regarding oxidative hypothesis on autism and raises the question of the place of antioxidants in autism treatment. Our results may suggest predictive usefulness of the plasma DTDH biomarkers in ASD, despite the study being conducted with a modestly small sample size that makes further research with a larger replication sample necessary to substantiate the findings.
Lay Summary
Dynamic thiol/disulfide homeostasis is a novel plasma marker used to determine the oxidative stress which is a natural result of disequilibrium between the oxidants and antioxidants in the human body. There is increasing interest regarding a central biological linking role of oxidative stress among the other etiological factors of autism. Our findings on the disturbed plasma dynamic thiol/disulfide homeostasis in children with autism and the absence of an expected antioxidant response against increased oxidative stress supports the data concerning the role of oxidative stress on the etiology of autism and the need of further research on the place of antioxidants in autism treatment.
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