Plasma Thiobarbituric Acid Reactive Substances Levels Research Articles

Assessment of oxidative stress markers in elderly patients with SARS-CoV-2 infection and potential prognostic implications in the medium and long term.

We aimed to evaluate the correlation of plasma levels of thiobarbituric acid reactive substances (TBARS) and reduced thiols with morbidity, mortality and immune response during and after SARS-CoV-2 infection. This was an observational study that included inpatients with SARS-CoV-2 infection older than 65 years. The individuals were followed up to the twelfth month post-discharge. Plasma levels of TBARS and reduced thiols were quantified as a measure of lipid and protein oxidation, respectively. Fatal and non-fatal events were evaluated during admission and at the third, sixth and twelfth month post-discharge. Differences in oxidative stress markers between the groups of interest, time to a negative RT-qPCR and time to significant anti-SARS-CoV-2 IgM titers were assessed. We included 61 patients (57% women) with a mean age of 83 years old. After multivariate analysis, we found differences in TBARS and reduced thiol levels between the comparison groups in fatal and non-fatal events during hospital admission. TBARS levels were also correlated with fatal events at the 6th and 12th months post-discharge. One year after hospital discharge, other predictors rather than oxidative stress markers were relevant in the models. The median time to reach significant anti-SARS-CoV-2 IgM titers was lower in patients with low levels of reduced thiols. Assessment of some parameters related to oxidative stress may help identify groups of patients with a higher risk of morbidity, mortality and delayed immune response during and after SARS-CoV-2 infection.

Form of Vitamin E Supplementation Affects Oxidative and Inflammatory Response in Exercising Horses

Vitamin E is an essential antioxidant that may benefit athletes by reducing oxidative stress and influencing cytokine expression. Supplements can be derived from natural or manufactured synthetic sources. This study aimed to determine (1) if supplemental vitamin E is beneficial to exercising horses and (2) if there is a benefit of natural versus synthetic vitamin E. After 2 weeks on the control diet (vitamin E–deficient grain and hay), 18 horses were divided into three groups and fed the control diet plus (1) 1000 IU/d synthetic α-tocopherol (SYN-L), (2) 4000 IU/d synthetic α-tocopherol (SYN-H), or (3) 4000 IU/d RRR-α-tocopherol (natural source [NAT]). On day 7, horses began a 6-week training protocol, with standard exercise tests (SETs) performed before and after the 6-week protocol. Venous blood samples were collected on days 0, 7, 29, and 49. Horses fed NAT had higher α-tocopherol (P < .05) at post-SET1 through post-SET2. Plasma thiobarbituric acid–reactive substance levels were lower in NAT versus SYN-L horses after SET2 (P = .02). Serum aspartate aminotransferase was lower after exercise in NAT horses versus SYN-L and SYN-H (P = .02), and less reduction in stride duration was seen after exercise in NAT as compared with SYN-L and SYN-H (P = .02). Gene expression of tumor necrosis factor α was lower in NAT compared with SYN-H (P = .01) but not SYN-L. In conclusion, feeding higher levels of natural vitamin E source resulted in higher serum α-tocopherol levels as well as some improvement in oxidative and inflammatory response and improved functional outcomes in response to an exercise test.

Antioxidants, endothelial dysfunction, and DCS: in vitro and in vivo study.

Reactive oxygen species (ROS) production is a well-known effect in individuals after an undersea dive. This study aimed to delineate the links between ROS, endothelial dysfunction, and decompression sickness (DCS) through the use of antioxidants in vitro and in vivo. The effect of N-acetylcysteine (NAC) on superoxide and peroxynitrite, nitric oxide (NO) generation, and cell viability during in vitro diving simulation were analyzed. Also analyzed was the effect of vitamin C and NAC on plasma glutathione thiol and thiobarbituric acid reactive substances (TBARS), plasma angiotensin-converting enzyme (ACE) activity, and angiotensin-II and DCS morbidity during in vivo diving simulation. During an in vitro diving simulation, vascular endothelial cells showed overproduction of superoxide and peroxynitrite, obvious attenuation of NO generation, and promotion of cell death, all of which were reversed by NAC treatment. After in vivo diving simulation, plasma ACE activity and angiotensin-II level were not affected. The plasma level of glutathione thiol was downregulated after the dive, which was attenuated partially by NAC treatment. Plasma TBARS level was upregulated; however, either NAC or vitamin C treatment failed to prevent DCS morbidity. During in vitro simulation, endothelial superoxide and peroxynitrite-mediated oxidative stress were involved in the attenuation of NO availability and cell death. This study is the first attempt to link oxidative stress and DCS occurrence, and the link could not be confirmed in vivo. Even in the presence of antioxidants, ROS and bubbles generated during diving and/or decompression might lead to embolic or biochemical stress and DCS. Diving-induced oxidative stress might not be the only trigger of DCS morbidity.

