thiobarbituric-acid and Body-Weight

The aim of this study was to evaluate the effects of a 12-week Nordic Walking (NW) intervention on nitric oxide synthase activity (eNOS), levels of antibodies against oxidatively modified low-density lipoproteins (oLAb), plasma antioxidant capacity (TAC), thiobarbituric acid reactive substance (TBARS) concentration, carbohydrate and lipid metabolism, and atherosclerosis risk factors (AIP) in postmenopausal women.. A sample of 39 women, divided into two comparable groups: training (N.=20) and control (N.=19), took part in the study. Participants in the training group performed a 12-week supervised NW training: 60-minute sessions of exercise, repeated three times per week. The biochemical and anthropometric data were obtained before and after the intervention. During the first and the last training sessions, the individual walking distance in trained group was measured.. After the intervention, significant differences in covered distance, body mass, BMI, fat mass, insulin level (P<0.01), systolic blood pressure and TBARS concentration (P<0.05) were found in trained women.. Applied training was able to improve functional capacity and body composition in healthy postmenopausal women. It appears to be no direct link between a significant decrease in the level of systolic blood pressure, the level of eNOS activity, TAC, oLAb and plasma TBARS concentration in trained women. It seems probable that NW training would be more effective for postmenopausal women with more severely impaired endothelial function.

Topics: Aged; Antioxidants; Biomarkers; Body Composition; Body Weight; Case-Control Studies; Endothelium, Vascular; Exercise; Female; Humans; Middle Aged; Nitric Oxide Synthase; Oxidative Stress; Postmenopause; Thiobarbiturates; Walking

Depression is frequently encountered during Parkinson's disease (PD) as a non-motor feature, which has been reported to cause and exaggerate motor deficits and neurodegenerative events in experimental PD models. We studied the effect of chronic mild stress (CMS) (pre, post and pre & post) exposure mediated depression on motor and non-motor symptoms, oxidative stress, inflammation and brain derived neurotrophic factor (BDNF) levels and its related signalling molecules against the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine/probenecid (MPTP/p) induced neurotoxicity in mice. CMS and MPTP/p-coexposed C57BL/6 mice exhibited low neuromuscular strength and stride length with enhanced oxidative stress and inflammation as compared to CMS or MPTP/p alone exposed mice. Coexposure diminished the levels of BDNF and expressions of p-TrkB, p-ERK/ERK, p-AKT/AKT and p-CREB in nigrostriatal regions as compared to those of the alone exposure. CMS alone exposed mice showed more anxiety related behaviour with diminished expression of serotonin transporter as compared to MPTP/p alone injected group. Post-stress exposure to MPTP/p mice exhibited lowest motor and reflecting higher anxiety state with greatest enhancement in inflammation and reduction in the protein expression of stress and cell signalling markers as compared to pre and pre & post stress exposed PD mice. However, pre- and pre & post CMS exposed PD animals are more vulnerable to oxidative stress as compared with post-stress experienced MPTP/p mice. CMS mediated depression exacerbates motor/non-motor symptoms in MPTP/p-PD animals by modulating oxidative stress and various signalling molecules. Our results suggested that stress induced NMS can accelerate neurodegenerative processes in the PD in a progressive or expedited manner.

Topics: 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; Adjuvants, Pharmaceutic; Animals; Body Weight; Brain-Derived Neurotrophic Factor; Calcium-Binding Proteins; Catalase; Disease Models, Animal; Exploratory Behavior; Glial Fibrillary Acidic Protein; Male; Maze Learning; Mice; Mice, Inbred C57BL; Microfilament Proteins; Muscle Strength; Parkinsonian Disorders; Probenecid; Signal Transduction; Stress, Psychological; Superoxide Dismutase; Thiobarbiturates; Thiobarbituric Acid Reactive Substances

