Lower serum zinc in major depression in relation to changes in serum acute phase proteins

There is now some evidence that major depression is accompanied by activation of the inflammatory response system (IRS). Other signs of IRS activation, which have been reported in major depression are lowered serum zinc (Zn) and serum albumin (Alb) concentrations. In serum, Zn is closely bound to Alb. The aims of the present study were to replicate previous findings that major depression is accompanied by lowered serum Zn and Alb and to examine whether the decrease in serum Zn may be explained by that in serum Alb. The above variables were determined in 48 major depressed patients and in 15 age-sex-matched healthy volunteers. Serum Zn and Alb were significantly lower in major depressed patients than in normal volunteers. In healthy volunteers and major depressed patients, there were significant and positive correlations between serum Zn and Alb. We found that 53.8% of the variance in serum Zn could be explained by the combined effects of serum Alb and diagnostic classification. The results suggest that lower serum Zn in depression is in part explained by lowered serum Alb and by another depression-related mechanism. It is suggested that lower serum Zn in depression may be secondary to sequestration of metallothionein in the liver, which may be related to increased production of interleukin-6.     

Antioxidant status and circulating lipids are altered in human gestational diabetes and macrosomia

Fetuses from mothers with gestational diabetes are at increased risk of developing neonatal macrosomia and oxidative stress. We investigated the modulation of antioxidant status and circulating lipids in gestational diabetic mothers and their macrosomic babies and in healthy age-matched pregnant women and their newborns. The serum antioxidant status was assessed by employing anti-radical resistance kit (KRL; Kirial International SA, Couternon, France) and determining levels of vitamin A, C, and E and the activity of superoxide dismutase (SOD). Circulating serum lipids were quantified, and lipid peroxidation was measured as the concentrations of serum thiobarbituric acid-reactive substances (TBARS). As compared with non-diabetic mothers, gestational diabetic women exhibited decreased levels of vitamin E and enhanced concentrations of vitamin C without any changes in vitamin A. Vitamin A and C levels did not change in macrosomic babies except vitamin E whose levels were lower in these infants than in the newborns of non-diabetic mothers. Gestational diabetes mellitus (GDM) and macrosomia were also associated with impaired SOD activities and enhanced TBARS levels. Globally, total serum antioxidant defense status in diabetic mothers and their macrosomic babies was diminished as compared with control subjects. Triglyceride and cholesterol concentrations did not differ significantly between gestational diabetic and control mothers; however, macrosomia was associated with enhanced plasma cholesterol and triglyceride levels. These results suggest that human GDM and macrosomia are associated with downregulation of antioxidant status, and macrosomic infants also exhibit altered lipid metabolism.     

维生素E对烧伤焦痂脂类引起肝线粒体呼吸功能障碍的保护作用

烧伤焦痂脂类组分D_1可抑制离体大鼠肝线粒体呼吸控制率(RCR)、ADP/O、第3态呼吸及ATP产生率,刺激第4态呼吸。预先加入维生素E(Vit.E)可非常显著地防止D_1对线粒体呼吸功能的抑制。后加Vit.E没有保护作用。D_1经热处理可非常显著地降低其对线粒体呼吸功能的抑制作用。氢过氧化枯烯(CHP)可非常显著地抑制线粒体呼吸功能。Vit.E可显著地防止较低浓度的CHP对线粒体RCR的抑制。还可使正常线粒体中以及加入D_1、HD_1和CHP,后线粒体中丙二醛含量显著减少。Vit.E为作用肯定的抗氧化剂,它的保护作用提示D_1和CHP极可能通过脂质过氧化作用这一共同途径损害线粒体功能。     

