Effects of Aluminum Exposure on the Adherence, Chemotaxis, and Phagocytosis Capacity of Peritoneal Macrophages in Rats

To investigate the effects of aluminum (Al) exposure on peritoneal macrophages of Wistar rats, four groups of ten rats each were orally exposed to 0, 13, 26, and 52?mg?kg(-1) Al(3+) in form of aluminum trichloride (AlCl(3)) in drinking water for 120?days. At the end of the experimental period, the Al concentration in serum, the adherence, chemotaxis, and phagocytosis capacity of peritoneal macrophages were determined. The results showed that the Al concentration in serum significantly increased in a dose-dependent manner; the adherence, chemotaxis, and phagocytosis capacity of peritoneal macrophages decreased with the increase of Al dose, and present a dose-effective relationship. Further, they were significantly lower in the high-dose groups (P?相似文献   

The influence of stress and methionine-enkephalin on macrophage functions in two inbred rat strains

The aim of our current study was to investigate the effect of acute exposure to electric tail shock stress (ES) and to a stress witnessing procedure (SW), as models for physical and psychological stress paradigms, respectively, on phagocytosis and H(2)O(2) production in peritoneal macrophages isolated from Albino Oxford (AO) and Dark Agouti (DA) rats. In addition, we studied the in vitro effects of methionine-enkephalin (ME) on phagocytosis and H(2)O(2) production in peritoneal macrophages isolated from both AO and DA rats that had been exposed to ES and SW procedures. The results showed that peritoneal macrophages isolated from DA rats were less sensitive to the suppressive effects of ES and SW than macrophages isolated from AO rats. In vitro treatment of macrophages isolated from AO rats with ME mimicked to some extent the suppressive effects of ES and SW on phagocytosis and H(2)O(2) production and additionally diminished H(2)O(2) release in macrophages isolated from AO rats previously exposed to ES or SW. ME did not have any effect on phagocytosis in macrophages isolated from DA rats, but changed H(2)O(2) production in a concentration-dependent manner. In macrophages isolated from DA rats previously exposed to stress the effect of ME was dependent on the macrophage function tested and the particular stress paradigm employed. Our results emphasise the fact that both beneficial and detrimental effects of stress on immune system functions could be attributed to the individual variations in the macrophage's response to stress mediators.     

Protective antioxidant effect of vitamins C and E in streptozotocin induced diabetic rats

We have investigated the protective effect of vitamin C and E together supplementation on oxidative stress and antioxidant enzyme activities in the liver of streptozotocin-induced diabetic rats, unsupplemented diabetic and control rats. We also determined the levels of both the vitamins and oxidative stress in plasma. Vitamin supplementation in diabetic rats lowered plasma and liver lipid peroxidation, normalised plasma vitamin C levels and raised vitamin E above normal levels. In liver, the activity of glutathione peroxidase was raised significantly and that of glutathione-S-transferase was normalised by vitamin supplementation in diabetic rats. The levels of lipid peroxidation products in plasma and liver of vitamin-supplemented diabetic rats and activities of antioxidant enzymes in liver suggest that these vitamins reduce lipid peroxidation by quenching free radicals.     

Complement-component-C3-opsonized immunoglobulin G anti-DNA antibodies do not bind effectively to red blood cells unless aggregated on a high-Mr DNA matrix.

The significance of microsomal vitamin E in protecting against the free-radical process of lipid peroxidation was evaluated with the low-level-chemiluminescence technique in microsomal fractions from vitamin E-deficient and control rats. The induction period that normally precedes the ascorbate/ADP/Fe3+-induced lipid peroxidation was taken as reflecting the microsomal vitamin E content and was found to be 5-6-fold decreased in microsomal fractions from vitamin E-deficient rats. Supplementation of microsomal fractions from vitamin E-deficient rats with exogenous vitamin E partially restores the induction period observed in that from control rats. The decrease in chemiluminescence intensity and the increase in the induction period both correlate linearly with the amount of vitamin E added. However, the efficiency of exogenous vitamin E is about 50-fold lower than that exerted by the naturally occurring vitamin E in microsomal membranes. These observations are discussed in terms of the process of re-incorporation of vitamin E into membranes, the experimental model for lipid peroxidation selected, and the method to evaluate lipid peroxidation, namely low-level chemiluminescence.     

