Levels Of Antioxidant Defenses Research Articles

Tidal height influences the levels of enzymatic antioxidant defences in Mytilus edulis

We investigated the potential variability of enzymatic antioxidant activities in blue mussels Mytilus edulis from a single intertidal population but living at different tidal heights. Activity levels of antioxidant enzymes (Cu/Zn superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione transferase) were measured in the gills and digestive gland of mussels sampled at high shore (HS, air-exposure > 6 h/12 h) and low shore (LS, air-exposure < 2 h/12 h) of an intertidal zone (Yport, Normandie, France) for two consecutive autumns. In both tissues, levels of each enzymatic activity (except GST) were clearly higher in HS mussels than in LS for the two years. These results suggest an ability to acclimate the enzymatic antioxidant defences to the degree of undergone stress, confirming the importance of environmental conditions in the antioxidant responses. Therefore, the location of organisms on the shore should be taken into account in sampling for ecotoxicological studies.

Overexpression of Glucose-6-phosphate Dehydrogenase Extends the Life Span of Drosophila melanogaster

The redox state of tissues tends to become progressively more prooxidizing during the aging process. The hypothesis tested in this study was that enhancement of reductive capacity by overexpression of glucose-6-phosphate dehydrogenase (G6PD), a key enzyme for NADPH biosynthesis, could protect against oxidative stress and extend the life span of transgenic Drosophila melanogaster. Overexpression of G6PD was achieved by combining a UAS-G6PD responder transgene at one of four independent loci with either a broad expression (armadillo-GAL4, Tubulin-GAL4, C23-GAL4, and da-GAL4) or a neuronal driver (D42-GAL4 and Appl-GAL4). The mean life spans of G6PD overexpressor flies were extended, in comparison with driver and responder controls, as follows: armadillo-GAL4 (up to 38%), Tubulin-GAL4 (up to 29%), C23-GAL4 (up to 27%), da-GAL4 (up to 24%), D42-GAL4 (up to 18%), and Appl-GAL4 (up to 16%). The G6PD enzymatic activity was increased, as were the levels of NADPH, NADH, and the GSH/GSSG ratio. Resistance to experimental oxidative stress was enhanced. Furthermore, metabolic rates and fertility were essentially the same in G6PD overexpressors and control flies. Collectively, the results demonstrate that enhancement of the NADPH biosynthetic capability can extend the life span of a relatively long-lived strain of flies, which supports the oxidative stress hypothesis of aging.

Adiposity Measures and Oxidative Stress Among Police Officers

Our objective was to investigate associations between adiposity measures (BMI, waist circumference, waist-to-hip ratio, waist-to-height ratio, and abdominal height) and biomarkers of oxidative stress (glutathione (GSH), GSH peroxidase (GSH-Px), vitamin C, thiobarbituric acid reactive substances (TBARS), and trolox equivalent antioxidant capacity (TEAC)) among police officers. This cross-sectional study included randomly selected police officers (43 policewomen; 67 policemen) from Buffalo, New York. Adiposity measures were performed using standardized methods. Biomarkers were measured on fasting blood specimens. An oxidative stress score (OSS) was created as a composite of the biomarkers. ANOVAs were used to compare mean levels of biomarkers across tertiles of the adiposity measures. Officers were 26- to 61-years old. GSH was inversely associated with waist circumference (trend P = 0.030) and waist-to-hip ratio (trend P = 0.026). GSH-Px was inversely associated with BMI (trend P = 0.004) and with waist-to-height ratio (trend P = 0.017). No associations were observed for TEAC, TBARS, or OSS with any adiposity measure. Significant interactions were observed by physical activity status for GSH with waist circumference and waist-to-hip ratio and for vitamin C with waist circumference, waist-to-hip and waist-to-height ratios. The above associations were inversely related only among officers who reported engaging in physical activity. Inverse associations were observed for BMI and waist circumference with GSH, but only among women; the interaction with gender was significant. Larger indices of adiposity were associated with increased levels of oxidative stress and decreased levels of antioxidant defense.