We have previously shown that low-dose fenofibrate treatment has an ability to prevent diabetes-induced nephropathy in rats. We investigated here the comparative pre- and post-treatment effects of low-dose fenofibrate (30 mg/kg/day p.o.) in diabetes-induced onset of nephropathy. Rats were made diabetics by single administration of streptozotocin (STZ, 55 mg/kg i.p.). The development of diabetic nephropathy was assessed biochemically and histologically. Moreover, lipid profile and renal oxidative stress were assessed. Diabetic rats after 8 weeks of STZ-administration developed apparent nephropathy by elevating serum creatinine, blood urea nitrogen and microproteinuria, and inducing glomerular-capsular wall distortion, mesangial expansion and tubular damage and renal oxidative stress. Fenofibrate (30 mg/kg/day p.o., 4 weeks) pretreatment (4 weeks after STZ-administration) markedly prevented diabetes-induced onset of diabetic nephropathy, while the fenofibrate (30 mg/kg/day p.o., 4 weeks) post-treatment (8 weeks after STZ-administration) was less-effective. However, both pre-and post fenofibrate treatments were effective in preventing diabetes-induced renal oxidative stress and lipid alteration in diabetic rats though the pretreatment was slightly more effective. Conversely, both pre-and post fenofibrate treatments did not alter elevated glucose levels in diabetic rats. It may be concluded that diabetes-induced oxidative stress and lipid alteration, in addition to a marked glucose elevation, play a detrimental role in the onset of nephropathy in diabetic rats. The pretreatment with low-dose fenofibrate might be a potential therapeutic approach in preventing the onset of nephropathy in diabetic subjects under the risk of renal disease induction. However, low-dose fenofibrate treatment might not be effective in treating the established nephropathy in diabetic subjects.

Topics: Animals; Blood Glucose; Blood Urea Nitrogen; Body Weight; Creatinine; Diabetic Nephropathies; Dose-Response Relationship, Drug; Female; Fenofibrate; Glutathione; Kidney; Lipids; Male; Organ Size; Proteinuria; Rats; Rats, Wistar; Thiobarbiturates; Time Factors

We have previously shown that treating streptozotocin-induced diabetic rats, an animal model of type 1 diabetes, with Ilepatril (an inhibitor of neutral endopeptidase and angiotensin converting enzyme (ACE)) improves vascular and neural functions. In this study we sought to determine the effect of Ilepatril treatment of high fat fed/low dose streptozotocin-diabetic rats, a model for type 2 diabetes, on vascular and neural complications. Following 8 weeks on a high fat diet rats were treated with 30 mg/kg streptozotocin (i.p.) and after 4 additional weeks a group of these rats was treated for 12 weeks with Ilepatril followed by analysis of neural and vascular functions. Included in these studies were age-matched control rats and rats fed a high fat diet and treated with or without Ilepatril. Diabetic and diet induced obese rats have characteristics of insulin resistance, slowing of nerve conduction velocity, thermal hypoalgesia, reduction in intraepidermal nerve fiber density in the hindpaw and impairment in vascular relaxation to acetylcholine and calcitonin gene-related peptide in epineurial arterioles of the sciatic nerve. Treatment with Ilepatril was efficacious in improving all of these endpoints although improvement of insulin resistance in diabetic rats was minimal. These studies suggest that dual inhibition of angiotensin converting enzyme and neutral endopeptidase activity of type 2 diabetic rats is an effective approach for treatment of diabetic neural and vascular complications.

Topics: Adipose Tissue; Animals; Arterioles; Blood Glucose; Blood Vessels; Body Weight; Carbohydrate Metabolism; Diabetes Complications; Diabetes Mellitus, Experimental; Diet, High-Fat; Dose-Response Relationship, Drug; Enzyme Inhibitors; Glucose Tolerance Test; Glutathione; Heterocyclic Compounds, 3-Ring; Insulin; Lens, Crystalline; Leptin; Male; Muscle, Skeletal; Nerve Fibers; Nervous System; Nociception; Organ Size; Rats; Rats, Sprague-Dawley; Sciatic Nerve; Superoxides; Thiobarbiturates; Tyrosine; Vasodilation

A feeding trial was conducted to determine the dietary vitamin E (DL-alpha-tocopheryl acetate, dl-alpha-TOA) requirement and its effect on the non-specific immune responses of juvenile grass shrimp, Penaeus monodon. Purified diets with eight levels (0, 25, 50, 75, 100, 150, 200, 400 mg vitamin E kg diet-1) of supplemental dl-alpha-TOA were fed to P. monodon (mean initial weight 0.29 +/- 0.01 g) for eight weeks. Each diet was fed to three replicate groups of shrimp. Weight gains and total haemocyte count (THC) were higher (P < 0.05) in shrimp fed diets supplemented with 75 and 100 mg vitamin E kg diet-1 than in shrimp fed diets supplemented with

