Thiobarbituric Acid Levels Research Articles

Supplementation with Vitamin C, Vitamin E or β-Carotene Influences Osmotic Fragility and Oxidative Damage of Erythrocytes of Zinc-Deficient Rats

Dietary zinc deficiency in rats causes increased osmotic fragility of their erythrocytes. In this study, the influence of supplementary antioxidants (vitamin C, vitamin E or β-carotene) on osmotic fragility, oxidative damage and components of the primary defense system of erythrocytes of zinc-deficient rats was investigated. Indicators of hemolysis in vivo were also examined. Five groups of 12 male rats were force-fed a zinc-adequate diet (control rats), a zinc-deficient diet or a zinc-deficient diet enriched with vitamin C, vitamin E or β-carotene. Compared with the control rats, the rats fed the zinc-deficient diet without supplementary antioxidants had greater red blood cell osmotic fragility, higher concentrations of thiobarbituric acid–reactive substances and alanine, higher glutathione S-transferase activity, lower concentration of glutathione and activity of glutathione peroxidase as well as lower activity of superoxide dismutase in plasma (P < 0.05). Supplementation with antioxidants generally improved osmotic fragility in zinc-deficient rats without influencing zinc concentration or alkaline phosphatase activity in plasma, indicators of zinc status. At some of the hypotonic saline concentrations tested, vitamin C and β-carotene significantly affected osmotic fragility. The zinc-deficient rats fed a diet without supplementary antioxidants had significantly higher concentrations of alanine in erythrocytes than the zinc-deficient rats supplemented with vitamin C, vitamin E or β-carotene and had significantly higher levels of thiobarbituric acid–reactive substances in erythrocytes than the rats supplemented with β-carotene. There was no indication of hemolysis in vivo in rats fed zinc-deficient diets. The results show that supplementary antioxidants decrease osmotic fragility and oxidative damage of erythrocytes in zinc-deficient rats.

Dose-related preventive and therapeutic effects of antioxidants-anticarcinogens on experimentally induced malignant tumors in Wistar rats.

A combination of antioxidants-anticarcinogens, consisting of vitamins C and E, selenium and 2-mercaptopropionyl glycine (2-MPG), was administered orally for the prevention (PRG) and treatment (TRG) of benzo(a)pyrene (BaP)-induced malignant tumors (leiomyosarcomas), in Wistar rats. In order to evaluate dose-related effects, a low dose vitamin (0.15 g/kg b.w. per day of vit.C and 0.05 g/kg b.w. per day of vit.E) and a high dose (1.5 g/kg b.w. per day of vit.C and 0.5 g/kg b.w. per day of vit.E) combination was administered, in prevention and treatment groups. Selenium was administered in doses of 2 microg/kg b.w. per day and 2-MPG in 15 mg/kg b.w. per day, in all groups. Daily estimations of 24 h urine volume levels of thiobarbituric acid reacting substances (MDA) were performed in 20 animals, divided into a control group, a BaP-injected group, a tricapryline-injected group and a BaP-injected and treated by the low dose combination group. Results revealed that the low dose combination failed to exert any beneficial effect on mean survival time of animals treated either preventitively or therapeutically. An increased number of animals bearing a second (lung) tumor was, in addition, found in autopsy and histological examination in the low dose combination (PRG and TRG) and the high dose TRG groups. The high dose combination groups manifested a significant prolongation of the mean survival time of animals; complete remission of tumors developed in 16.8% of the animals in the treatment group and a 5.2% prevention of tumor formation in the preventive group, without any evidence of an increased number of double tumor formation in the PRG group. Urine MDA increased significantly in animals injected by BaP during the first 10 days and since the 90th day (formation of palpable tumors) after injection, in relation to control and tricapryline-injected groups. Complete prevention of urine MDA-increased values was obtained in BaP-injected and treated by the low dose combination animals. Results indicate that high doses (megadoses) of the antioxidant-anticarcinogen vitamins C and E in combination with carefully selected other antioxidants possessing supplementary actions, are probably needed in order to achieve a sufficient prevention and treatment of malignant diseases.