Autotomy reduces immune function and antioxidant defence

Costs of autotomy, an antipredator defence, are typically explained by impaired mobility; yet physiologically mediated costs may also play a role. Given the resemblance to wounding, a decreased immune function and an associated reduction in antioxidant defence is expected after autotomy. In line with this, after lamellae autotomy, larvae of the damselfly Lestes viridis showed lower levels of innate immunity (i.e. phenoloxidase, PO) and antioxidant defence (superoxide dismutase, SOD). Levels of catalase (CAT) remained, however, unaffected. In line with its cytotoxicity, PO covaried positively with CAT, yet negatively with SOD. We identified a novel cost of autotomy in terms of a reduced innate immunity, which may provide an alternative explanation for the often observed costs of autotomy and which may generate indirect interactions between predators and parasites.

Respiratory Deficiency Enhances the Sensitivity of the Pathogenic Fungus Candida to Photodynamic Treatment

Mucosal infections caused by the pathogenic fungus Candida are a significant infectious disease problem and are often difficult to eradicate because of the high frequency of resistance to conventional antifungal agents. Photodynamic treatment (PDT) offers an attractive therapeutic alternative. Previous studies demonstrated that filamentous forms and biofilms of Candida albicans were sensitive to PDT using Photofrin as a photosensitizer. However, early stationary phase yeast forms of C. albicans and Candida glabrata were not adversely affected by treatment. We report that the cationic porphyrin photosensitizer meso-tetra (N-methyl-4-pyridyl) porphine tetra tosylate (TMP-1363) is effective in PDT against yeast forms of C. albicans and C. glabrata. Respiratory-deficient (RD) strains of C. albicans and C. glabrata display a pleiotropic resistance pattern, including resistance to members of the azole family of antifungals, the salivary antimicrobial peptides histatins and other types of toxic stresses. In contrast to this pattern, RD mutants of both C. albicans and C. glabrata were significantly more sensitive to PDT compared to parental strains. These data suggest that intact mitochondrial function may provide a basal level of anti-oxidant defense against PDT-induced phototoxicity in Candida, and reveals pathways of resistance to oxidative stress that can potentially be targeted to increase the efficacy of PDT against this pathogenic fungus.

Genetic variation and gene expression in antioxidant related enzymes and risk of COPD: a systematic review

Background:Observational epidemiological studies of dietary antioxidant intake, serum antioxidant concentration and lung outcomes suggest that lower levels of antioxidant defences are associated with decreased lung function. Another approach to understanding...

Antioxidant response of the seagrass Posidonia oceanica when epiphytized by the invasive macroalgae Lophocladia lallemandii

The aim was to evaluate the antioxidant defences and the occurrence of oxidative damage in Posidonia oceanica under a stress situation due to the epiphytism of the invasive macroalgae Lophocladia lallemandii. P. oceanica leaves were collected in the absence (control station) and in the presence of the epiphytic algae L. lallemandii and the antioxidant enzyme activities, markers of oxidative damage, and hydrogen peroxide production were determined. Antioxidant enzyme - catalase, glutathione peroxidase and superoxide dismutase – activities were significantly higher in Posidonia epiphytized by L. lallemandii. Malondialdehyde, protein carbonyl derivates, and glutathione levels were also higher in L. lallemandii epiphytized P. oceanica leaves compared to control samples. The production of hydrogen peroxide was also significantly increased when Posidonia was epiphytized by L. lallemandii. The invasion of P. oceanica meadows by L. lallemandii appeared to induce oxidative stress in the seagrass as evidenced by increased levels of oxidative stress markers and antioxidant defences.