Topics: Analysis of Variance; Animal Nutritional Physiological Phenomena; Animals; Body Weight; Diet; Dose-Response Relationship, Drug; Hemocytes; Hepatopancreas; Immunity, Innate; Muscles; Nutritional Requirements; Penaeidae; Regression Analysis; Superoxide Dismutase; Thiobarbiturates; Vitamin E

The aim of this study was to determine the amount of excess dietary copper (Cu) necessary to experimentally induce liver lesions characteristic of Cu-associated disease in Fischer 344 rats. Male weanling Fischer 344 rats of uniform age were divided into 6 groups (n = 5) and fed a rodent diet containing 18 (control), 750, 1000, 1250, 1500, and 2000 microg/g Cu added as CuSO4. Rats were euthanized after 3 months on the experimental diets and their livers processed for histology, histochemistry, Cu analysis (by atomic absorption spectrophotometry), and quantification of malondialdehyde (MDA) by the thiobarbituric acid reaction. Hepatic Cu levels were significantly higher (P < 0.01) in rats receiving over 1000 microg/g Cu compared to the controls (means for each diet: control = 4.8 microg/g, 750 microg/g Cu = 39.6 microg/g, 1000 microg/g Cu = 111.2 microg/g, 1250 microg/g Cu = 389 microg/g, 1500 microg/g Cu = 509.4 microg/g, and 2000 microg/g Cu = 766 microg/g). Histological lesions increased gradually according to the level of dietary Cu. Significant morphologic changes (necrosis, portal inflammation, hyaline remnants) and reduced growth rate occurred in rats receiving over 1250 microg/g Cu. However, no significant differences were found for MDA levels between groups. The present study demonstrates that compared to other species, very high levels of excess dietary Cu are needed to induce significant liver injury in Fischer 344 rats. Increased MDA content was not detected in rats with morphologic evidence of liver damage, suggesting that lipid peroxidation may not play a major role in this model of Cu toxicity.

Topics: Animals; Body Weight; Copper; Dose-Response Relationship, Drug; Histocytochemistry; Lipid Peroxidation; Liver; Male; Malondialdehyde; Rats; Rats, Inbred F344; Spectrophotometry, Atomic; Thiobarbiturates; Time Factors

This study was designed to investigate the alterations in thiobarbituric acid reactants (TBA-reactants) and enzymatic and nonenzymatic antioxidant levels induced by dexamethasone (Dex) in heart and kidney and to find out whether these alterations induced by Dex and its hypertensive effect had any role in the maintenance of hypertension in this model. Administration of dexamethasone induced severe loss of body weight, significant increase in heart and kidney weights and also marked electrocardiographic changes. The protein content in heart and kidney increased significantly during Dex administration and returned to near normalcy after withdrawal. Total activity of lactate dehydrogenase showed a significant increase in heart till day 8 of treatment, whereas in serum, it exhibited a significant decrease. The activity of CK in heart showed an increase till day 8 of treatment and approached normalcy thereafter. In serum, CK exhibited a decrease till day 8, remaining insignificant thereafter. CKMB in heart showed an insignificant increase initially, reaching normal levels on Dex withdrawal, whereas in serum, it showed a significant decrease throughout the experimental period. Mean arterial pressure (MAP) and heart rate increased significantly, while a significant elevation in the ST segment was noticed during administration as well as after withdrawal of Dex. The TBA-reactants levels were found to increase in heart and kidney during days 12 and 16 of administration with Dex and even after withdrawal of Dex, the levels were insignificantly elevated. The level of glutathione in heart and kidney increased from day 4 onwards and reached normalcy during the later stages of treatment and after withdrawal of Dex. The total sulfhydryl groups exhibited a significant increase in both heart and kidney throughout the experiment. The antioxidant enzymes such as catalase, superoxide dismutase, glutathione peroxidase and glutathione S-transferase exhibited a significant decrease in heart during Dex administration whereas, in kidney, they exhibited a significant increase during treatment and after withdrawal of Dex. Thus, Dex induced rise in mean arterial pressure, significant alterations in electrocardiographic parameters and also marked alterations in enzymatic and nonenzymatic antioxidant levels and in the TBA-reactants level in heart and kidney.