Effect of Desferrioxamine Cardioplegia on Ischemia-Reperfusion Injury in Isolated Rat Heart

Background. The protective effect of desferrioxamine against myocardial ischemia-reperfusion injury remains uncertain. In this study we examined a broad range of ischemia-reperfusion indices to determine the effect of desferrioxamine cardioplegia in a model that reflects surgical practice.Methods. Isolated rat hearts were subjected to 90 minutes of ischemia with cold cardioplegia, with or without 0.5-mmol/L desferrioxamine. Left ventricular mechanical function and the levels of thiobarbituric acid–reactive substances and nonprotein thiol compounds were measured after reperfusion. Electron microscopic analysis of mitochondria was performed using diaminobenzidine staining, together with histochemical staining for glycogen and marker enzymes in left ventricular muscle and the atrioventricular node.Results. The desferrioxamine group showed better preservation of diastolic function (chamber stiffness coefficient at 15 minutes and maximum rate of decrease of left ventricular pressure at 45 minutes of reperfusion). Histochemical analysis showed that mitochondria-specific succinate dehydrogenase and the nonspecific esterase of the atrioventricular node were better preserved in the desferrioxamine group.Conclusions. The findings from this study indicate that there is added protection against ischemia-reperfusion injury when desferrioxamine is added to the cardioplegic solution; however, the study also highlighted that, in this clinically applicable model, desferrioxamine is not universally protective against all aspects of ischemia-reperfusion injury.(Ann Thorac Surg 1997;63:1003–11)

Renoprotective effects of the 21-aminosteroid U74389G in ischemia-reperfusion injury and cold storage preservation.

Free radical mediated lipid peroxidation (LPO) has been implicated in the pathogenesis of ischemic-reperfusion injury (IRI). To address the renoprotective effect(s) of LPO inhibition, the efficacy of the 21 aminosteroid U74389G was evaluated in three IRI models. In Model 1 51 unilateral nephrectomized rats that underwent 60 min of warm ischemia followed by a 72-hr reperfusion interval were treated with the test vehicle only, or 3, 6, or 12 mg/kg of U74389G intravenously, 5 min pre- or postischemia. In Model 2 Sprague-Dawley rats underwent sham operation (n=9), or 45 min of warm ischemia and 10 min of reperfusion with U74389G (6 mg/kg; n=10) or test vehicle only (n=10) administered intravenously over 10 min beginning 5 min prior to clamp release. After reperfusion, LPO was determined by assay of snap frozen tissue for thiobarbituric acid (TBA) concentrations (nmol/g tissue weight). In Model 3 domestic lean maid pigs (14-18 kg) underwent left nephrectomy with 30 min of warm ischemia, Collins C-4 flush, and 24 hr of cold storage preservation. Heterotopic autotransplantation and immediate contralateral nephrectomy was then performed in Group A-nonischemic controls (n=4), Group B-ischemic controls (n=5), and Group C-U74389G (6 mg/kg) administered preischemia and at autotransplantation (n=5). In Model 1 maximal renoprotection was demonstrated with the 6 mg/kg dose of U74389G administered after ischemia (ischemic control 72-hr serum creatinine (Cr) = 8.01+/-1.1 mg% vs. 3.32+/-0.96 mg%; ischemic control creatinine clearance = 0.069+/-0.03 ml/min vs. 0.206+/-0.04 ml/min; P<0.05). In Model 2 TBA levels were significantly lower in U74389G treated animals (88.5+/-10.0 vs. ischemic controls = 296.8+/-81.4; P=0.02). In Model 3 graft survivals were 100%, 0%, and 60% respectively. Peak Cr and BUN (mg%) were significantly greater in Group C vs. Group A, (Group A Cr = 8.59+/-0.63 vs. Group C = 12.8+/-1.01; Group A BUN = 64.1+/-2.73 vs. Group C = 104.9+/-12.21)--however, by day 10, thee were no significant differences in renal function: (Group A Cr = 2.15+/-0.3 vs. Group C = 2.10+/-0.06; Group A BUN = 27.0+/-6.0 vs. Group C = 31.1+/-6.4). These results support the beneficial effects of LPO inhibitors in models of ischemia-reperfusion, as well as preservation/transplantation, and suggest that this renoprotection correlates with decreased membrane lipid peroxidation.

Ischemia/reperfusion injury in the rat colon.