Seasonal variations in markers of stress and oxidative stress in rats

High ambient temperature has been reported to increase oxidative stress by increasing lipid peroxidation and decreasing antioxidant defence in transition dairy cows. It is also known to cause an increase in plasma cortisol levels in goats, European hedgehog and human volunteers. High levels of glucocorticoids have been reported to decrease blood glutathione and erythrocyte superoxide dismutase activity in rats. Although institutional animal houses in research laboratories of developed countries maintain animals in air-conditioned rooms at constant temperature, the same is not true of animal houses in the developing countries especially those belonging to smaller institutions and this could affect the results of the experiments being conducted on these animals. The present research study was done to assess the effects of seasonal variations on the status of erythrocyte oxidative damage, antioxidant defence and plasma cortisol levels in adult female Wistar rats. Rats were kept in their home cages and were left in non-air-conditioned procedure rooms in two different seasons, Hot season (March-May) and Cool season (June to September). Erythrocyte Thiobarbituric acid reactive substances and plasma cortisol levels were significantly increased in rats exposed to high ambient temperature and humidity of the hot season as compared to the rats of the cool season. Erythrocyte reduced glutathione levels, erythrocyte glutathione peroxidase and superoxide dismutase activities were significantly decreased in the hot season group of rats. The results of our experiments showed that exposure of adult female Wistar rats to high ambient temperature and humidity of the hot season increases neuroendocrine stress, oxidative stress and decreases antioxidant defence in them.

Efficacy of caffeic acid in preventing nickel induced oxidative damage in liver of rats

Nickel (Ni), a major environmental pollutant, is known for its wide toxic manifestations. In the present study caffeic acid (CA), one of the most commonly occurring phenolic acids in fruits, grains and dietary supplements, was evaluated for its protective effect against the Ni induced oxidative damage in liver. In this investigation, Ni (20 mg/kg body weight) was administered intraperitoneally for 20 days to induce toxicity. CA was administered orally (15, 30 and 60 mg/kg body weight) for 20 days with intraperitoneal administration of Ni. Ni induced liver damage was clearly shown by the increased activities of serum hepatic enzymes namely aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), gamma glutamyl transferase (GGT) and lactate dehydrogenase (LDH) along with increased elevation of lipid peroxidation indices (thiobarbituric reactive acid substances (TBARS) and lipid hydroperoxides). The toxic effect of Ni was also indicated by significantly decreased levels of enzymatic (superoxide dismutase (SOD), catalase (CAT) glutathione peroxidase (GPx) and glutathione S-transferase (GST)) and non-enzymatic antioxidants (glutathione (GSH), vitamin C and vitamin E). CA administered at a dose of 60 mg/kg body weight significantly reversed the activities of hepatic marker enzymes to their near normal levels when compared with other two doses. In addition, CA significantly reduced lipid peroxidation and restored the levels of antioxidant defense in the liver. All these changes were supported by histological observations. The results indicate that CA may be beneficial in ameliorating the Ni induced oxidative damage in the liver of rats.

Oxidative Stress in the Thyroid Gland: From Harmlessness to Hazard Depending on the Iodine Content

In basal conditions, thyroid epithelial cells produce moderate amounts of reactive oxygen species (ROS) that are physiologically required for thyroid hormone synthesis. They are not necessarily toxic because they are continuously detoxified either in the process of hormone synthesis or by endogenous antioxidant systems. Using a rat model of goiter formation and iodine-induced involution, we found that compared with control thyroids, the oxidative stress, assessed by the detection of 4-hydroxynonenal, was strongly enhanced both in hyperplastic and involuting glands. The level of antioxidant defenses (glutathione peroxidases and peroxiredoxins) was also up-regulated in both groups, although somewhat less in the latter. Of note, increased oxidative stress came along with an inflammatory reaction, but only in involuting glands, suggesting that although antioxidant systems can adequately buffer a heavy load of ROS in goiter, it is not necessarily the case in involuting glands. The effects of 15-deoxy-Delta(12,14)-prostaglandin J2 (15dPGJ2), an endogenous ligand of peroxisome proliferated-activated receptor gamma (PPARgamma) with antiinflammatory properties, were then investigated in involuting glands. This drug strongly reduced both 4-hydroxynonenal staining and the inflammatory reaction, indicating that it can block iodine-induced cytotoxicity. When experiments were carried out with the PPARgamma antagonist, bisphenol A diglycidyl ether, 15dPGJ2-induced effects remained unchanged, suggesting that these effects were not mediated by PPARgamma. In conclusion, thyroid epithelial cells are well adapted to endogenously produced ROS in basal and goitrous conditions. In iodine-induced goiter involution, the increased oxidative stress is accompanied by inflammation that can be blocked by 15dPGJ2 through PPARgamma-independent protective effects.