Levels of lipid peroxidation products in a chronic inflammatory disorder

We have examined the plasma levels of the lipid peroxidation products 4-hydroxy-nonenal and malondialdehyde in a carefully controlled study of age and sex-matched subjects with rheumatoid arthritis in whom potentially confounding influences such as disease modifying anti-rheumatic drugs (DMARDs), self-medication and vitamin supplements were eliminated. The plasma concentrations of the antioxidants uric acid and vitamin E were also measured. The results reveal a strong and consistent inverse correlation between the levels of lipid peroxidation products in the plasma and erythrocyte sedimentation rate (ESR). There is no indication that vitamin E or urate function as the major antioxidant agent in arthritis, as has been suggested in more seriously affected patients. It is concluded that there is no evidence that vitamin E is more important, and urate less important as an antioxidant in mild arthritis. The correlation between lipid peroxidation and ESR suggests a more complex relationship than has been assumed.     

Erythrocyte susceptibility to lipid peroxidation in patients with coronary atherosclerosis

In recent years it has been reported that free oxygen radicals play an important role in the pathogenesis of degenerative diseases and that antioxidant vitamins such as vitamins E or C prevent their harmful effects. In this study, we evaluated the following: Erythrocyte susceptibility to lipid peroxidation; the role of erythrocyte glutathione (GSH) as an antioxidant; plasma lipid fractions; and the relationship between plasma lipid peroxides and antioxidant vitamin levels. Thiobarbituric acid-reactive substance (TBARS) levels were measured to determine the levels of plasma lipid peroxides and the susceptibility to lipid peroxidation when erythrocytes were stressed by hydrogen peroxide for 2 h in vitro. Erythrocyte TBARS production was significantly higher in patients with coronary atherosclerosis than in the controls. On the other hand, the levels of plasma high-density lipoproteins, vitamin C, vitamin E and erythrocyte GSH were significantly lower, and the levels of plasma total cholesterol, triglycerides, low-density lipoproteins and TBARS were significantly higher in the patients with coronary atherosclerosis than in the controls. In conclusion, our results indicate that erythrocytes from patients with coronary atherosclerosis are more susceptible to oxidation than those of controls and that these patients have lowered antioxidant capacity as revealed by decreased plasma levels of vitamins C and E.     

Depression and folate status in the US Population

BACKGROUND: Folate deficiency and low folate status have been linked in clinic studies to depression, persistent depressive symptoms, and poor antidepressant response. These relationships have not been demonstrated in general populations. This study examined associations between depression and folate status indicators in an ethnically diverse general US population sample aged 15-39 years. METHODS: Healthy subjects whose red blood cell (RBC) folate concentrations had been measured were determined to have no depression (n = 2,526), major depression (n = 301), or dysthymia (n = 121) using a diagnostic interview schedule. Serum concentrations of folate and total homocysteine (tHcy) were also measured. RESULTS: After adjustment for sociodemographic factors, serum vitamin B(12) concentration, alcohol consumption over the past year and current status as to overweight and use of vitamin/mineral supplements, cigarettes and illegal drugs, subjects who met criteria for a lifetime diagnosis of major depression had folate concentrations in serum and RBCs that were lower than those of subjects who had never been depressed. Subjects who met criteria for dysthymia alone had lower RBC folate concentrations than never-depressed subjects, but the serum folate concentrations of the two groups were comparable. Serum tHcy concentration was not related to lifetime depression diagnoses. Low folate status was found to be most characteristic of recently recovered subjects, and a large proportion of such subjects were folate deficient. CONCLUSIONS: Low folate status was detectable in depressed members of the general US population. Folate supplementation may be indicated during the year following a depressive episode.     