Topics: Animals; Antioxidants; Blood Pressure; Body Weight; Dexamethasone; Electrocardiography; Glucocorticoids; Glutathione; Heart; Hypertension; Kidney; Male; Myocardium; Organ Size; Proteins; Rats; Rats, Wistar; Sulfur; Thiobarbiturates

The present study was carried out to examine whether nitrofurantoin-induced pulmonary toxicity in normal rats was mediated via oxidant stress mechanisms. The relative importance of the cellular antioxidant enzymes in nitrofurantoin toxicity was also assessed. For this, the pulmonary toxicity induced by nitrofurantoin in rats was evaluated at various time intervals after a single subcutaneous injection. Data from this study showed that nitrofurantoin (200 mg/kg, s.c.) resulted in transient but measurable lung damage as evidenced by the increases in wet lung weight/body weight ratio and decreases in lung angiotensin converting enzyme activity. A transient decrease in GSH concentrations with a concurrent increase in GSSG concentrations as well as an increase in lipid peroxidation levels (measured by the formation of diene conjugates and thiobarbituric acid reactants) were also evident in lungs of nitrofurantoin-treated rats. In addition, nitrofurantoin did not alter the pulmonary superoxide dismutase and glutathione peroxidase activities, but it did produce transient decreases in catalase and glutathione reductase activities. These data indicate that impairment of the ability of the lung to detoxify reactive oxygen species may play an important role in the development of nitrofurantoin-induced pulmonary toxicity. The results of the present study suggest that nitrofurantoin can damage the lungs of rats, probably through oxidative stress-mediated mechanisms. Also, our data have provided in vivo evidence for substantiating lipid peroxidation as a possible cause of lung damage.

Topics: Animals; Body Weight; Catalase; Glutathione Peroxidase; Glutathione Reductase; Injections, Subcutaneous; Lipid Peroxidation; Lung; Male; Models, Chemical; Nitrofurantoin; Organ Size; Oxidation-Reduction; Peptidyl-Dipeptidase A; Rats; Rats, Inbred Strains; Superoxide Dismutase; Thiobarbiturates

The effect of maternal copper (Cu) deficiency on various proteins was studied to determine if the changes were reversible or persistent with Cu repletion. The functional consequences of these alterations were assessed by exposing the animals to an oxidative stress (endotoxin), and by measuring the formation of benzo[a]pyrene-DNA adducts in vitro. Throughout gestation and lactation, mice were fed a Control diet (10 micrograms Cu/g diet) or a Low Cu diet (1 microgram Cu/g diet). On day 18, the offspring were killed or switched to the Control diet and killed on day 42 following a single injection of saline or endotoxin on day 41. In day-18 offspring, Cu deficiency resulted in decreased hematocrit values, ceruloplasmin activity, liver and tissue Cu levels, and metallothionein concentrations. Cu repletion restored all but metallothionein levels. Early Cu deficiency led to higher brain CuZn superoxide dismutase activity on day 42, and higher levels of brain thiobarbituric acid reactive substances (TBARS) in endotoxin-treated mice. Liver TBARS were lower in day-18 Low Cu offspring and in day-42 Low Cu offspring treated with endotoxin than age-matched Controls. Cytochrome P-450 concentrations were lower in Low Cu, endotoxin-treated males than in Controls. These results show that Cu deficiency-mediated alterations during early development are not immediately reversed with Cu repletion.

Topics: 7-Alkoxycoumarin O-Dealkylase; Animals; Benzo(a)pyrene; Body Weight; Brain; Ceruloplasmin; Copper; Cytochrome P-450 Enzyme System; Embryonic and Fetal Development; Female; Hematocrit; Hemoglobins; Kidney; Liver; Metallothionein; Mice; Mice, Inbred Strains; Organ Size; Pregnancy; Pregnancy Complications; Superoxide Dismutase; Thiobarbiturates; Trace Elements