Mitochondrial activity and oxidative stress markers in peripheral blood mononuclear cells of patients with bipolar disorder, schizophrenia, and healthy subjects

Evidence suggests that mitochondrial dysfunction is involved in the pathophysiology of psychiatric disorders such as schizophrenia (SZ) and bipolar disorder (BD). However, the exact mechanisms underlying this dysfunction are not well understood. Impaired activity of electron transport chain (ETC) complexes has been described in these disorders and may reflect changes in mitochondrial metabolism and oxidative stress markers. The objective of this study was to compare ETC complex activity and protein and lipid oxidation markers in 12 euthymic patients with BD type I, in 18 patients with stable chronic SZ, and in 30 matched healthy volunteers. Activity of complexes I, II, and III was determined by enzyme kinetics of mitochondria isolated from peripheral blood mononuclear cells (PBMCs). Protein oxidation was evaluated using the protein carbonyl content (PCC) method, and lipid peroxidation, the thiobarbituric acid reactive substances (TBARS) assay kit. A significant decrease in complex I activity was observed (p = 0.02), as well as an increase in plasma levels of TBARS (p = 0.00617) in patients with SZ when compared to matched controls. Conversely, no significant differences were found in complex I activity (p = 0.17) or in plasma TBARS levels (p = 0.26) in patients with BD vs. matched controls. Our results suggest that mitochondrial complex I dysfunction and oxidative stress play important roles in the pathophysiology of SZ and may be used in potential novel adjunctive therapy for SZ, focusing primarily on cognitive impairment and disorder progression.

Positive influence of a natural product as propolis on antioxidant status and lipid peroxidation in senescent rats

Given the importance of oxidative stress associated to aging, it would be interesting to assess the effect of oral supplementation with antioxidant substances capable of diminishing oxidative aggression and free radicals generation associated to this condition. This study investigated the effects of AIN-93 M diet supplemented either with 2 % of propolis, or with 4 % of a natural product obtained from lyophilizate vegetables, selected by its antioxidant properties, in senescent healthy Wistar rats fed ad libitum over 3 months. Propolis supplementation leads to a lower level of glucose and cholesterol concentrations together with a reduction in protein oxidation. Plasma thiobarbituric acid-reactive substance levels were lower in the rats consuming the natural vegetable product and propolis possibly due to its antioxidant components, neutralizing the free radical produced, and thus preventing cellular damage. The results of the present study suggest a synergic effect of overall propolis compounds reducing the oxidative stress and glucose and cholesterol plasma levels associated with aging.

Oxidative stress is associated with visceral adipose tissue and subclinical atherosclerosis in a healthy multi-ethnic population

Oxidative stress plays an important role in the development of atherosclerosis. Excess visceral adipose tissue (VAT) and increased carotid intima-media thickness (IMT) are risk factors for coronary artery disease. We tested the hypothesis that VAT and IMT were associated with systemic oxidative stress. Healthy men and women (n = 565) matched for ethnicity (Aboriginal, Chinese, European, and South Asian) were recruited. Plasma malondialdehyde, a biomarker of oxidative stress, was measured as thiobarbituric acid reactive substances (TBARS). VAT and IMT were determined by computerized tomography and ultrasound scans, respectively. Plasma TBARS levels correlated with VAT and total atheroma burden (sum of IMT area and plaque area) in the entire cohort. When stratified by ethnicity, plasma TBARS levels correlated with distinct body composition and arterial measures in different ethnic populations with more associations present amongst Chinese and Europeans relative to Aboriginals and South Asians. VAT was associated with plasma TBARS levels independent of age, sex, ethnicity, smoking, and body mass index. Plasma TBARS levels were associated with IMT, the presence of plaques, and total atheroma burden, independent of age, sex, ethnicity, smoking, body mass index, and VAT. The association with total atheroma burden remained significant even when adjusted for apolipoprotein B. Results from the present study indicate that oxidative stress is positively associated with VAT as well as diffuse and focal carotid atherosclerosis in apparently healthy men and women.