Age-related increases in DNA repair and antioxidant protection: A comparison of the Boyd Orr Cohort of elderly subjects with a younger population sample

One commonly held theory of ageing is that it is caused by oxidative damage to critical molecules in the body, including proteins, lipids and nucleic acids. Accumulation of oxidative DNA damage with age will occur if there is an increase in reactive oxygen species in the body, or a decline in antioxidant defences, or a reduced efficiency of DNA repair. Using the comet assay, we have measured DNA breaks and oxidised purines in lymphocytes from subjects of different age groups: 20-35 (n = 40), 63-70 (n = 35), and 75-82 (n = 22). We also measured the resistance of lymphocyte DNA to H(2)O(2)-induced oxidative damage, and the repair activity of cell-free lymphocyte extracts on a substrate containing 8-oxoguanine. We found an increase in oxidative base damage in old age, but this apparently does not result from deterioration of either antioxidant defence or DNA repair. In fact, both of these tend to increase with age. There were few age-related differences in plasma levels of dietary antioxidants: tocopherols and retinol were higher in the older subjects, while lycopene was highest in the youngest age group. It is possible, that in old age, antioxidant defences and DNA repair are induced, in response to a higher level of oxidative damage, as mitochondria become more leaky and release more reactive oxygen. It is equally possible that older people, as survivors, had relatively high levels of antioxidant defences and DNA repair earlier in their lives, compared with those who did not survive to such an age.

Effects of diallyl tetrasulfide on cadmium-induced oxidative damage in the liver of rats

The protective efficacy of diallyl tetrasulfide (DTS) from garlic on liver injury induced by cadmium (Cd) was investigated. In this study, Cd (3 mg/kg body weight) was administered subcutaneously for 3 weeks to induce toxicity. DTS was administered orally (10, 20 and 40 mg/kg body weight) for 3 weeks with subcutaneous (sc) injection of Cd. Cd-induced liver damage was evidenced from increased activities of serum hepatic enzymes, namely aspartate transaminase, alanine transaminase, alkaline phosphatase and lactate dehydrogenase, with significant elevation of lipid peroxidation indices (thiobarbituric acid reactive substances and hydroperoxides) and protein carbonyl groups in the liver. Rats subjected to Cd toxicity also showed a decline in the levels of total thiols, reduced glutathione (GSH), vitamin C and vitamin E, accompanied by an increased accumulation of Cd, and significantly decreased activities of superoxide dismutase, catalase (CAT), glutathione peroxidase, glutathione-S-transferase (GST), glutathione reductase, and glucose-6-phosphate dehydrogenase in the liver. Administration of DTS at 40 mg/kg body weight significantly normalised the activities of hepatic marker enzymes, compared to other doses of DTS (10 and 20 mg/kg body weight). In addition, DTS (40 mg/kg body weight) significantly reduced the accumulation of Cd and the level of lipid peroxidation, and restored the level of antioxidant defense in the liver. Histological studies also showed that administration of DTS to Cd-treated rats resulted in a marked improvement of hepatocytes morphology with mild portal inflammation. Our results suggest that DTS might play a vital role in protecting Cd-induced oxidative damage in the liver.

Differential susceptibility following β-amyloid peptide-(1–40) administration in C57BL/6 and Swiss albino mice: Evidence for a dissociation between cognitive deficits and the glutathione system response