This study investigated metabolic and biochemical consequences of colonic ischemia/reperfusion (I/R) in the rat and evaluated whether antioxidants prevent I/R-induced functional damage in the rat colon. The surgical preparation involved a 10 cm segment of the colon and occlusion of the superior mesenteric artery (SMA) to induce I/R. Arterial blood from the aorta and venous blood from the superior mesenteric vein (SMV) was collected to measure blood gases, lactic acid (LA) and arachidonic acid (AA) metabolites. Tissue xanthine oxidase (XO) and thiobarbituric acid (TBA) derivatives were measured before and after reperfusion. In addition, vascular and mucosal permeability, and the effect of MDL 73404 (a water soluble vitamin E analog) and 5-aminosalicylic acid on LA, AA, XO and TBA was measured. After ischemia, the colon displayed a metabolic shift from aerobic to anaerobic course by increasing lactic acid production in the colon (183% increase in SMV lactate level compared 87% in the SMA; p < 0.03). After 10 minutes of reperfusion, circulating 6-keto-prostaglandin F1 alpha increased by 3.85 fold (p < 0.001) and thromboxane B2 increased by 2 to 3 fold. An Ischemia time longer than 60 minutes was required to cause changes in tissue XO levels. Tissue TBA levels showed a good dose response corresponding with I/R time. I/R (60 minutes) caused a three and 16 fold increase (p < 0.01) in vascular and mucosal permeability, respectively. MDL 73404 and 5-aminosalicylic acid significantly inhibited the vascular permeability and decreased LA, AA, XO and TBA. These observations provide the first direct experimental evidence for I/R-induced damage in the colon and some of its effects can be reversed by conventional and novel antioxidants.

Hypotensive activity of aqueous extract of Andrographis paniculata in rats.

1. The hypotensive activity of an aqueous extract of Andrographis paniculata was studied using chronic intraperitoneal (i.p.) infusions by osmotic pumps. The extract exhibited a dose-dependent hypotensive effect on the systolic blood pressure (SBP) of spontaneously hypertensive rats (SHR). 2. The optimum hypotensive dose determined was repeated in a study in SHR and their normotensive controls, Wistar-Kyoto (WKY) rats, to demonstrate its comparative effects on the SBP, plasma and lung angiotensin-converting enzyme (ACE) activities, as well as on lipid peroxidation in the kidneys, as measured by the thiobarbituric acid (TBA) assay. 3. The extract significantly lowered the SBP of both SHR and WKY rats. 4. Plasma, but not lung, ACE activity and kidney TBA level were significantly lower in extract-treated SHR when compared with vehicle-treated SHR controls. 5. Plasma and lung ACE activities as well as kidney TBA levels were not significantly different between extract- and vehicle-treated WKY rats. 6. This study indicates that the aqueous extract of A. paniculata lowers SBP in the SHR possibly by reducing circulating ACE in the plasma as well as by reducing free radical levels in the kidneys. The mechanism(s) of hypotensive action seems to be different in WKY rats.

Immobilization stress-induced antioxidant defense changes in rat plasma: Effect of treatment with reduced glutathione

1. 1. We examined immobilization stress-induced antioxidant defense changes in rat plasma and observed the antioxidant effect of reduced glutathione (GSH) administration on these changes. 2. 2. Immobilization stress induced severe bleeding in the stomach and a significant increase in plasma levels of thiobarbituric acid receives substances (TBARS). 3. 3. Immobilization stress induced a significant decrease in plasma iron-binding, ironoxidizing protections and radical scavenging activity. 4. 4. Plasma levels of ascorbic acid, ascorbyl radical and superoxide dismutase activity remained unchanged following immobilization stress. 5. 5. Treatment with GSH showed a significant protective effect on stomach bleeding, on the increase in plasma TEARS, and on the decrease of iron-binding, iron-oxidizing protection and radical scavenging activity in plasma. 6. 6. These results suggest that immobilization stress induces generation of reactive oxygen species and decreases the endogenous antioxidant defenses, which can be attenuated by extracellular administration of antioxidant GSH.

Magnesium deficiency in vitro enhances free radical-induced intracellular oxidation and cytotoxicity in endothelial cells

The effect of magnesium (Mg)-deficient culture on endothelial cell susceptibility to oxidative stress was examined. Bovine endothelial cells were cultured in either control sufficient (0.8 mM) or deficient (0.4 mM) levels of MgCl 2. Oxygen radicals were produced extracellularly by the addition of dihydroxyfumarate and Fe 3+-ADP. Isolated Mg-deficient endothelial cells produced 2- to 3-fold higher levels of thiobarbituric acid (TBA)-reactive materials when incubated with this free radical system. Additional studies were performed using digitized video microscopy and 2′,7′-dichlorofluorescin diacetate (DCFDA) as an intracellular indicator for oxidative events at the single cell level. In response to the exogenous oxidative Stress, endothelial cells exhibited a time-dependent increase in fluorescence, suggestive of intracellular lipid peroxidation. The increase in cellular fluorescence began within 1 min or free radical addition; the Mg-deficient cells exhibited a more rapid increase in fluoresence than that of Mg-sufficient cells. In separate experiments, cellular viability was assessed using the Trypan blue exclusion assay. Mg deficiency increased cytotoxicity of the added oxyradicals, but the loss or cellular viability began to occur only after 15 min of free radical exposure, tagging behind the detection of intracellular oxidation products. These results suggest that increased oxidative endothelial cell injury may contribute to vascular injury during Mg deficiency.