Selenium and Vitamin E Modulates Radiation-Induced Liver Toxicity in Pregnant and Nonpregnant Rat: Effects of Colemanite and Hematite Shielding

The levels of liver lipid peroxidation, glutathione peroxidase, reduced glutathione, and vitamins A and E were used to follow the level of oxidative damage caused by ionizing radiation in pregnant rats. The possible protective effects of selenium and vitamin E supplemented to rats housed in concrete-protected cages using hematite and colemanite were tested and compared to untreated controls. Ninety-six rats were randomly divided into four main equal groups namely control (A), normal concrete (B), concrete containing colemanite (C), and concrete containing hematite (D). Except group A, all groups exposed to 7 Gy radiation. The four main groups were divided into four subgroups each as follows: subgroups 1 (n?=?6): nonpregnant control rats. Subgroups 2 (n?=?6): selenium and vitamin E combination was intraperitoneally (i.p.) given to the nonpregnant rats for 20 days. Subgroups 3 (n?=?6): pregnant control rats. Subgroups 4 (n?=?6): selenium and vitamin E combination was i.p. given to the pregnant rats for concessive 20 days. Lactate dehydrogenate, alkaline phosphates, and lipid peroxidation values were higher in subgroups 1 and 3 than in no radiation group although glutathione peroxidase and vitamin E levels in liver were lower in radiation group than in no radiation group. Lactate dehydrogenate activity and lipid peroxidation levels were found to be decreased in subgroups 2 and 4 protected with concrete containing hematite and colemanite when compared to subgroup 1 and 3 with normal concrete. The radiation doses in rats housed by concrete without colemanite and hematite exposed radiation clearly showed liver degeneration. In conclusion, selenium and vitamin E supplementations and housing by concrete with colemanite was found to offer protection against gamma-irradiation-induced liver damage and oxidative stress in rats, probably by exerting a protective effect against liver necrosis via its free radical scavenging and membrane stabilizing. Protective effects of colemanite in the liver seem to be more important than in hematite.     

Chromium-induced excretion of urinary lipid metabolites,DNA damage,nitric oxide production,and generation of reactive oxygen species in Sprague-Dawley rats

Chromium and its salts induce cytotoxicity and mutagenesis, and vitamin E has been reported to attenuate chromate-induced cytotoxicity. These observations suggest that chromium produces reactive oxygen species which may mediate many of the untoward effects of chromium. We have therefore examined and compared the effects of Cr(III) (chromium chloride hexahydrate) and Cr(VI) (sodium dichromate) following single oral doses (0.50 ld₅₀) on the production of reactive oxygen species by peritoneal macrophages, and hepatic mitochondria and microsomes in rats. The effects of Cr(III) and Cr(VI) on hepatic mitochondrial and microsomal lipid peroxidation and enhanced excretion of urinary lipid metabolites as well as the incidence of hepatic nuclear DNA damage and nitric oxide (NO) production were also examined. Increases in lipid peroxidation of 1.8- and 2.2-fold occurred in hepatic mitochondria and microsomes, respectively, 48 hr after the oral administration of 25 mg Cr(VI)/kg, while increases of 1.2- and 1.4-fold, respectively, were observed after 895 mg Cr(III)/kg. The urinary excretion of malondialdehyde (MDA), formaldehyde (FA), acetaldehyde (ACT) and acetone (ACON) were determined at 0–96 hr after Cr administration. Between 48 and 72 hr post-treatment, maximal excretion of the four urinary lipid metabolites was observed with increases of 1.5- to 5.4-fold in Cr(VI) treated rats. Peritoneal macrophages from Cr(VI) treated animals 48 hr after treatment resulted in 1.4- and 3.6-fold increases in chemiluminescence and iodonitrotetrazolium reduction, indicating enhanced production of Superoxide anion, while macrophages from Cr(III) treated animals showed negligible increases. Increases in DNA single strand breaks of 1.7-fold and 1.5-fold were observed following administration of Cr(VI) and Cr(III), respectively, at 48 hr post-treatment. Enhanced production of NO by peritoneal exudate cells (primarily macrophages) was monitored following Cr(VI) administration at both 24 and 48 hr post-treatment with enhanced production of NO being observed at both timepoints. The results indicate that both Cr(VI) and Cr(III) induce an oxidative stress at equitoxic doses, while Cr(VI) induces greater oxidative stress in rats as compared with Cr(III) treated animals.     