Considerable evidence supports the role of oxidative stress in the pathogenesis of Alzheimer's disease (AD). Previous studies suggest that the central nervous system (CNS) administration of β-amyloid peptide, the major constituent of senile plaque in AD, induces oxidative stress in rodents which may contribute to the learning and memory deficits verified in the β-amyloid model of AD. In the present study, we compared the effects of a single intracerebroventricular (i.c.v.) injection of aggregated β-amyloid peptide-(1–40) (Aβ 1–40) (400 pmol/mouse) on spatial learning and memory performance, synaptic density and the glutathione (GSH)-dependent antioxidant status in adult male C57BL/6 and Swiss albino mice. Seven days after Aβ 1–40 administration, C57BL/6 and Swiss mice presented similar spatial learning and memory impairments, as evaluated in the water maze task, although these impairments were not found in Aβ 40–1-treated mice. Moreover, a similar decline of synaptophysin levels was observed in the hippocampus (HC) and prefrontal cortex (PFC) of both Swiss and C57BL/6 mice treated with Aβ 1–40, which suggests synaptic loss. C57BL/6 mice presented lower levels of glutathione-related antioxidant defences (total glutathione (GSH-t) levels, glutathione peroxidase (GPx) and glutathione reductase (GR) activity) in the HC and PFC in comparison to Swiss mice. Despite the reduced basal GSH-dependent antioxidant defences observed in C57BL/6 mice, Aβ 1–40 administration induced significant alterations in the brain antioxidant parameters only in Swiss mice, decreasing GSH-t levels and increasing GPx and GR activity in the HC and PFC 24 h after treatment. These results indicate strain differences in the susceptibility to Aβ 1–40-induced changes in the GSH-dependent antioxidant defences in mice, which should be taken into account in further studies using the Aβ model of AD in mice. In addition, the present findings suggest that the spatial learning and memory deficits induced by β-amyloid peptides in rodents may not be entirely related to glutathione-dependent antioxidant response.

Antioxidant Effects of Metronidazole in Colonic Tissue

Reactive oxygen species, primarily generated in the mitochondria, contribute to tissue injury in inflammatory bowel diseases. The efficacy of metronidazole (MTZ) in some situations of inflammatory bowel disease may result not only from its antibiotic effect, but also from an antioxidant effect. We evaluated, under physiologic conditions, the antioxidant potential of MTZ on the biomarkers of oxidative damage to proteins (protein carbonyls), lipids (malondialdehyde), and the levels of antioxidant defense (glutathione) in the small bowel, large bowel, and liver of control and MTZ-treated rats. Basal levels of protein carbonyls and malondialdehyde were significantly higher in the colon compared with those in the small intestine, whereas glutathione levels were quite similar along the bowel. MTZ reduced significantly the colonic oxidative damage to proteins without any side effect in the liver. This is the first evidence of an antioxidant effect of MTZ on oxidative protein damage in the colon under physiologic conditions.

Skeletal muscles in chronic obstructive pulmonary disease: Deconditioning, or myopathy?

In recent years, COPD has become increasingly thought of as a systemic disease affecting many tissues and organs in addition to the lungs. The skeletal muscles in particular have been the target of much research focusing on whether the universally observed exercise limitation reflects a systemic myopathic effect of COPD, or simply the consequences of extreme, long-term inactivity. In this paper, the evidence is reviewed for COPD patients without loss of muscle mass and who are not taking systemic steroids. While altered levels of antioxidant defences (lower), circulating inflammatory biomarkers (higher) and anabolic hormones (lower) have been found in COPD, cause and effect remains to be established for the link of inflammation/oxidative stress to muscle dysfunction. Other evidence used to propose a myopathic state (early lactate release, reduced power output, lower metabolic enzyme capacities, greater phosphocreatine breakdown and slower phosphocreatine restoration after exercise, and altered fibre type distribution) also occur in normal subjects who are extremely inactive. Furthermore, intense small muscle mass training can normalize small muscle function in these patients. Based on these data, it remains to be shown that the muscles in COPD patients without loss of muscle mass are myopathic. The interesting discussion about systemic effects of COPD should not get in the way of systematic muscle training, which has been shown to be an effective component of rehabilitation.