Free Radicals in Reperfusion Injury After Acute Aortic Occlusion

This investigation aims to evaluate the role of free radicals and the influence of radical scavengers in reperfusion injury of the skeletal muscle in male Wistar rats. Various parameters, including tissue blood flow, serum and calf muscle tissue levels of thiobarbituric acid (TBA) reactants, and the water content of calf muscles, were measured in the experimental setting, where infrarenal abdominal aorta was occluded for two hours followed by reperfusion with and without intraperitoneal administration of radical scavengers (superoxide dismutase or catalase). The rats were divided into four groups: group A: single laparotomy; group B: two-hour occlusion; group C: two-hour occlusion with superoxide dismutase; group D: two-hour occlusion with catalase. The increases in both serum and calf muscle tissue levels of TBA reactants following reperfusion were diminished in groups C and D as compared with those in group B. The water content of calf muscles showed a significant increase after reperfusion in group B, whereas it did not change in group D. The calf muscle tissue blood flow after reperfusion was significantly lower in group C than that in group B. These results indicate that oxygen-derived free radicals may be responsible for reperfusion injury in the lower extremity and that the attenuated blood flow during reperfusion produced by these scavengers seems to play an important role in reducing lipid peroxidation . In a clinical setting, limiting the rate of reperfusion blood flow may reduce the reperfusion injury in skeletal muscle.

Induction of metallothionein synthesis by menadione or carbon tetrachloride is independent of free radical production

The relationship between induction of hepatic metallothionein (MT) synthesis and lipid peroxidation by free radical production following an injection of menadione or carbon tetrachloride (CCl 4) in mice was studied. The hepatic concentration of MT was increased by menadione significantly at 25 mg/kg or higher. A significant increase in thiobarbituric acid (TBA) value, indicative of lipid peroxidation, was observed in the liver at menadione doses of 62.5 mg/kg or higher. Both the MT and the TBA value in the liver were significantly increased at the low dose of CCl 4. The concentration of MT was increased significantly 4–8 hr after administrations of these compounds. The increase of TBA value over time was similar to that of MT concentration after administration of CCl 4, but not after administration of menadione. The MT concentration in the menadione group was higher than that in the CCl 4 group, and the TBA level in the menadione group was lower than that in the CCl 4 group. Pretreatment with vitamin E caused a significant reduction in the TBA value, but did not affect the MT level in the liver. The concentration of MT did not significantly correlate with the TBA value in either the menadione or the CCl 4 group. Pretreatment with phenobarbital, which promotes free radical production, did not influence induction of MT synthesis following an injection of menadione or CCl 4. Neither l-buthionine sulfoximine nor 2-cyclohexen-1-one, which decreases hepatic glutathione, influenced the induction of MT by menadione. These data suggest that induction of MT synthesis by menadione or CCl 4 is independent of free radical production in the liver.

Induction of colitis in rats by 2-2'-azobis(2-amidinopropane) dihydrochloride.

Reactive oxygen metabolites (ROM) may play a role in the pathophysiology of inflammatory bowel disease (IBD) and ischemia-reperfusion-induced intestinal injury. Although there are many reports of intestinal mucosal injury associated with neutrophil-derived ROM, free radicals themselves have not been reported to induce intestinal mucosal injury. We administered intrarectally 2,2'-azobis(2-amidinopropane) dihydrochloride (AAPH) to rats, an azo compound that generates free radicals in vitro. Acute mucosal injury was assessed histologically by light microscopy and biochemically by myeloperoxidase (MPO) activity. Intrarectal administration of AAPH (60, 90, 150 mg/kg) caused erythema, edema, and histologically verifiable mucosal inflammation. MPO activity was increased 9- to 18-fold above the control level. The levels of thiobarbituric acid (TBA) reactants and sulfhydryls (SH) were significantly (P less than 0.01) increased and decreased, respectively, by 90 mg/kg AAPH. Sulfasalazine, 5-aminosalicylic acid, the LTB4 receptor antagonist SC-41930, and the antioxidant glutathione prevented the inflammation. This model of mucosal inflammation may be useful in evaluating new therapeutic agents for the treatment of IBD.