1. Blood antioxidants were measured in venous blood samples from 20 runners and six sedentary individuals. All subjects were male, between 20 and 40 years old, and in steady state with respect to body weight and physical activity patterns. Dietary analysis was undertaken using a 7-day weighed food intake. Correlations were sought between antioxidants in blood and (1) weekly training distance and (2) maximum oxygen uptake. In addition, 12 runners could be classified into two groups undertaking either low (range 16-43 km, n = 6) or high (80-147 km, n = 6) weekly training. 2. Body weight (range 55.3-90.0 kg) and percentage body fat (range 7-19%) both showed negative correlations with the weekly training distance (both P less than 0.001). Energy intake and maximum oxygen uptake were both correlated with the weekly training distance (both P less than 0.001). 3. Plasma creatine kinase activity, an indicator of muscle damage, was significantly correlated with the weekly training distance (P less than 0.01), whereas the plasma concentration of thiobarbituric acid-reactive substances, an indicator of free-radical-mediated lipid peroxidation, decreased with increased maximum oxygen uptake (P less than 0.01). 4. Erythrocyte alpha-tocopherol content was greater in the two running groups (P less than 0.05) compared with the sedentary group, and lymphocyte ascorbic acid concentration was significantly elevated in the high-training group (P less than 0.01) compared with the low-training group. 5. Erythrocyte activities of the antioxidant enzymes, glutathione peroxidase and catalase, were significantly and positively correlated with the weekly training distance (P less than 0.01 and P less than 0.05, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Antioxidants; Ascorbic Acid; Body Mass Index; Body Weight; Catalase; Creatine Kinase; Energy Intake; Erythrocytes; Glutathione; Glutathione Peroxidase; Humans; Lymphocytes; Male; Muscles; Oxygen Consumption; Physical Endurance; Running; Thiobarbiturates; Vitamin E

The effects of dietary pantethine levels on the contents and compositions of fatty acids and on the levels of lipid peroxides were investigated with rat liver and its S-9 fraction under administration of 0 (non), 0.2 (low dose), and 0.35 ml (high dose) of autoxidized linoleate (AL) per 100 g body weight of the rats per day for 5 days. AL having 800 meq/kg of peroxide value (PV) and 1,700 meq/kg of carbonyl value (CV) was dosed to the rats of each group given drinking water containing 0 mg% (deficient), 6.25 mg% (adequate), and 125 mg% pantethine (excess). In the pantethine-deficient and -adequate groups, the contents of fatty acids both in the liver homogenate and in the S-9 fraction were correspondingly decreased by increasing dose levels of AL, and the decrease was remarkable especially in the pantethine-deficient group, but was not significant in the pantethine-excess group even by a high dose of AL. Particularly, in the high dose of AL, the notable decreases of oleic acid (C18:1) contents in both the liver and the S-9 fraction were observed in rats of the pantethine-deficient and -adequate groups. The thiobarbituric acid (TBA) values in the liver homogenate and the S-9 fraction were increased correspondingly by increasing dose levels of AL, and the increases were repressed in the pantethine-excess group.

Topics: Administration, Oral; Animals; Body Weight; Chromatography, Gas; Fatty Acids; In Vitro Techniques; Linoleic Acid; Linoleic Acids; Liver; Male; Malondialdehyde; Pantetheine; Rats; Rats, Inbred Strains; Thiobarbiturates

To determine whether beta blockade protects against the acceleration of lipid peroxidation in hyperthyroid rat soleus (slow-oxidative) muscle, in vivo chronic (3 weeks) effects of 3 beta blockers with different ancillary properties on mitochondrial oxidative enzymes, antioxidant enzymes, and thiobarbituric acid-reactive substances were investigated. The rats were rendered hyperthyroid by the administration of thyroxine and treated simultaneously with either carteolol (a nonselective blocker with partial agonist activity; 30 mg/kg/day), atenolol (a beta 1-selective blocker; 50 mg/kg/day), or arotinolol (a nonselective blocker with weak alpha-blocking action; 50 mg/kg/day) over a 3 week period. Hyperthyroidism induced tachycardia, an increase in the mitochondrial oxidative enzymes, manganese (mitochondrial) superoxide dismutase and thiobarbituric acid-reactive substances, and a decrease in the other antioxidant enzymes. The tachycardia was alleviated completely by either atenolol or arotinolol, but partially by carteolol. Arotinolol, but neither carteolol nor atenolol, inhibited the increase in oxidative enzymes and thiobarbituric acid-reactive substances. The levels of antioxidant enzymes were minimally affected by the beta-blocker treatment. Beta 2-, and possibly alpha- as well, but not beta 1-, blockade suppressed mitochondrial hypermetabolism and protected against peroxidative injury in the hyperthyroid soleus muscle. Partial agonist activity was not beneficial.