Antioxidative Effects of Benidipine Hydrochloride in Patients with Hypertension Independent of Antihypertensive Effects

This study investigated the significance of measuring plasma level of thiobarbituric acid reactive substance (TBARS) in patients with hypertension and compared the clinical effects of benidipine hydrochloride (CAS 91599-74-5, Coniel) and amlodipine besylate (CAS 111470-99-6) on plasma TBARS. At first, blood pressure and plasma TBARS were measured in 85 untreated patients (48 males and 37 females, 68 years old on average) with at least one risk factor of cardiovascular disease to investigate factors which had influence on plasma TBARS. As the result, plasma TBARS was significantly higher in those with hypertension, which was also true when adjusted for other factors (r = 0.359, p< 0.01). Among these patients, benidipine hydrochloride at the dose of 4 mg/day was administered to 49 patients with hypertension or angina pectoris. All patients stratified for each factor showed significantly decreased plasma TBARS after benidipine hydrochloride treatment. Second, 40 untreated patients with essential hypertension were randomly assigned to the amlodipine group (5-7.5 mg/day) or benidipine group (4-8 mg/day) to compare the plasma TBARS levels. Plasma TBARS levels were significantly decreased in both groups. The amlodipine group showed a positive correlation between the decrease in plasma TBARS level and those in both diastolic and systolic blood pressures after treatment. On the other hand, benidipine hydrochloride decreased plasma TBARS to a greater degree than both diastolic and systolic blood pressures. These findings suggest that patients with hypertension have high plasma TBARS, and benidipine hydrochloride decreases not only blood pressure but also oxidative stress in the clinical practice.

Mitochondrial DNA copy number correlates with oxidative stress and predicts mortality in nondiabetic hemodialysis patients

Oxidative stress is highly prevalent in hemodialysis patients and may contribute to atherosclerosis and mortality. The copy number of mitochondrial DNA (mtDNA) is affected by oxidative stress in blood circulation. This study aimed to test whether mtDNA copy number correlates with oxidative stress and predicts all-cause mortality in nondiabetic hemodialysis patients. Ninety-five nondiabetic hemodialysis patients and 95 healthy subjects were enrolled. Plasma thiobarbituric acid-reactive substances (TBARS) and plasma free thiol were used as indicators of oxidative stress and antioxidant defense, respectively. Mitochondrial DNA copy number in peripheral blood leukocytes was measured by determining relative amounts of mtDNA to nuclear DNA by quantitative real-time PCR. All-cause mortality of hemodialysis patient was recorded during a follow-up of 3 years. Nondiabetic hemodialysis patients showed higher TBARS levels, lower free thiol levels and higher mtDNA copy numbers compared with normal control subjects. The plasma TBARS level was a significant factor correlating positively to the mtDNA copy number (p=0.024). Patients with a mtDNA copy number higher than the median had a higher all-cause mortality than patients with a lower mtDNA copy number (17.0% vs. 4.2%; log-rank test: p=0.038). A 1-log increase in mtDNA copy number was independently related to an increase in the risk for mortality (hazard ratio 21.360; 95% confidence interval, 1.298-351.572). Nondiabetic hemodialysis patients had higher oxidative stress and mtDNA copy numbers than healthy subjects. The mtDNA copy number correlates with oxidative stress and predicts mortality in nondiabetic hemodialysis patients.