Antioxidative enzyme activities and lipid peroxidation in major depression: alterations by antidepressant treatments

BACKGROUND: Reactive oxygen species (ROS) may play a role in some neuropsychiatric disorders. There is some evidence that the activation of immune-inflammatory process, increase of monoamines catabolism, and abnormalities in lipid compounds may cause overproduction of ROS and, in turn, antioxidative enzyme activities (AEAs) and lipid peroxidation (LP), and that these phenomena may be related to pathophysiology of major depression. METHODS: The aims of this study were (i) to examine the AEAs and LP levels of the major depressed (MD) patients, and to compare these with healthy controls; and (ii) to investigate the effect of subchronic treatment with selective serotonin reuptake inhibitors (SSRIs) on AEAs and LP levels in MD subjects. Thirty MD patients, and 32 healthy controls (HC) participated in this study. AEAs and LP levels were determined by measuring several antioxidative enzymes and malondialdehyde (MDA) levels in plasma and/or in red blood cells. RESULTS: Major depressed patients, especially melancholic patients, had higher AEA and LP levels than those of healthy controls. After treatment for 3 months with SSRIs, AEA and LP levels of the patients were significantly decreased to normal levels. CONCLUSION: These findings suggest that (i) major depression, especially with melancholia, is associated with elevated AEAs and LP, and that (ii) subchronic treatment with SSRIs may have a suppressive effect on AEA and LP. CLINICAL IMPLICATION AND LIMITATION: AEAs might be used for monitoring SSRIs effects.     

Vitamin E supplementation, exercise and lipid peroxidation in human participants

The theoretical benefits of using antioxidant vitamin supplements to quench oxygen free radicals appear large. The major function of vitamin E is to work as a chain-breaking antioxidant in a fat soluble environment so as to protect polyunsaturated fatty acids within membrane phospholipids and in plasma lipoproteins. The purpose of this critical review was to determine whether vitamin E supplementation decreases exercise-induced lipid peroxidation in humans. If vitamin E alone is ineffective, researchers can turn their efforts to other individual antioxidants or combinations. Using the search words vitamin E, exercise, lipid peroxidation and antioxidant, all relevant studies since 1985 were identified through a computer search using Pub Med and Sport Discuss databases. Additional articles were reviewed from the reference list of the retrieved articles. Nine vitamin E studies met the criteria of using human participants in an experimental design. Studies were analyzed to determine the strength of evidence regarding the efficacy of vitamin E supplementation. Strength of evidence was based on: (1) number of participants, (2) intensity of the exercise test, (3) type of research design, (4) other controls, (5) the biomarker of lipid peroxidation, (6) the timing of the biomarker measurement, (7) measurement of vitamin E status and (8) correction for plasma volume change. Overall, the six studies showing no effect of vitamin E supplementation had a much higher total score (67) in comparison to the three studies showing positive effects (38). Although limitations have plagued much of the research, vitamin E supplementation does not appear to decrease exercise-induced lipid peroxidation in humans.     

Antioxidant role of vitamin E and carbon tetrachloride hepatotoxicity

Five hours after administration of a single large dose of Vitamin E, the content of the vitamin in rat liver microsomes and “mitochondria fractions” was more than 10 times control levels. Despite these exceptionally high levels of vitamin E, carbon tetrachloride administration nevertheless produced liver microsomal lipid peroxidation. This result suggests various possibilities: (a) that vitamin E does not act as an antioxidant intracellularly, (b) that despite high overall levels, the vitamin could not gain access to the critical sites, and (c) that microsomal lipid peroxidation initiated by carbon tetrachloride is highly localized and that localized stores of vitamin E are exhausted, thus permitting lipid peroxidation to proceed. The last possibility is supported by data which show a marked drop in vitamin E content of liver microsomal lipids in the carbon tetrachloride poisoned rat.     