Topics: Adrenergic beta-Antagonists; Animals; Atenolol; Body Weight; Carteolol; Hyperthyroidism; Lipid Peroxidation; Male; Mitochondria, Muscle; Muscles; Organ Size; Propanolamines; Rats; Rats, Inbred Strains; Thiobarbiturates

In hepatic iron overload, iron-catalyzed lipid peroxidation has been implicated in the mechanisms of hepatocellular injury. Lipid peroxidation may produce reactive aldehydes such as malondialdehyde (MDA) and 4-hydroxynonenal (4-HNE), which may form aldehyde-protein adducts. We investigated whether lipid peroxidation occurred in rats fed a diet containing 3% carbonyl iron for 5-13 wk, and if this resulted in the formation of MDA- and 4-HNE- protein adducts. Chronic iron feeding resulted in hepatic iron overload (greater than 10-fold) and concomitantly induced a 2-fold increase in hepatic lipid peroxidation. Using an antiserum specific for MDA-lysine protein adducts, we demonstrated by immunohistochemistry the presence of aldehyde-protein adducts in the cytosol of periportal hepatocytes, which co-localized with iron. In addition, MDA- and 4-HNE-lysine adducts were found in plasma proteins of animals with iron overload. Only MDA adducts were detected in albumin, while other plasma proteins including a approximately 120-kD protein had both MDA and 4-HNE adducts. In this animal model of hepatic iron overload, injury occurs primarily in periportal hepatocytes, where MDA-lysine protein adducts and excess iron co-localized.

Topics: Aldehydes; Animals; Body Weight; Electrophoresis, Gel, Two-Dimensional; Fluorescence; Iron; Lipid Peroxides; Liver; Lysine; Male; Malondialdehyde; Molecular Weight; Proteins; Rats; Rats, Inbred Strains; Thiobarbiturates

Parenteral administration of iron nitrilotriacetate (FeNTA) to rats resulted in marked loss in body weight, and increases in liver/and kidney/body weight ratios. Fatalities, due to renal failure, depended on dosage and age of the animals, and were greater (70%) after a single large dose (12 mg iron) than after repeated smaller doses (30%). FeNTA administered subchronically gave rise to an increase in ethane exhalation, and to decreased liver glutathione peroxidase activity, and decreased cytochrome P-450 concentration and benzphetamine N-demethylase activity. It also resulted in severe renal tubular necrosis, with deposition of iron in the tubular cells and loss of brush border alkaline phosphatase activity, resulting in a dose-dependent diuresis, with increased urinary excretion of glucose, iron and lipid peroxidation products, and decreased urine creatinine concentration. NTA alone had none of these effects but slightly decreased the hepatic concentration of iron.

Topics: Acetates; Alkaline Phosphatase; Animals; Blood Cell Count; Body Weight; Copper; Cytochrome P-450 CYP1A1; Cytochrome P-450 Enzyme System; Ferric Compounds; gamma-Glutamyltransferase; Hematopoiesis; Iron; Iron Chelating Agents; Kidney; Kidney Tubules; Liver; Male; Nitrilotriacetic Acid; Organ Size; Oxidoreductases; Oxidoreductases, N-Demethylating; Rats; Rats, Inbred Strains; Thiobarbiturates; Zinc