A RAPID, DIRECT CHEMICAL ASSAY FOR THE QUANTITATIVE DETERMINATION OF THIOBARBITURIC ACID REACTIVE SUBSTANCES IN RAW, COOKED, AND COOKED/STORED MUSCLE FOODS

ABSTRACTA study was performed to compare two procedures for the determination of thiobarbituric acid (TBA) levels in meat, i.e., the widely accepted distillation procedure versus a more rapid and direct extraction technique. Both methods produced statistically identical values for the rate of increase in TBA levels upon storage of precooked muscle foods. Addition of the antioxidant propyl gallate (PG) and the chelator ethylenediaminetetraacetic acid (EDTA) at concentrations of 200 ppm and 400 ppm, respectively, to the tissue samples prior to homogenization was found to be necessary both to retard further lipid oxidation and to serve as a ‘blank’or control to distinguish the color products formed between malondialdehyde (MDA) and TBA with those produced between other peroxides and TBA. The need for use of a control appears to be species dependent.

Aging-related changes in brain metabolism are altered by early developmental exposure to diazepam

To study the long-term effects of prenatal diazepam (DZ) exposure, 31P NMR (nuclear magnetic resonance) spectra and levels of thiobarbituric acid (TBA)-reactive material were measured in the brains of rats from 3 to 26 months of age. In control rats, there were aging-related increases in levels of TBA-reactive material, decreases in intracellular pH (pH i) and alterations in phosphocreatine (PCr) utilization. Prenatal (late gestational) DZ exposure induced lasting, dose-related and age-related alterations in levels of TBA-reactive material and pH i. The results indicate that the prenatal chemical environment can influence cellular metabolism throughout the lifetime of the organism, and that the process of aging can in turn interact with the consequences of prenatal drug exposure.

Early developmental exposure to benzodiazepine ligands alters brain levels of thiobarbituric acid-reactive products in young adult rats

Levels of thiobarbituric acid (TBA)-reactive material were measured in brain regions of 3-4 month-old rats following prenatal exposure to several benzodiazepine (BDZ) receptor ligands over gestational days 14-20. Prenatal exposure to diazepam (DZ) at 1.0 mg/kg/day markedly elevated levels of brain TBA-reactive material while exposure to a higher dose (2.5 mg/kg) induced a significant increase only in the hippocampus. Early exposure to the central-type BDZ agonist clonazepam as well as to the central-type antagonist Ro 15-1788 also increased brain levels of TBA-reactive material. Concurrent exposure to the higher dose of DZ partially attenuated the effect of Ro 15-1788. Prenatal exposure to the peripheral-type BDZ ligand PK11195 produced a profound increase in TBA-reactive products in all regions, and concurrent DZ exposure did not attenuate this effect, except in the basal ganglia. Measurement of TBA-reactive material from birth to 3 months indicated that the effect of prenatal exposure to DZ was not apparent until after 8 weeks of age. Acute in vitro exposure of adult and fetal tissue to DZ had no effect on TBA-reactive material. The results suggest an interference in the organization of cellular metabolism in the brain by developmental exposure to BDZ ligands.

Comparative Studies on Lipid Peroxidation in the Kidney of Rats, Mice, and Hamsters and on the Effect of Cysteine, Glutathione, and Diethyl Maleate Treatment on Mortality and Nephrotoxicity After Administration of Potassium Bromate

As an index of lipid peroxidation (LPO), levels of thiobarbituric acid (TBA)-reactive substances were examined in the kidneys of male F344 rats, BDF1, CDF1, and B6C3F1 mice, and Syrian golden hamsters after a single intravenous (IV) administration of potassium bromate (KBrO3) at various doses. In the rats, LPO levels were significantly increased in both a dose-dependent and time-dependent manner. However, when the rats were given intraperitoneal (IP) injection of cysteine, the levels of LPO were not significantly different between KBrO3-treated animals and controls. In CDF1 mice, the slight increases in LPO levels observed were much weaker and not statistically significant. On the other hand, treatment of BDF1 and B6C3F1 mice or hamsters with KBrO3 resulted in decreased values as compared to controls. The effect of treatment with cysteine, glutathione (GSH), or diethyl maleate (DEM) on mortality was tested in male F344 rats given IV injection of KBrO3 at various doses. Significant reduction and elevation in the mortality were observed in rats treated with cysteine or GSH and DEM, respectively. Significant dose-dependent and time-dependent increases were observed in the levels of serum non-protein nitrogen (NPN), blood urea nitrogen (BUN), and creatinine, and absolute and relative weight of the kidneys in male F344 rats administered KBrO3 IV. Microscopically, the appearance of numerous eosinophilic droplets in the cytoplasm of proximal tubular epithelium of KBrO3-treated rats was noteworthy. All these changes were reduced and exacerbated by treatment with cysteine or GSH and DEM, respectively. The possibility of LPO formation in the kidney by active oxygen radicals generated by KBrO3 is suggested. A possible relationship between LPO levels in the kidney and species differences in the renal toxicity and carcinogenicity of KBrO3 is implicated.