Effect of ghrelin administration on phagocytic activity in acute cold-restraint stress exposed rats

Ghrelin, an endogenous ligand for growth hormone secretagogue receptor, was identified in the rat stomach. This peptide acts through nitric oxide (NO) by expressing endothelial nitric oxide synthase (eNOS) and down regulating inducible nitric oxide synthase (iNOS) at its gastroproprotective effect against restraint stress induced damage. Recently the ghrelin receptor has also been detected in peripheral systems including immune tissue. We have investigated the possible effect of ghrelin on phagocytic activity of peritoneal macrophages in acute cold-restraint stress (ACRS) exposed rats. The rats were divided into control, stress and ghrelin groups. In ghrelin groups, single dose and three days consecutive dose of ghrelin (20 microg/kg. i.p.) were applied to rats that were exposed to ACRS for 4 h. 1 ml of saline was injected i.p. after ACRS for 3 consecutive days to the rats of the stress groups. Ghrelin administration reduced the increased phagocytic activity induced by ACRS. We conclude that ghrelin exerts an important role at macrophage phagocytic activity in ACRS exposed rats.     

Effect of oral methionine and vitamin E on blood lipid peroxidation in vitamin B6 deficient rats

Lipid peroxidation in blood of vitamin B6 deficient rats was significantly increased when compared to pair-fed controls. The observed increased lipid peroxidation in vitamin B6 deficiency was correlated with high levels of lipids, metal ions and low levels of antioxidants, alpha-tocopherol, ascorbic acid and reduced GSH. Supplementation of methionine or vitamin E along with the vitamin B6 deficient diet restored the levels of antioxidants to near normal and also protected against oxidative stress. However plasma TBARS level as well as total lipids were still elevated in M-B6 diet fed rats and normalized in E-B6-d rats.     

Mitochondrial respiratory chain dysfunction in ageing; influence of vitamin E deficiency

The causes and consequences of ageing are likely to be complex and involve the interaction of many processes. It has been proposed that the decline in mitochondrial function caused by the accumulation of oxidatively damaged molecules plays a significant role in the ageing process. In agreement with previous reports we have shown that the activities of NADH CoQ₁ reductase and cytochrome oxidase declined with increasing age in both rat liver and gastrocnemius muscle mitochondria. However, only in the liver were the changes in lipid peroxidation and membrane fluidity suggestive of an age-related increase in oxidative stress.

After 12 weeks on a vitamin E deficient diet, vitamin E levels were undetectable in both gastrocnemius muscle and liver. In skeletal muscle, this was associated with a statistically significant increase in lipid peroxidation, a decrease in cytochrome oxidase activity after 48 weeks, and an exacerbation in the age-related rate of decline of NADH CoQ₁ reductase activity. This was consistent with the suggestion that an imbalance between free radical generation and antioxidant defence may contribute to the mitochondrial dysfunction with age. In contrast to this, vitamin E deficiency in the liver caused a significant increase in mitochondrial respiratory chain activities with increasing age despite evidence of increased lipid peroxidation. Comparison of other features in these samples suggested vitamin E deficiency; did not have a significant impact upon mtDNA translation; induced a compensatory increase in glutathione levels in muscle, which was less marked in the liver, but probably most interestingly caused a significant decrease in the mitochondrial membrane fluidity in muscle but not in liver mitochondria.

