Oxidative stress is described as disturbed oxidative balance between increased reactive oxygen species such as hydroxyl radical (OH•), superoxide radical (O 2 −), hydrogen peroxide (H 2 O 2) which occurs during normal cellular metabolism and decreased antioxidants which have scavenging effects on free radicals. Reactive oxygen species resulted from increased oxidative stress attacks on to the double bonds of lipids, proteins and DNA bases, removing one hydrogen atom from structure and initiate to oxidative chain reactions. This process leads to cellular damage and death damaging intracellular macromolecules such as lipids, proteins and DNA. The damage of free radicals is detected measuring oxidative products such as malondialdehyde (MDA), protein carbonyl (PCO) and 8-hydroxyguanine derivatives (8-OHG, 8-hidroksi-2′deoksiguanozin) in body fluids and various tissues. Although considerable amount of studies in this field, the effects of oxidative stress on cellular structures still remain unknown. In this review, we aimed to evaluate the biochemical aspects of oxidative stress, antioxidant systems and their mechanism of actions and oxidative products.
Background Vitamin B12 is an important vitamin for metabolism and affects many mechanisms in the body including neuronal migration, DNA synthesis, neurotransmitter synthesis, brain and cognitive development. Increased oxidative stress in the body leads to the damage of the child development, but also plays a crucial role in the pathogenesis of many diseases encountered in the childhood period. Our aim is to investigate whether or not B12 deficiency is associated with dynamic thiol/disulfide homeostasis in adolescent patients. Methods This is a case-controlled observational study consisting of 45 adolescent patients with vitamin b12 deficiency and a control group consisting of 45 healthy adolescent. Patients between 11 and 18 ages who applied to the outpatient clinic for the first time with one of the complaints of headache were selected due to their decreased school performance, dizziness, and fatigue. Hemogram, vitamin B12, homocysteine levels and oxidative stress parameters such as native and total thiol disulfide levels and ratios of disulfide/native thiol, disulfide/total thiol, and native thiol/total thiol were measured from the patients. Results Vitamin B12 level was found to be significantly lower in vitamin B12 deficiency group (p < 0.001). The serum disulfide level was found to be 27.5 ± 8.38 in the case group and 20.5 ± 8.36 in the control group (p < 0.001). In the multiple linear regression analysis, it was determined that the independent variables of native thiol, homocysteine and disulfide levels effected of vitamin B12 levels (p < 0.001, p < 0.001, p < 0.005 respectively; R2 = 0.62). Conclusion The results obtained in terms of the effect of vitamin B12 deficiency on oxidative stress in adolescents are remarkable. The increase in oxidative stress parameters in the patient group may also suggest that oxidative stress plays a vital role in vitamin B12 deficiency in adolescence.
Objective:Sickle cell disease (SCD), described as a group of inherited blood disorders, affects millions of people throughout the world and is particularly common in the southern part of Turkey. We aimed to determine the relationship between ischemia-modified albumin (IMA) and the dynamic thiol/disulfide balance in SCD.Materials and Methods:Fifty-four adult SCD patients and 30 healthy controls were included in the study. The 54 adult patients included 30 (56%) males and 24 (44%) females with a mean age of 28.3±8.4 years (minimum-maximum: 18-46 years). Of the 54 patients, 46 had homozygous sickle cell anemia (HbSS) and 8 had sickle/β-thalassemia (HbS/β+-thalassemia). Fasting blood samples were collected. After centrifugation at 1500×g for 10 min, plasma samples were portioned and stored at -80 °C. IMA levels were determined by albumin cobalt binding test, a colorimetric method. Total and native thiols and disulfide were analyzed with a novel spectrophotometric method.Results:We found significantly lower levels of native thiol (-SH) (284.0±86.3 µmol/L), disulfide levels (14.6±7 µmol/L), and total thiols (-SH + -S-S-) (313.0±89.3 µmol/L) in SCD patients compared to healthy controls (respectively 417.0±54.2, 22.7±11.3, and 462.0±58.7 µmol/L). Plasma albumin levels (34.9±7.9 g/L) were lower and IMA levels (13.6±3.1 g/L) were higher in SCD patients compared to controls (respectively 43.5±3.1 and 8.4±1.6 g/L). Plasma albumin levels were strongly correlated with both plasma native (r=0.853; p=0.0001) and total thiols (r=0.866; p=0.0001).Conclusion:Decreased plasma native and total thiol levels and increased IMA levels are related to increased oxidative stress and provide an indirect and quick reflection of the oxidative damage in SCD patients.
This is the first study to evaluate both the dynamic thiol-disulfide homeostasis and ischemia-modified albumin (IMA) levels in patients with chronic lymphocytic leukemia (CLL). Twenty-nine patients with CLL and 20 controls were included in the study. The dynamic thiol-disulfide balance was determined by the newly developed colorimetric method by Erel. IMA levels were determined by the cobalt binding test. We found that total antioxidant status levels were lower while total oxidant status (TOS) and oxidative stress index (OSI) levels were significantly higher in patients with CLL than controls. Moreover, native and total thiol levels were found to be statistically significant between the study and control groups (p<0.001), whereas no statistically significant difference was noted for IMA levels (p=0.365). A negative correlation was observed between native and total thiol levels, leukocyte, lymphocyte, and TOS. Total bilirubin showed positive correlation with direct bilirubin and alkaline phosphatase. In addition, IMA levels showed a positive correlation with OSI. This study highlights measurement of native and total thiol and IMA levels in patients with CLL for the first time. Dynamic thiol-disulfide homeostasis may contribute in the pathophysiological mechanism, and follow-up to disease in patients with CLL.
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