Oxidative stress and antioxidant defenses in mild cognitive impairment: A systematic review and meta-analysis

This study aims to systematically review and meta-analyze the nitro-oxidative stress (O&NS)/antioxidant (ANTIOX) ratio in the peripheral blood of people with mild cognitive impairment (MCI). We searched PubMed, Scopus, Google Scholar, and Web of Science for articles published from inception until July 31, 2021. Forty-six studies on 3.798 MCI individuals and 6.063 healthy controls were included. The O&NS/ANTIOX ratio was significantly higher in MCI than in controls with a Standardized Mean Difference (SMD)= 0.378 (95% CI: 0.250; 0.506). MCI individuals showed increased lipid peroxidation (SMD=0.774, 95%CI: 4.416; 1.132) and O&NS-associated toxicity (SMD=0.621, CI: 0.377; 0.865) and reduced glutathione (GSH) defenses (SMD=0.725, 95%CI: 0.269; 1.182) as compared with controls. MCI was also accompanied by significantly increased homocysteine (SMD=0.320, CI: 0.059; 0.581), but not protein oxidation, and lowered non-vitamin (SMD=0.347, CI: 0.168; 0.527) and vitamin (SMD=0.564, CI: 0.129; 0.999) antioxidant defenses. The results show that MCI is at least in part due to increased neuro-oxidative toxicity and suggest that treatments targeting lipid peroxidation and the GSH system may be used to treat or prevent MCI.     

Effects of vitamin E supplementation on oxidative stress in streptozotocin induced diabetic rats: investigation of liver and plasma

This experimental study was designed to investigate the effects of vitamin E supplementation, especially on lipid peroxidation and antioxidant status elements 3/4 namely, glutathione (GSH), CuZn superoxide dismutase (CuZn SOD), and glutathione peroxidase (GSH Px), both in blood and liver tissues of streptozotocin (STZ) diabetic rats. The extent to which blood can be used to reflect the oxidative stress of the liver is also investigated. In diabetic rats, plasma lipid peroxide values were not significantly different,from control,whereas erythrocyte CuZn SOD (p < 0.01), GSH Px (p < 0.001) activities and plasma vitamin E levels (p < 0.001), were significantly more elevated than controls. Vitamin E supplementation caused significant decreases of erythrocyte GSH level (p < 0.01) in control rats and of erythrocyte GSH Px activity (p < 0.05) in diabetic rats. Liver findings revealed significantly higher lipid peroxide (p < 0.001) and vitamin E (p < 0.01) levels and lower GSH (p < 0.001), CuZn SOD (p < 0.001) and GSH Px (p < 0.01) levels in diabetic rats. A decreased hepatic lipid peroxide level (p < 0.01) and increased vitamin E/lipid peroxide ratio (p < 0.001) were observed in vitamin E supplemented, diabetic rats. A vitamin E supplementation level which did not cause any increase in the concentration of the vitamin in the liver or blood, was sufficient to lower lipid peroxidation in the liver. Vitamin E/lipid peroxide ratio is suggested as an appropriate index to evaluate the efficiency of vitamin E activity,independent of tissue lipid values. Further, the antioxidant components GSH, GSH Px and CuZn SOD and the relationships among them, were affected differently in the liver and blood by diabetes or vitamin E supplementation.     

Rejuvenation of antioxidant system in central nervous system of aged rats by grape seed extract

Oxidative stress is considered as a major risk factor that contributes to age-related increase in lipid peroxidation and declined antioxidants in the central nervous system during aging. Grape seed extract, one of the bioflavonoid, is widely used for its medicinal properties. In the present study, we evaluated the role of grape seed extract on lipid peroxidation and antioxidant status in discrete regions of the central nervous system of young and aged rats. Male albino rats of Wistar strain were divided into four groups: Group I-control young rats, Group II-young rats treated with grape seed extract (100 mg/kg body weight) for 30 days, Group III-aged control rats and Group IV-aged rats supplemented with grape seed extract (100 mg/kg body weight) for 30 days. Age-associated increase in lipid peroxidation was observed in the spinal cord, cerebral cortex, striatum and the hippocampus regions of aged rats (Group III). Activities of antioxidant enzymes like superoxide dismutase, catalase, glutathione peroxidase and levels of non-enzymic antioxidants like reduced glutathione, Vitamin C and Vitamin E were found to be significantly decreased in all the brain regions studied in aged rats when compared to young rats. However, normalized lipid peroxidation and antioxidant defenses were reported in the grape seed extract-supplemented aged rats. These findings demonstrated that grape seed extract enhanced the antioxidant status and decreased the incidence of free radical-induced lipid peroxidation in the central nervous system of aged rats.     