These data suggest that while increased lipid peroxidation exacerbated the age-related decline in muscle respiratory chain function this relationship was not observed in liver. Consequently other factors are likely to be contributing to the age-related decline in mitochondrial function and specific stimuli may influence or even reverse these age-related effects as observed with vitamin E deficiency in the liver.     

Impairment of Brain Mitochondrial Oxidative Phosphorylation Accompanying Vitamin E Oxidation Induced by Iron or Reactive Nitrogen Species: A Selective Review

Mitochondria are exposed to large fluxes of iron, and reactive oxygen and nitrogen species. Hence they are susceptible to oxidative stress, a process inhibited by vitamin E. Our investigations show that iron uncouples oxidative phosphorylation whereas peroxynitrite and nitrite are inhibitors of oxidative phosphorylation. Oxidation of mitochondrial vitamin E is accompanied by generation of lipid peroxidation products, altered enzyme activity and electrical conductance etc., and result in inefficient oxidative phosphorylation. Vitamin E is important for mitochondrial function because: (1) Prior investigations have shown that vitamin E is essential for maintaining mitochondrial respiration. (2) Vitamin E is the most potent, lipid-soluble antioxidant localized ideally in mitochondrial membranes. (3) The decline in respiratory control ratios (RCR) of rat brain mitochondria exposed to peroxynitrite closely paralleled the oxidative elimination of vitamin E. (4) Finally, iron is a strong uncoupler of oxidative phosphorylation in brain mitochondria from vitamin E deficient animals and not from controls.Special issue dedicated to Lawrence F. Eng.     

Regulation of expression of antioxidant enzymes by vitamin E and curcumin in <Emphasis Type="SmallCaps">l</Emphasis>-thyroxine-induced oxidative stress in rat renal cortex

The present study investigates the antioxidative effects of vitamin E and curcumin against l-thyroxine (T₄)-induced oxidative stress in renal cortex of adult male rats. Rats were made hyperthyroid by administration of l-thyroxine (0.0012%) in their drinking water for 30 days. Vitamin E (200 mg/kg body weight/day) and curcumin (30 mg/kg body weight/day) were supplemented singly or in combination orally for 30 days along with l-thyroxine treatment. The elevated level of oxidative stress parameters (lipid peroxidation and protein carbonylation) and decline level of small antioxidant molecules (reduced glutathione and ascorbic acid) in renal cortex of T₄-treated rats were restored back by supplementation of vitamin E or/and curcumin. Increased superoxide dismutase and catalase activities in kidney cortex of T₄-treated rats were ameliorated in response to vitamin E or/and curcumin treatment. The elevated translated product of Cu/Zn-SOD, Mn-SOD and catalase in T₄-treated rats were differentially reduced by the administration of vitamin E and curcumin independently or in combination. Cu/Zn-SOD expression was ameliorated by both vitamin E and curcumin independently or in combination, whereas Mn-SOD expression was ameliorated by the supplementation of vitamin E or curcumin independently. However, the expression of catalase was alleviated by only supplementation of vitamin E to T₄-treated rats. The results suggest that both vitamin E and curcumin may play an important role in protecting T₄-induced oxidative stress in rat renal cortex by differentially modulating the activities of antioxidant enzymes and oxidative stress parameters.     