Vitamin E prevents steroid-induced osteonecrosis in rabbits

Background and purpose Prevention of osteonecrosis after corticosteroid administration would be important. We examined the potential of vitamin E (α-tocopherol) to reduce the incidence of corticosteroid-induced osteonecrosis in an animal model.Methods Japanese white rabbits were divided into 2 groups; the control group was fed a normal diet and the experimental group was fed α-tocopherol-supplemented diet in which α-tocopherol (600 mg/kg diet) was added to the normal diet. To induce osteonecrosis, high-dose methylprednisolone acetate (MPSL) (20 mg/kg body weight) was injected once into the right gluteus medius muscle of all rabbits. 4 weeks after the injection of MPSL, the presence or absence of osteonecrosis of bilateral femurs was examined histopathologically. The tocopherol/cholesterol ratios were calculated. The plasma levels of thiobarbituric acid-reactive substances (TBARS) were measured.Results Alpha-tocopherol-supplemented diet reduced the incidence of osteonecrosis, which developed in 14 of 20 rabbits in the control group and 5 of 21 rabbits in the experimental group (p = 0.004). The tocopherol/cholesterol ratio was higher in the experimental group than in the control group after the α-tocopherol administration. The plasma TBARS level was lower in the experimental group than in the control group at 4 weeks after the MPSL administration.Interpretation Our findings may offer a new approach for the prevention of corticosteroid-induced osteonecrosis.

Lycopene in the Prevention of Gastrointestinal Toxicity of Radiotherapy

We conducted a study to investigate if lycopene could reduce gastrointestinal toxicity of abdominal and pelvic radiation in Wistar albino rats. Animals received either a control diet (Group 1), lycopene-supplemented diet (Group 2), control diet and radiation (Group 3), and lycopene-supplemented diet plus radiation (Group 4). In Groups 2 and 4, the rats received 5 mg/kg/day lycopene for 10 days. In Groups 3 and 4, the rats received single fraction 8 Gy abdominal and pelvic radiation (RT) on Day 10. Study endpoints included weight loss, diarrhea, duration of diarrhea, survival, and an oxidative stress marker, plasma level of thiobarbituric acid reactive substance (TBARS). The rats receiving RT only had significantly higher weight loss rate compared to the lycopene plus RT group (P = 0.001). Plasma TBARS levels after RT were also significantly higher in the RT only group compared to lycopene plus RT group (P = 0.001). In conclusion, lycopene supplementation significantly reduced the weight loss and prevented oxidative stress in rats treated with abdominopelvic radiation.

Increased plasma concentrations of soy isoflavones by increased doses of soy isoflavones are irrelevant to lipid peroxidation and aberrant crypt foci formation in colonic cancer model rats

We have investigated whether soy isoflavones supplemented to diets increase plasma concentrations of soy isoflavones and equol, and whether increased plasma concentration of soy isoflavones suppresses tissue levels of lipid peroxides and aberrant crypt foci (ACF) formation in colon cancer model rats. Sprague Dawley male rats were injected with 1,2‐dimethylthydrazine (DMH) and given one of AIN93‐based experimental diets (0, 10, 50, 150, or 500 mg isoflavones per kg diet) for 12 weeks. Thiobarbituric acid reactive substances (TBARS) of plasma and homogenates of liver and kidneys were determined using TBARS assay kit. Plasma concentrations of genistein, daidzein and equol were determined using kits by competitive time‐resolved fluoroimmunoassay technique. Plasma concentrations of genistein (R2=0.521 by genistein intake, p&lt;0.001), daidzein (R2=0.623 by daidzein intake, p&lt;0.001) and equol (R2=0.528 by daidzein intake, p&lt;0.001) were increased dose‐dependently. However, the numbers of ACF decreased significantly (p&lt;0.01) in 10 or 50 mg isoflavones‐fed groups as compared with the control group, and there was no significant correlation between the number of ACF and plasma concentration of genistein, daidzein or equol. Plasma TBARS level was not influenced by either dose or plasma level of soy isoflavones. Hepatic levels of TBARS were significantly lower in 10 and 50 mg isoflavones‐fed groups as compared with the control group. The level of kidney TBARS was significantly lower in only 50 mg isoflavones‐fed group as compared with the control group. Therefore, the results indicate that optimal level of soy isoflavones seemed to be most effective in suppressing ACF formation and lipid peroxidation in DMH‐induced colon cancer model rats.