Vitamin E as an antioxidant agent in CAPD patients

Oxidative stress, increased lipid peroxidation and decreased activity of antioxidant systems may contribute to the accelerated development of atherosclerosis in chronic renal failure patients during renal replacement therapy. The aim of the study was to investigate the influence of vitamin E (400 mg/day) on some antioxidant defense parameters in CAPD patients. In fourteen CAPD patients, erythrocyte antioxidant enzymes, superoxide dismutase (SOD), glutathione peroxidase (GPX) and catalase (CAT), the concentration of plasma malondialdehyde (MDA), vitamin A, vitamin C and vitamin E were investigated. The study was divided into two periods. Each period lasted six weeks. In the first period patients received orally vitamin E 400 mg/day, in the second period they did not receive vitamin E or other antioxidant drugs. Each parameter was determined at the beginning of the study and at the end of each period. Six CAPD patients were treated by erythropoietin (EPO) and received orally pyridoxine 20 mg/day and the others without EPO treatment received pyridoxine 5 mg/day. Six-week treatment by vitamin E (400 mg/day) led to the significant increase of serum vitamin E (from 33.6+/-9.0 to 49.3+/-15.5 micromol/L) and to the significant decrease of MDA (from 2.62+/-0.5 to 2.36+/-0.4 micromol/L). The mean values of erythrocyte enzymes were in or under the lower margin of normal range and were not influenced by vitamin E in CAPD patients. The results of our study showed that orally administered vitamin E is a very important antioxidant agent for CAPD patients.     

Age effects on cortisol levels in depressed patients with and without comorbid post-traumatic stress disorder, and healthy volunteers

BACKGROUND: Post-traumatic stress disorder (PTSD) and major depression are frequently comorbid. Age and major depression are associated with higher cortisol levels and dexamethasone resistance, whereas PTSD is associated with lower cortisol and dexamethasone supersensitivity. Therefore, we examined the effect of age on the hypothalamic-pituitary-adrenal (HPA) system in depressed patients with and without PTSD. METHODS: Thirty-one depressed patients without PTSD, 12 depressed patients with PTSD, and 23 healthy volunteers were studied on 2 days. Subjects received single-blind placebo on day 1 and fenfluramine on day 2. Cortisol levels were drawn before challenge and for 5 h thereafter. RESULTS: Cortisol levels increase with age in depressed patients without PTSD but not in depressed patients with PTSD or in healthy volunteers. Number of previous major depressive episodes was a predictor of the cortisol response to fenfluramine administration in depressed patients without PTSD. CONCLUSIONS: The results of our study highlight the importance of considering age in psychobiology. Further research is needed to fully delineate the role of age in abnormalities of the HPA axis found in major depression and PTSD.     

Oxidative stress markers in preovulatory follicular fluid in humans.

Intensified peroxidation in the Graafian follicle may be a factor compromising the normal development of the oocyte. The aim of this study was to measure concentrations of three oxidative stress markers: conjugated dienes, lipid hydroperoxides and thiobarbituric acid-reactive substances, in preovulatory follicular fluids and sera of 145 women attending an in-vitro fertilization programme, and to correlate these concentrations with pregnancy outcome. Determinations were conducted either with or without an antioxidant (10 microM butylated hydroxytoluene) and an iron chelate (10 microM deferoxamine mesylate) to examine peroxidation associated with the methods used. Concentrations of conjugated dienes, lipid hydroperoxides and thiobarbituric acid-reactive substances in follicular fluid were all significantly lower than those in serum, both in the presence or absence of the antioxidant and iron chelate. These concentrations did not correlate with pregnancy outcome. In conclusion, the intensity of peroxidation in the Graafian follicle is much lower than that in serum. This gradient is the result of the lower rate of initiation of peroxidation in the follicular fluid, suggestive of the presence of efficient antioxidant defence systems in the direct milieu of the oocyte before ovulation. The concentrations of investigated oxidative stress markers in follicular fluid do not reflect the reproductive potential of oocytes.     