Blood Antioxidant Status and Lipid Peroxidation in Patients with Chronic Pancreatitis

Purpose: The role of immune system in pathogenesis of chronic pancreatitis is unclear. The aim of this study was to establish the main determinants of plasma antioxidant potential in different types of chronic pancreatitis: alcoholic pancreatitis (ACP, N = 25), biliary pancreatitis (BCP, N = 37). Methods: We measured blood plasma levels of lipid peroxide oxidation and antioxidant defense: malondialdehyde (MD), hydroperoxide of lipids (HL); ceruloplasmine (CP) and myeloperoxidase (MPO). Measurements were performed by using colorimetric methods. Results: In comparison to healthy volunteers (HV, N = 18) the average concentration of plasma free-radical oxidation determinants (MD and HL) in both groups of chronic pancreatitis were significantly higher (by 45%-91%). Ceruloplasmine activity was higher (approximately 35%) in patients with alcoholic chronic pancreatitis, and lower (49%) in case of biliary chronic pancreatitis. MPO levels were lower in 2,5 and 2,1 times in case of alcoholic pancreatitis and biliary pancreatitis accordingly. Conclusions: Low levels of antioxidant defense in patients suffering from different types of chronic pancreatitis show the exhaustion of immune defense, high indices of blood plasma lipid peroxidation underline important role of immune system in pathogenesis of chronic pancreatitis and determine strategy of therapy.

Long-term antipsychotic treatments and crossover studies in rats: Differential effects of typical and atypical agents on the expression of antioxidant enzymes and membrane lipid peroxidation in rat brain

Short-term (<45 days) treatment studies in rats have reported increased oxidative stress and oxidative (i.e., oxygen free radical-mediated) neural cell injury with typical antipsychotics such as haloperidol, but not with the atypicals such as clozapine, olanzapine or risperidone. However, now these and several other atypical antipsychotics that differ in their neurotransmitter receptor affinity profiles are being used for a long-term treatment of schizophrenia. Therefore, understanding of their long-term treatment effects on the expression of antioxidant enzymes and oxidative neural cell injury in rats may be important to explain the possible differential mechanisms underlying their long-term clinical and side effects profiles. The effect of 90 and 180 day exposure to haloperidol (HAL, 2 mg/kg/day), a representative typical antipsychotic was compared to exposure to chlorpromazine (CPZ, 10 mg/kg/day), ziprasidone (ZIP, 12 mg/kg/day), risperidone (RISP, 2.5 mg/kg/day), clozapine (CLOZ, 20 mg/kg/day) or olanzapine (OLZ, 10 mg/kg/day) on the expression of antioxidant defense enzymes and levels of lipid peroxidation in the rat brain. The drug-induced effects on various antioxidant defense enzymes; manganese-superoxide dismutase (MnSOD), copper–zinc superoxide dismutase (CuZnSOD) and catalase (CAT) were assessed by determination of their enzymatic activity and protein content. Immunohistochemical analysis was also carried out to assess the cellular levels of MnSOD and CuZnSOD and cellular morphology. The oxidative membrane damage was assessed by determination of levels of the lipid peroxidation product, hydroxyalkanals (HAEs) in the rat brain. Both 90 and 180 days of HAL treatment very significantly decreased the levels of MnSOD (50%) and CuZnSOD (80%) and increased the levels of HAEs compared to vehicle treatment. Smaller reduction was found in CAT (25%) and no change in the glutathione peroxidase (GSHPx). The levels of enzymatic activity correlated generally well with the levels of enzyme protein indicating that the changes were in the expression of net protein. Though atypical antipsychotics like ZIP, RISP and OLZ did not show any change in the HAEs levels up to 90 days, further treatment up to 180 days resulted in significantly increased levels of HAEs in CPZ, ZIP and RISP, but not in OLZ treated rats. Post-treatment with several atypical antipsychotics (OLZ = CLOZ > RISP) for 90 days after 90 day of HAL treatment significantly restored the HAL-induced loss in MnSOD and CuZnSOD activities and increase in lipid peroxidation products as well as cellular morphology. These data may be very helpful in planning long-term use as well as switch over of these antipsychotics for the management of schizophrenia.