Among vertebrates, adult amphibians are known to be especially tolerant to exposure to high environmental oxygen tensions. To clarify the basis for this high O2 tolerance, adult Rana ridibunda perezi frogs were acclimated for 15 days to water-air phases with either 149 mm Hg O2 (normoxia) or 710 mm Hg O2 (hyperoxia). At the end of the acclimation, various morphometric and biochemical parameters related to oxidative stress were measured in seven organs and tissues. Hyperoxia acclimation did not change either the total weight of the animals or the total and relative wet weights of the organs studied, except for the brain, which showed weight increases in the hyperoxic group. In vivo tissue peroxidation increased in the kidney; decreased in the skeletal muscle and skin; and did not change in the liver, lung, brain, and heart after hyperoxic exposures. Whereas liver, lung, and skin showed glutathione peroxidase (GSH-Px) activities with both cumene hydroperoxide (cumene-OOH) and H2O2 as substrates, skeletal muscle only showed H2O2 GSH-Px activity. Hyperoxia acclimation did not change either catalase (CAT) or GSH-Px activities in any organ, except for the liver in which CAT activity was induced by hyperoxia. Thus hyperoxia tolerance in this species does not need the induction of H2O2-detoxifying enzymes in the majority of the organs. It is suggested that the high O2 tolerance of this amphibian species is related to its comparatively high constitutive GSH-Px activities.

Topics: Adaptation, Physiological; Animals; Benzene Derivatives; Body Weight; Catalase; Glutathione Peroxidase; Hydrogen Peroxide; Organ Size; Oxygen; Partial Pressure; Rana ridibunda; Ranidae; Thiobarbiturates

Male and female rats were dosed once a day for 2 days with injections of 1.5 mg Cd/kg. Formation of thiobarbituric acid reactive substances (TBA-RS) was significantly increased in male rat liver but not in the females. NADPH-dependent lipid peroxidation in vitro in microsomes derived from untreated rat liver was greater in males than in females. Furthermore, addition of cadmium (Cd) to microsomes isolated from male rat liver produced a dose-dependent potentiation of NADPH-dependent lipid peroxidation from low concentrations of Cd. In microsomes derived from females a significant increase in lipid peroxidation was observed only at high Cd concentrations. NADPH-dependent lipid peroxidation enhanced by Cd was greater in the males than in the females. These data suggest that a sex-related difference in the ability of Cd to induce lipid peroxidation in vivo in rat liver appears to be mediated partly through differences in hepatic microsomal NADPH-dependent lipid peroxidation.

Topics: Animals; Body Weight; Cadmium; Female; Lipid Peroxides; Liver; Male; NADP; Rats; Rats, Inbred Strains; Sex Factors; Thiobarbiturates

The influence of dietary vitamin E and Santoquin on lipid peroxidation and liver regeneration in partially-hepatectomized rats was studied. Rats were fed either a basal 10% tocopherol-stripped corn oil diet, the basal diet plus 40 mg dl-alpha-tocopheryl acetate/kg, or the basal diet plus 2 g Santoquin (6-ethoxy-1,2-dihydro-2,2,4-trimethylquinoline)/kg. After 6 weeks, rats fed the antioxidant-deficient diet produced more of the lipid peroxidation product, pentane, than did the rats fed antioxidants. Partial hepatectomy was performed after six and one-half weeks or ten weeks of feeding the diets. At 3 and 6 days after surgery, pentane production was significantly elevated over pre-surgery levels in rats fed the antioxidant-deficient or vitamin E-supplemented diets, but not in rats fed the Santoquin-supplemented diet. Six days after surgery, there were fewer thiobarbituric acid reactants in regenerating liver of Santoquin-fed rats than of vitamin-E fed rats or antioxidant-deficient rats. There was no increase in the 6-day level of thiobarbituric acid reactants over the 3-day level in livers of rats fed Santoquin, while there was an increase in livers of the antioxidant-deficient and vitamin E-supplemented rats. Liver sulfhydryl levels were higher at 3 and 6 days post surgery in the Santoquin-fed rats than in the antioxidant-deficient or vitamin E-supplemented rats. Plasma gamma-glutamyl-transpeptidase activity was not different among the groups of rats. Between the third and sixth day following surgery, liver regeneration was significantly stimulated in Santoquin-fed, but not vitamin E-fed rats. After 11 days, a stimulatory, but not statistically significant, effect of vitamin E was found. Although DNA content of liver was higher at 6 days than at 3 days post surgery, it was not different among the dietary groups, indicating that cell proliferation rather than hypertrophy had occurred. Partial hepatectomy could have altered the ability of the liver to metabolize pentane, thus explaining part of the increased production of pentane. However, the results obtained support the interpretation that elevated levels of dietary antioxidants can be beneficial in terms of reduced lipid peroxidation and increased rates of liver regeneration following liver surgery.