Effects of potential dietary inhibitors of endogenous DNA damage on mutagenesis and lipid peroxidation in lacZ mice

The effects of a nine month administration of dietary: (1) 3H-1,2-dithiole-3-thione (D3T), (2) N-acetylcysteine (NAC), (3) antioxidant vitamin mix, (vitamin C+E), (4) free radical scavenger, amifostine, and (5) calorie restriction, (CR), on mutagenesis and lipid peroxidation in lung, kidney, spleen and liver of lacZ transgenic mice were examined. These agents/diets were chosen because they might inhibit certain proposed mechanisms of endogenous damage to DNA. The agents were added to a high fat, reduced antioxidant AIN-76 diet, to better approximate a Western style diet than the conventional AIN-76 diet. As the lacZ gene is not expressed, mutations in that gene are neutral, and simply accumulate over time. The mutant fractions in control mice increased about 50-100%. Most of the agents inhibited to various extents the age-related increase in mutagenesis in lung, kidney, and/or spleen, but no inhibition was observed in liver. There was no significant effect of age on lipid peroxidation levels in controls, possibly reflecting steady state turnover of lipid peroxidation products. Almost all of the treatments except D3T inhibited lipid peroxidation in most organs to different degrees. The vitamin C+E mix was the most effective at inhibiting lipid peroxidation, but a single most effective inhibitor of mutagenesis could not be discerned. Some associations were observed between the reduction in lipid peroxidation and the inhibition of mutagenesis. The results are consistent with a partial role for oxidative stress in the age-related increase in mutagenesis. These observations may have implications for chemoprevention of carcinogenesis.     

Effect of vitamin E supplementation on post-exercise plasma lipid peroxidation and blood antioxidant status in smokers: with special reference to haemoconcentration effect

The oxidative effects were investigated of exhausting exercise in smokers, and the possible protective role of 400?mg?·?day^?1 vitamin E (Vit E) supplementation over a period of 28 days. The subjects exercised to exhaustion including concentric-eccentric contractions following maximal cycling. The haematocrit and haemoglobin, leucocyte (WBC), plasma lactic acid (La) and malondialdehyde (MDA), erythrocyte superoxide dismutase (SOD) and glutathione peroxidase (GPx), serum Vit E and ceruloplasmin (CER) concentrations were measured pre and post exercise. Supplementation increased Vit E concentrations 28% and 31% in the controls and the smokers, respectively. Cigarette smoking and/or Vit E supplementation did not influence plasma lipid peroxidation or the antioxidant status at rest. Exercise caused significant haemoconcentration in all groups. When the post-exercise concentrations were adjusted for haemoconcentration, a significant elevation in La concentrations due to exercise was observed in all groups. Similarly, there were significant elevations in the adjusted WBC counts in all groups except the Vit E supplemented controls. The MDA concentrations on the other hand, when adjusted for haemoconcentration, did not exhibit any difference due to exercise. Exercise did not affect the GPx and CER activities either, while causing a SOD activity loss in all groups except the Vit E supplemented non-smokers. Serum Vit E concentrations diminished significantly in all groups after exercise. Post-exercise plasma MDA and blood antioxidant concentrations were not altered by smoking. The results would suggest that plasma volume changes should always be taken into account when assessing post-exercise plasma concentrations and that smoking and exercise do not have an additional collective effect on plasma lipid peroxidation and the dose of Vit E administered was insufficient to maintain the serum concentrations after exercise.     