Increase in liver antioxidant enzyme activities in non‐alcoholic fatty liver disease

Steatosis may increase oxidative stress, which is counteracted by cellular enzymatic (cytosolic and mitochondrial superoxide dismutases (Cu/Zn-SOD and Mn-SOD), glutathione peroxidase (GPx), catalase) and non-enzymatic antioxidant systems. We aimed to determine, in patients with non-alcoholic fatty liver disease (NAFLD), the level of antioxidant defenses (1) in liver biopsies, to demonstrate the existence of oxidative stress; (2) in erythrocytes and plasma, to determine whether their antioxidant defenses reflect liver oxidative stress. Erythrocyte and plasma antioxidant defenses were prospectively studied in two groups of 16 patients: patients with NAFLD and controls. Liver biopsies were performed in eight NAFLD patients; liver antioxidant enzyme activities were measured and compared with those in 12 control livers used for transplantation. Cu/Zn-SOD, GPx and catalase activities were significantly higher in NAFLD livers than in controls whereas no significant differences were observed in Mn-SOD activity, and thiobarbituric acid-reactive substance (TBARS) concentration. No differences were observed in erythrocyte antioxidant enzyme activities (GPx, catalase, Cu/Zn-SOD), erythrocyte TBARS concentration, and plasma alpha-tocopherol concentration. Liver antioxidant enzyme activities were high in patients with NAFLD, reflecting an oxidative stress possibly involved in inflammation and fibrogenesis. However, erythrocyte and plasma antioxidant defenses did not reflect intrahepatic peroxidation.

Total Antioxidant Capacity and Levels of Epidermal Growth Factor and Nitric Oxide in Blood and Saliva of Insulin-Dependent Diabetic Patients

The aim of this study was to examine how type 1 diabetic patients have altered levels of lipid peroxidation, antioxidant defense, NO and EGF in their plasma and saliva. We tested the differences in lipid peroxidation level, antioxidant power, and concentrations of epidermal growth factor (EGF) and nitric oxide (NO) in saliva and blood of type 1 diabetic subjects in comparison to healthy control subjects. Nineteen subjects with type 1 diabetes mellitus and 19 healthy age- and sex-matched control subjects were included in the study. Blood and saliva samples were obtained and analyzed for thiobarbituric reactive substances (TBARS) as a marker of lipid peroxidation, ferric reducing ability (total antioxidant power), EGF and NO levels. TBARS levels did not show a significant difference between the two groups. Analysis of antioxidant power revealed that saliva and plasma of diabetic patients had more antioxidant power (p <0.01) than the healthy control population (107 +/- 10.35 vs. 11.14 +/- 4.66 and 192 +/- 12.3 vs. 142 +/- 15.2 mmol/L, respectively). Concentration of EGF was increased (p <0.01) in saliva whereas it was reduced (p <0.01) in plasma of diabetic patients in comparison to those of healthy subjects (2423 +/- 322 vs. 1513 +/- 341 and 125 +/- 14 vs. 346 +/- 60 pg/mL, respectively). NO level increased in both saliva and plasma of diabetic patients in comparison to those of healthy subjects (46.61 +/- 7 vs. 72.89 +/- 13 and 62.11 +/- 4.6 vs. 76.25 +/- 5 micromol/L, respectively). Blood HbA1c (%) of patients was significantly higher than that of controls (8.3 +/- 0.32 vs. 5.4 +/- 0.24, p <0.01). Existence of increased total antioxidant power in the presence of normal lipid peroxidation in plasma and saliva of type 1 diabetic patients indicates the existence of oxidative stress. Increased salivary EGF and NO levels in association with elevated TAOP is interesting and should be further studied.

Plasma Antioxidant Activity and Chromosome Aberrations in Humans Exposed to Long-Term Low-Dose γ-Irradiation

Plasma antioxidant activity was evaluated in the lecithin-Fe(2+) model system and cytogenetic studies were carried out in 16 men. A relationship between elevated antioxidant activity of the plasma and increased level of chromatid aberrations and with percentage of aberrant cells was detected in the experimental group, but no correlation was found between antioxidant activity and the integral dose of gamma-irradiation and rate of its accumulation. An assumption was made about exhaustion of the buffer capacity of the antioxidant defense system resulting from long-term exposure to unidentified factors of technogenic nature increasing plasma antioxidant activity and level of chromosome aberrations. In subjects with high level of antioxidant defense, naturally low antioxidant activity and low percentage of chromatid aberrations were probably maintained.