Anomalous antioxidant effects in selenium- and vitamin E-deficient liver mitochondria

In this study, we investigate the mechanisms of two anomalous protective effects of exogenous vitamin E that had previously been postulated to involve either a specific antioxidant effect or a non-antioxidant function of the vitamin. These atypical vitamin E effects were observed during the prevention of NAD-induced respiratory decline occurring in homogenates and mitochondria prepared from vitamin E- and selenium-deficient rat liver. The study showed neither hypothesis to be true; rather, the two effects, one in homogenates and the other in isolated mitochondria, were explained by other mechanisms. The protective effect against respiratory decline in homogenates was found to result from interference in the thiobarbituric acid assay for lipid peroxidation by ethanol (the conventional solvent for vitamin E addition). With other non-interfering solvents, inhibition of lipid peroxidation by vitamin E, in contrast to previous studies, correlated perfectly with prevention of respiratory decline. The atypical vitamin E effect occurring in isolated mitochondria—and consisting of a requirement for cytosol proteins for the prevention of respiratory decline by exogenous vitamin E—was found to be caused by the prevention of adverse glass effects and not by the action of vitamin E-specific binding proteins. Frequent failures in the combined protective effect of vitamin E and cytosol, which had been a major complication of respiratory decline studies, were found to be caused by phospholipase activity generated during isolation procedures. Irreversible deactivation of respiratory enzymes by lipid peroxidation was found not to be involved in the respiratory decline mechanism. In memoriam: Klaus Schwarz, MD, 1914–1978.     

Prophylactic effects of magnesium and vitamin E in rat spinal cord radiation damage: evaluation based on lipid peroxidation levels

This study investigated the neuroprotective effects of magnesium sulfate prophylaxis and vitamin E prophylaxis in a rat model of spinal cord radiation injury. Groups were subjected to different treatment conditions for 5 days prior to irradiation, and outcomes were evaluated on the basis of lipid peroxidation levels in cord tissue. Four groups of rats were investigated: no radiation/treatment (n = 4), intraperitoneal (i.p.) saline 1 ml/day (n = 6), i.p. vitamin E 100 mg/kg/day (n = 6), and i.p. magnesium sulfate 600 mg/kg/day (n = 6). The thoracic cord of each non-control rat was exposed to 20 Gy radiation in a LINAC system using 6 MV x-rays, and malondialdehyde (MDA) levels (reflecting lipid peroxidation level) were determined 24 hours post-irradiation. The MDA levels in thoracic cord segments from the control rats were used to determine baseline lipid peroxidation. The mean levels in the control, saline-only, vitamin E, and magnesium sulfate groups were 12.12 +/- 0.63, 27.0 +/- 2.81, 17.71 +/- 0.44, and 14.40 +/- 0.47 nmol/mg tissue, respectively. The MDA levels in the saline-only group were significantly higher than baseline, and the levels in the vitamin E group were significantly lower than those in the saline group (P < 0.05 for both). The levels in the magnesium sulfate group were dramatically lower than those in the saline group (P < 0.001). The results indicate that i.p. magnesium sulfate has a marked neuroprotective effect against radiation-induced oxidative stress in the rat spinal cord.     

The effect of vitamin E on lipid peroxidation in the copper-deficient rat

The present study was designed to determine whether the supplementation of vitamin E in the copper-deficient diet would ameliorate the severity of copper deficiency in fructose-fed rats. Lipid peroxidation was measured in the livers and hearts of rats fed a copper-deficient diet (0.6 microg Cu/g) containing 62% fructose with adequate vitamin E (0.1 g/kg diet) or supplemented with vitamin E (1.0 g/kg diet). Hepatic lipid peroxidation was significantly reduced by vitamin E supplementation compared with the unsupplemented adequate rats. In contrast, myocardial lipid peroxidation was unaffected by the level of vitamin E. Regardless of vitamin E supplementation, all copper-deficient rats exhibited severe signs of copper deficiency, and some of the vitamin E-supplemented rats died of this deficiency. These findings suggest that although vitamin E provided protection against peroxidation in the liver, it did not protect the animals against the severity of copper deficiency induced by fructose consumption.     