Correlation of Oxidative Stress Biomarkers and Peritoneal Urea Clearance with Mitochondrial DNA Copy Number in Continuous Ambulatory Peritoneal Dialysis Patients

Background/Aims: The influence of oxidative stress and peritoneal clearance on alterations in mitochondrial DNA (mtDNA) copy number in continuous ambulatory peritoneal dialysis (CAPD) patients was investigated. Methods: Ninety-one CAPD patients (age, 30–57 years) and 99 age-matched healthy subjects were enrolled. Biochemical variables, plasma thiobarbituric-acid-reactive substances (TBARS), free thiol levels and mtDNA copy number in peripheral leukocytes were measured. Results: CAPD patients showed higher TBARS levels, lower free thiol levels and a higher mtDNA copy number than control subjects. Plasma TBARS levels and peritoneal urea clearance were significant factors contributing positively to leukocyte mtDNA copy number (p = 0.024, R² = 0.238). The CAPD patients were further categorized into 4 groups depending on whether the TBARS and free thiol plasma levels were above or below the mean values for these parameters. Patients with higher TBARS levels and lower free thiol levels had a significantly higher number of leukocyte mtDNA copies than patients with lower TBARS levels and higher free thiol levels (multi-covariate ANOVA, p = 0.008). Conclusion: This study demonstrated that CAPD patients have higher oxidative stress than healthy subjects; such elevated oxidative stress and peritoneal urea clearance have a positive correlation with mtDNA copy number in peripheral leukocytes.

Ant-Altherogenic Effects of Morelloflavone from Garcinia dulcis Leaves in Cholesterol Fed Rabbits

A biflavonoid, morelloflavone isolated from leaves of Garcinia dulcis Kurz was investigated for its ability to reduce plasma lipids and prevent progression of atherosclerotic lesions in hypercholesterolemic rabbits. Male rabbits were divided into 6 groups. Group 1 received a regular diet, Group 2 received a regular diet with 0.02% (w/w) of G. dulcis derived morelloflavone, Group 3 was fed a diet containing 1% (w/w) cholesterol to induce hypercholesterolemia, and Group 4 to Group 6 had their 1% cholesterol diets supplemented with morelloflavone at concentrations of 0.005%, 0.01% and 0.02%, respectively. During a 4 month-experimental period, rabbits were monitored for their body weights and plasma cholesterol, triglycerides and thiobarbituric acid-reactive substances (TBARS) levels monthly and the extent of aortic atherosclerotic lesions were analysed at the end of the period. The levels of plasma cholesterol, triglycerides and TBARS as well as intimal thickening within aortas were increased in all animals fed with cholesterol diets. Such increases, however, were reduced in the presence of morelloflavone. The concentrations of morelloflavone that showed inhibitory effects in all cases were 0.005% and 0.01%, whereas the 0.02% dosage was ineffective.

Antioxidant effects and insulin resistance improvement of chromium combined with vitamin C and e supplementation for type 2 diabetes mellitus.

To determine the effects of combined supplementation with chromium (Cr) and vitamins C and E on oxidative stress in type 2 diabetes, adult subjects with HbA1c >8.5%. Subjects (n = 30) in this randomized, double blind, placebo-control study were divided into three groups (placebo, Cr or Cr + C + E) on daily treatment. The Cr group received 1000 µg of Cr (as Cr yeast); the Cr + C + E group received Cr (1000 µg as Cr yeast) together with vitamins C (1000 mg) and E (800 IU); and, a control group received a placebo. Baseline plasma Cr levels were not significant differences comparing the supplementation and placebo groups. Thiobarbituric acid reactive substances (TBARS) and total antioxidative status (TAS) were also not significant different. Following the 6-month study period, the plasma TBARS levels, fasting glucose, HbA1c and insulin resistance were significantly decreased in the Cr and Cr + C + E groups, but not for the placebo group. Plasma TAS and glutathione peroxidase were significantly higher for Cr and Cr + C + E groups relative to the placebo group. These findings suggest that Cr supplementation alone and combined of Cr together with vitamins C and E was effective for minimization of oxidative stress and improvement of glucose metabolism in type 2 DM patients.