Production of thiobarbituric acid-reactive material during experimental cardiopulmonary bypass in cows.

Increased levels of thiobarbituric acid (TBA)-reactive material were found in the plasma of cows during experimental cardiopulmonary bypass. The levels of TBA-reactive substance decreased during the postoperative period to levels statistically lower (50%; p less than 0.001) than the preoperative values. The increased TBA reactivity of the plasma is indicative of lipid peroxidation during the perfusion period, owing either to exposure of the blood to increased PO2 or to oxygen radical formation. Activation of phagocytic cells by membrane contact and complement activation can induce phagocytic killing processes with the release of oxygen radicals. Although the absolute neutrophil count increased during the perfusion period, convincing correlation with the TBA reactivity was not found, and the origin of the TBA-reactive material remains speculative.

Effect of vitamin E on adjuvant arthritis in rats

Adjuvant arthritis was induced in rats fed a diet deficient in or supplemented with vitamin E, and its severity was scored according to the macroscopic findings of their legs, tails, and ears. The average score so obtained was higher in the vitamin E-deficient diet group than in the group of rats supplemented with vitamin E. Whereas the A G ratio remained depressed in vitamin E-deficient rats, rats on a vitamin E-supplemented diet showed a fast recovery from A G -ratio depression. The serum levels of β-glucuronidase and acid phosphatase were elevated after administration of an adjuvant. The serum levels of these lysosomal enzymes showed a remarkable increase in rats fed a vitamin E-deficient diet, while the elevation in lysosomal enzyme levels in rats fed a vitamin E-supplemented diet was inhibited. The levels of thiobarbituric acid (TBA) reactants in the synovia were elevated at 2 weeks after exposure to the adjuvant and were decreased thereafter. In rats maintained on a diet supplemented with vitamin E, on the other hand, the increase in synovial level of TBA reactive substances was inhibited. These observations suggest that the aggravation of adjuvant arthritis may be associated with lipid peroxidation and that antioxidants, such as vitamin E, may be beneficial for arthritis.

Immunopotentiators and the protection they give against carbon tetrachloride hepatotoxicity.

Immunopotentiators such as BCG, levamisole, PS-K and OK-432 prevent carbon tetrachloride (CCl4) hepatotoxicity, and in spite of exposure to CCl4 the liver tissue levels of thiobarbituric acid (TBA) reactive substances were not increased in rats pretreated with such immunopotentiators.

The increase of thiobarbituric acid reacting substances in rats with experimental chronic hypoxia.

Feeding under conditions of reduced oxygen supply prompted an increase in serum, arterial and brain tissue levels of thiobarbituric acid (TBA)-reacting substances. These observations indicated the possibility that hypoxia might be one of the factors predisposing to the accumulation of lipid peroxide.

Influence of vitamin E on rat adjuvant arthritis

Adjuvant arthritis was induced in rats fed on a diet deficient in or supplemented with vitamin E. The severity of arthritis was scored according to the macroscopic findings of the rat's legs, tail and ears. In the vitamin E deficient diet group, the score was higher than that of the rats supplemented with vitamin E. Wheres the A/G ratio remained depression in vitamin E deficient rats, it showed a fast recovery in the rats supplemented with vitamin E. The levels of serum β-glucuronidase and acid phosphatase activity of rats were elevated after the injection of adjuvant. Though, the increase of these lysosomal enzymes was remarkable in the rats fed on a diet deficient in vitamin E, the elevation was inhibited in the group supplemented with vitamin E. The levels of thiobarbituric acid (TBA) reactants in the synovia was elevated at 2 weeks after the exposure to adjuvant, and decreased thereafter. In contrast, the increase of TBA reactants in the synovia was inhibited in the rats supplemented with vitamin E.These observations suggest not only that peroxidation be positively associated with the aggravation of adjuvant arthritis but also that antioxidants, such as vitamin E, are beneficial for arthritis.