Stimulation of lipid peroxidation by methyl mercury in rats

As an index lipid peroxidation, thiobarbituric acid (TBA)-reactive substances in the liver, kidney, and serum, and hydrocarbons (ethane and pentane) in the exhalation of rats injected subcutaneously with 10 mg/kg/day of methylmercuric chloride (MMC) were determined. Formation of TBA-reactive substances in the liver and kidney of rats was significantly increased 4 and 2 days after initial injection of MMC, respectively. The result for serum was similar to that for the kidney. The maximum ethane production in the exhaled gases was observed 4 days after initial injection of MMC, and thereafter decreased slowly. Pentane production was significantly increased 5 days after initial injection of MMC, and thereafter continued to increase. Glutathione peroxidase activity and amount of vitamin C in the liver were depleted 4 days after initial injection of MMC; vitamin E was not depleted. In the kidney, significant decreases of glutathione peroxidase activity and vitamin C content were also seen 4 days after initial injection of MMC, but vitamin E content was unaltered.Thus, a clear increase of lipid peroxidation as determined by measurement of TBA-reactive substances in tissues and of hydrocarbons in the exhaled gases of rats after MMC treatment was demonstrated, though there was a lag phase of several days before the increase of lipid peroxidation. It is suggested that the significant increase of lipid peroxide formation may be a result of depletion of defending factors against lipid peroxidation.     

Effects of vitamin E, ascorbic acid and mannitol on alloxan-induced lipid peroxidation in rats

ω6- and ω3-unsaturated lipid hydroperoxides decompose to yield pentane and ethane, respectively. Alloxan toxicity was studied in rats in relation to pentane and ethane produced during lipid peroxidation induced by intraperitoneal injection of 20 mg of alloxan/100 g body wt. Fifteen minutes after injection, vitamin E-deficient rats exhaled 102- and 11.2-fold more pentane and ethane, respectively, than prior to injection. Injection of 75 mg ascorbic acid/100 g body wt 30 min prior to alloxan treatment prolonged the time over which peroxidation occurred and all vitamin E-deficient rats died before 4 h. Vitamin E-deficient rats injected with 100 mg of the radical scavenger mannitol/ 100 g body wt 30 min prior to alloxan treatment were completely protected against lipid peroxidation, and none of the rats died by 4 h. Rats fed 40 iu dl-α-tocopherol acetate/kg diet or injected with 100 mg dl-α-tocopherol/100 g body wt were either totally protected against alloxan and alloxan-ascorbic acid-induced peroxidation or were only slightly affected as shown by very low-level pentane and ethane production. Thiobarbituric acid reactants in plasma, liver and pancreas 4 h after alloxan treatment reflected the prooxidant nature of ascorbic acid and alloxan, the vitamin E status of the rats and the protective effect of mannitol. Plasma glucose levels 4 h after alloxan injection were lowest in vitamin E-injected rats and highest in vitamin E-deficient rats. Only in vitamin E-deficient rats were both lipid peroxidation and significantly elevated plasma glucose levels observed by 4 h post-alloxan treatment.     

A diet high in cholesterol and deficient in vitamin E induces lipid peroxidation but does not enhance antioxidant enzyme expression in rat liver

Expression of antioxidant enzymes (AOE), an important mechanism in the protection against oxidative stress, could be modified by the redox status of the cells. The aim of this project was to evaluate the role of vitamin E deficiency in association with a high-cholesterol diet in the hepatic lipid peroxidation and the expression of AOE. Two groups of 6 male rats were fed with a high-cholesterol or a high-cholesterol vitamin E-deficient diet. All animals were sacrificed at 72 days of treatment. Liver lipid peroxidation index (Malondialdehyde; MDA) and hepatic AOE were evaluated. Total liver RNA was extracted, and the steady state messenger RNA (mRNA) levels of glutathion peroxydase, manganese superoxide dismutase, Cu/Zn superoxide dismutase and catalase were examined by northern blot. After 72 days on the diet, a significant increase in the lipid peroxidation index was observed in the vitamin E deficient group (MDA : 4.45 +/- 0.29 nmol/mg protein versus 3.65 +/- 0.1 nmol/mg protein in vitamin E normal group). Despite this oxidative stress, the activities and mRNA levels of liver AOE were not significantly different in the 2 groups. These preliminary results show that chronic vitamin E deficiency associated with high cholesterol diet is able to increase lipid peroxidation without modulation of AOE expression and activity in the liver. This suggests that beneficial effects of dietary vitamin E are due to a plasma antioxidant effect or a cell mediated action, rather than to a specific modulation of cellular enzymes.     