Antioxidant parameters and ageing in some animal species

Connection between ageing and some tissue antioxidant parameters have been studied in four experiments on different animal species. Prenatal studies on the developing chick embryos showed discrepancies between the lipid-rich liver and brain antioxidant defence. In the liver, high levels of reduced glutathione (GSH), vitamins A and E and high activities of the antioxidant enzymes glutathione peroxidase (GPX) and superoxide dismutase (SOD) were found whereas brain expressed a high vitamin C concentration. In newborn healthy calves during the first two days of life, atmospheric oxygen tension did not cause either increased lipid peroxidation as reflected in a high malondialdehyde (MDA) level or any changes in GSII, GPX, SOD and catalase (CAT) activities in red blood cells (RBC). Plasma vitamin E and carotene concentrations also did not change. In growing healthy calves during two months after birth increasing MDA, decreasing GSH, GPX and CAT are leading features, whereas plasma vitamin E and carotene concentrations significantly increased. In young (1-year-old) and old (9-year-old) dogs RBC results showed significant differences with the highest MDA and lowest GSH levels in the old males. Activity of GPX and SOD was higher in old dogs than in the young ones, especially in the females.     

Increased oxidative stress and altered levels of antioxidants in asthma

BACKGROUND: Reactive oxygen species might play an important role in the modulation of airway inflammation. There is evidence of an oxidant-antioxidant imbalance in asthma. Although several oxidants and antioxidants are likely to be involved, alterations in only limited parameters have been studied in isolation. OBJECTIVE: We investigated changes in a wide range of oxidants and antioxidants to create a comprehensive picture of oxidant-antioxidant imbalance. METHODS: In the peripheral blood of 38 patients with bronchial asthma and 23 control subjects, oxidative stress was measured in terms of superoxide anion generation by leukocytes, lipid peroxidation products, total nitrates and nitrites, total protein carbonyls, and total protein sulfhydrils in plasma. Antioxidant status was evaluated by measuring red blood cell superoxide dismutase and catalase activity, total blood glutathione, and glutathione peroxidase activity in red blood cells and leukocytes and total antioxidant capacity in plasma. RESULTS: Asthmatic patients showed increased superoxide generation from leukocytes, increased total nitrites and nitrates, increased protein carbonyls, and increased lipid peroxidation products and decreased protein sulfhydrils in plasma, indicating increased oxidative stress. They also showed increased superoxide dismutase activity in red blood cells and increased total blood glutathione and decreased glutathione peroxidase activity in red blood cells and leukocytes. Red blood cell catalase activity and the total antioxidant capacity of plasma were not altered. CONCLUSION: There are alterations in a wide array of oxidants and antioxidants, with balance shifting toward increased oxidative stress in asthma. Therapeutic augmentation of the antioxidant defenses might be beneficial.     

Protection of human peripheral blood leukocytes with vitamin E and C from toxic effects of fenarimol in vitro]

The work was undertaken in a trial to protect leukocytes against the toxic effect of fenarimol with vitamin E and C. The experiment was carried out in vitro. These vitamins were chosen since they are the components of the physiological antioxidative mechanism in the cell. The protective effect of the vitamins varied depending on the type of the cell and the studied structure as well as on the dose of the antioxidant used. Improvement of the phagocytic activity of the granulocytes was observed after preincubation with vitamin E and using vitamin C it was possible to achieve control values of the phagocytosis index and per cent of non-phagocytizing granulocytes. Both these vitamins in a satisfactory degree improved the morphological and quantitative pattern of lysosomes in cultured lymphocytes treated with fenarimol. The use of vitamin E in doses of 15 micrograms/ml and vitamin C - 0.5 microgram/ml, made possible achieving of complete normalization of the nucleologram in the lymphocytes. The observed effective protection of the leukocytes against the effects of fenarimol by means of antioxidants suggests that these cells are damaged by the mechanism of lipid peroxidation.