Altered antioxidant defense system in clinically stable patients with schizophrenia and their unaffected siblings

Objective To determine Red Blood Cell (RBC) antioxidant enzyme activities and plasma Thiobarbituric Acid Reactive Substances (TBARS) in clinically stable patients with schizophrenia and their unaffected siblings. Methods A case-control study carried out on three groups: 60 schizophrenic patients treated with neuroleptics, 33 of their unaffected siblings and 30 healthy controls with no family psychiatric history. Biological markers were measured on fasting patients after a period of tobacco abstinence: RBC antioxidant enzyme activities – superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT) – by spectrophotometry and plasma levels of TBARS by spectrofluorimetry. Results RBC SOD and CAT activities were significantly lower in schizophrenic patients and their unaffected siblings compared to the control group ( P < 0.001). Schizophrenic patients also had significantly lower RBC GSH-Px activity than controls ( P = 0.03), whereas their unaffected siblings had significantly higher RBC GSH-Px activity than controls ( P = 0.04). Plasma TBARS were higher in schizophrenic patients than their unaffected siblings: 2.1 ± 0.8 μmol/l vs. 1.7 ± 0.6 μmol/l ( P = 0.06). Conclusions Our results showed a decrease in antioxidant enzyme activities and an increase in lipid peroxidation confirming the existence of oxidative stress in schizophrenic patients treated with neuroleptics. Additionally, this suggests that the increase in GSH-Px activity in unaffected siblings would be a protective mechanism against oxidative stress and damage. Other studies are necessary to confirm these findings.

Swimming reduces the severity of atherosclerosis in apolipoprotein E deficient mice by antioxidant effects

It was shown that aerobic exercise training may protect against the development of atherosclerosis. However, the precise mechanisms are still unknown. We assessed the hypothesis that exercise training reduced the severity of experimental atherosclerosis in apolipoprotein (apo) E-deficient mice by antioxidant effects. Exercise training (45 min swimming, 3 times/week) was conducted on apo E-deficient mice fed a high fat diet. Over 8 and 16 weeks on alternate days, mice were treated with and without exercise, and additional exercise-treated mice were orally given 25 mg/kg/day of NG-nitro-L-arginine methylester (L-NAME), an inhibitor of nitric oxide synthase (NOS). In addition, the effect of L-arginine against L-NAME was also tested. Fatty streak formation at 8 weeks and fibrofatty plaques at 16 weeks developed in apo E-deficient mice fed a high fat diet, and were suppressed in mice treated with swimming for 8 and 16 weeks. In contrast, atherosclerotic lesions were not ameliorated in mice treated with exercise training associated with oral L-NAME. However, in mice treated with swimming associated with L-NAME and L-arginine, the atherosclerotic lesions were reduced. Immunohistochemical analysis revealed that macrophage and CD4+ cell accumulation in the fatty streak lesions was suppressed in mice treated with exercise, but not in those treated with exercise associated with L-NAME administration. The severity of atherosclerotic lesions was inversely correlated with the endothelial NOS expression and the expression of an endogenous antioxidant protein, thioredoxin. Namely, the expression of thioredoxin in mice treated with exercise was suppressed compared with mice without exercise. Plasma thiobarbituric acid-reactive substance levels were significantly lower in groups with exercise than in those without exercise or with exercise associated with L-NAME administration, suggesting exercise-induced less lipid peroxidation. Differences in lesion area did not correlate with any significant alterations in serum lipid levels. The exercise load used in the current study did not affect energy metabolism efficacies in the hearts. Exercise training, in which the load did not affect energy metabolism efficacy of the heart, suppressed atherosclerosis by antioxidant effects via the vascular NO system.

Plasma Thiobarbituric Acid-Reactive Substance Levels in Subclinical Hypothyroidism

Objective: The purpose of this study was to determine thiobarbituric acid-reactive substance (TBARS) levels in subclinical hypothyroidism and to examine the effect of levothyroxine replacement on TBARS levels. Subjects and Methods: A cohort of 28 female patients with subclinical hypothyroidism and 24 healthy controls were enrolled in this study. The levels of plasma TBARS, serum lipids, and high-sensitive C-reactive protein (CRP) in patients with subclinical hypothyroidism at baseline and after achieving euthyroid state by levothyroxine were assessed. Results: TBARS levels of the patients were similar to those of the control group in the subclinical hypothyroid state and after restoration of euthyroidism by levothyroxine replacement. TBARS levels decreased after levothyroxine treatment, but did not reach statistical significance. There was no significant correlation between TBARS, lipid and CRP levels. Serum CRP levels were higher in subclinical hypothyroidism (4.28 ± 0.9 mg/l) than in the control group (1.95 ± 0.34 mg/l) and the difference was statistically significant (p = 0.03). After achieving euthyroid state, CRP levels decreased significantly in patients with subclinical hypothyroidism from 4.28 ± 0.9 to 2.32 ± 0.6 mg/l (p = 0.006). Conclusion: Our findings suggest that there is no significant alteration of plasma TBARS levels neither in subclinical hypothyroid state nor after achieving euthyroid state. Serum CRP level is higher in patients with subclinical hypothyroidism than in the control group. Normalization of thyroid state seems to effectively reduce serum CRP levels in subclinical hypothyroidism without any correlation with TBARS activity.