Synaptosomes isolated from Goto-Kakizaki diabetic rat brain exhibit increased resistance to oxidative stress: role of vitamin E

Increased oxidative stress is believed to be an important factor in the development of diabetic complications. In this study, the effect of diabetes on the susceptibility of synaptosomes to oxidative stress, induced by the oxidizing system ascorbate/Fe2+, on the activity of antioxidant enzymes and on the levels of glutathione and vitamin E was investigated. Synaptosomes were isolated from brain of 29-weeks-old Goto-Kakizaki (GK) rats, a model of non-insulin dependent diabetes mellitus and from normal Wistar rats. Synaptosomes isolated from GK rats displayed a lower susceptibility to lipid peroxidation, as assessed by quantifying thiobarbituric acid reactive substances (TBARS), than normal rats (5.33 +/- 0.79 and 7.58 +/- 0.7 nmol TBARS/mg protein, respectively). In the absence of oxidants, no significant differences were found between the levels of peroxidation in synaptosomes of diabetic or control rats. Superoxide dismutase (SOD), glutathione peroxidase and glutathione reductase activities were unaltered in the brain of diabetic rats. There were no statistically significant differences in fatty acid composition of total lipids and reduced glutathione levels in synaptosomes of diabetic and control rats. The decreased susceptibility to membrane lipid peroxidation of diabetic rats synaptosomes correlated with a 1.3-fold increase in synaptosomal vitamin E levels. Vitamin E levels in plasma were also higher in diabetic rats (21.32 micromol/l) as compared to normal rats (15.13 micromol/l). We conclude that the increased resistance to lipid peroxidation in GK rat brain synaptosomes may be due to the increased vitamin E content, suggesting that diabetic animals might develop enhanced defense systems against brain oxidative stress.     

Effect of nitric oxide on 1 ml: peritoneal macrophages activity in normal pregnancy in white rats

The activity of peritoneal macrophages, nitrotyrosine concentration and condition of free radical processes in normal pregnancy in white rats against the background of the introduction of donator (sodium nitrite) and inhibitor (Nw-nitro-L-arginine methyl ester) of nitric oxide was studied. During normal pregnancy in animals, nitrotyrosine concentration, the activity of free radical processes, and phagocytosis increase. With the introduction of nitric oxide donator, NO level increases and after the injection of antagonist of nitric oxide it is reduced. These changes are accompanied by increased lipid peroxidation and activation of phagocytic activity of macrophages.     

Lipid peroxidation, vitamins C, E and reduced glutathione levels in patients with pulmonary tuberculosis

The present study examined the relationship between lipid peroxidation and vitamin C, vitamin E and reduced glutathione levels in plasma, erythrocytes and erythrocyte membranes of pulmonary tuberculosis patients and an equal number of age-and sex-matched healthy subjects. Enhanced plasma, erythrocytes and erythrocyte membrane lipid peroxidation with concomitant decline in vitamin C, vitamin E and reduced glutathione levels were found in pulmonary tuberculosis patients. The elevated lipid peroxidation and decreased vitamin C, vitamin E and reduced glutathione levels indicate the potential of oxidative damage to erythrocytes and erythrocyte membranes of pulmonary tuberculosis patients.