The Relationship Between Lipid Peroxidation and LDL Desialylation in Experimental Atherosclerosis

ABSTRACTHigh serum total cholesterol concentration has been strongly connected with atherosclerosis in numerous studies. Being the main carrier of cholesterol in blood, low-density lipoprotein (LDL) is also the principal lipoprotein causing atherosclerosis. Sialic acids are a family of amino sugars that are commonly found as terminal oligosaccharide residues on glycoproteins and are sialylated on their apolipoprotein and glycolipid constituents. In several studies, it was demonstrated that LDL has a 2.5- to 5-fold lower content of sialic acid in patients with coronary artery disease compared with healthy subjects. The role of oxidatively modified LDL in the pathogenesis has been well documented. These studies have focused on modifications in the lipid and protein parts of LDL. But recently, desialylated LDL and its relation with the oxidation mechanisms have received attention in the pathogenesis of atherosclerosis and coronary artery disease (CAD). From these points, we have performed atheroma plaques in an experimental atherosclerosis model with rabbits and examined the LDL and plasma sialic acid and thiobarbituric acid reactive substance (TBARS) levels in the same model. We also have determined serum sialidase enzyme activities relevant with these parameters. LDL sialic acid levels were significantly decreased in the progression of the atherosclerosis (by the 30th, 60th, and 90th days). LDL and plasma TBARS levels and plasma sialidase enzyme activities were significantly elevated by the same time periods. In conclusion, serum sialidase enzyme may play an important role in the desialylation mechanism, and reactive oxygen substance (ROS) may affect this reaction.

Association of plasma level of thiobarbituric acid reactive substances with extent of hepatocellular injury in preterm infants with cholestatic jaundice

The present study was designed to determine the association between extent of hepatocellular injury and plasma level of thiobarbituric acid reactive substances (TBARS) in pre term infants with cholestasis. Preterm infants (<35 weeks gestation) admitted to the neonatal intensive care unit were enrolled (with their parents informed consent) in either the 'cholestasis' group (if their direct bilirubin was >2 mg/dl) (n=25) or in the control group (n=16). Blood samples for measurement of TBARS, direct bilirubin and transaminases were obtained with-in 24 hours of enrollment. The cholestasis and control groups were comparable with respect to gestational age, birth weight and Apgar score. Serum direct bilirubin, SGOT (EC 2.6.1.1) and SGPT (EC 2.6.1.2) levels were significantly high in the cholestasis group. Plasma levels of TBARS in cholestasis group were correlated with SGOT (F=276.92; P<0.0001) and SGPT (F=355.17; P<0.0001) and differed significantly between cholestatic and control infants. Our findings suggest that oxidative stress in preterm infants with cholestasis is associated with hepatocellular injury.

Comparative study on lipid peroxidation and antioxidant vitamins E and C inFalciparum andVivax malaria

Reactive oxygen species are thought to be involved in the pathogenesis of Malaria. To assess the extent of oxidative stress, a study was conducted in patients withPlasmodium falciparum malaria andPlasmodium Vivax malaria. Plasma Thiobarbituric acid reactive substances (TBARS) were measured to assess the degree of lipid peroxidation. Antioxidant status was measured by estimating the levels of Vitamins E and C. Results were compared with age and sex matched control subjects. This study suggests that plasma TBARS levels were significantly increased in malaria patients. The patients withP. falciparum infection showed significantly increased levels of lipid peroxides when compared toP. vivax malaria. The antioxidant Vitamins E and C were decreased significantly in malaria patients in both the groups. Maximum decline in Vitamin C was observed inP. vivax malaria. Therefore it is been hypothesized that antioxidant Vitamins E and C could provide protection against the oxidative stress induced by malaria.