Topics: Animals; Antioxidants; Body Weight; Breath Tests; Diet; Ethoxyquin; gamma-Glutamyltransferase; Lipid Peroxides; Liver; Liver Regeneration; Male; Pentanes; Quinolines; Rats; Rats, Inbred Strains; Sulfhydryl Compounds; Thiobarbiturates; Time Factors; Vitamin E

Gold (Au) thioglucose, which has been used in the treatment of rheumatoid arthritis, inhibits selenium (Se)-glutathione peroxidase. Since Au and Se play roles in inflammation, the effects of dietary Se (0, 0.2, and 2.0 ppm for 10 weeks) and injected gold thioglucose (5 mg Au/day/kg body weight for 28 days) in adjuvant-treated rats were investigated. Au toxicity was evidenced by lower body weights and higher tissue weight/body weight ratios for kidneys and spleens of Au-treated rats. Adjuvant-induced inflammation, measured by paw thickness, was not influenced by dietary Se, although Au decreased inflammation in Se-deficient rats. Liver glutathione peroxidase activity was depressed by Se deficiency and by Au. Sulfhydryl levels in liver soluble fraction and plasma were highest for Se-deficient rats. Among liver, kidney, spleen, and plasma, thiobarbituric acid reactants were highest in kidneys of Au-treated rats and lowest in plasma of rats fed 2 ppm Se. gamma-Glutamyltranspeptidase activity in plasma indicated liver damage in Se-deficient rats. Kidney PGE2 output in 24-hour urine samples was unaffected by Au, Se, or adjuvant. Au-Se interactions in vivo are complex, but decreased glutathione peroxidase activity in Au-injected rats suggests that Se nutrition of Au-treated rheumatoid arthritis patients may be a practical concern.

Topics: Animals; Aurothioglucose; Body Weight; Diet; Dinoprostone; Freund's Adjuvant; gamma-Glutamyltransferase; Glutathione Peroxidase; Gold; Inflammation; Kidney; Liver; Male; Organ Size; Prostaglandins E; Rats; Rats, Inbred Strains; Selenium; Thiobarbiturates

Adjuvant arthritis was induced in rats by the injection of Mycobacterium tuberculosis, and its severity was scored according to the macroscopic findings of the legs, tail, and ears. The average score so obtained was lower in SOD-injected rats than in the control group. The depression of albumin/globulin ratio was inhibited significantly in rats treated with 10.0 mg/kg of SOD. The levels of acid phosphatase and beta-glucuronidase were elevated after the administration of an adjuvant, and these lysosomal enzymes showed a remarkable increase in the control rats, while the elevation was inhibited in rats injected with 10.0 mg/kg of SOD. The levels of TBA-reactive substances in the sera and synovia were elevated at 2 weeks after the injection of adjuvant and decreased thereafter. In rats injected with 5.0 mg/kg or 10.0 mg/kg of SOD, the increase in both serum and synovial levels of TBA reactants was inhibited significantly. These observations suggest that the aggravation of adjuvant arthritis may be associated with lipid peroxidation due to superoxide, and that SOD may be beneficial for the treatment of arthritis.

Topics: Acid Phosphatase; Animals; Arthritis; Arthritis, Experimental; Blood Proteins; Body Weight; Female; Glucuronidase; Lipid Peroxides; Rats; Rats, Inbred Strains; Superoxide Dismutase; Thiobarbiturates

Pentane production was used as an index of lipid peroxidation in male rats fed either 0 or 1000 ppm copper in diets with and without vitamin E. Pentane production by vitamin E-deficient rats not fed copper was greater than that by vitamin E-supplemented rats not fed copper. Pentane production was low by all groups of rats. Copper-fed, vitamin E-deficient and vitamin E-supplemented rats produced more pentane than did respective controls not fed copper. After 9 weeks of feeding the diets, more pentane was produced by vitamin E-deficient than by vitamin E-supplemented rats following intraperitoneal injection of 5 mg of copper/kg of body weight, and vitamin E-deficient rats fed copper produced 5-fold more pentane than did those not fed copper. Thiobarbituric acid-reactants were highest in blood, kidney and liver from copper-fed rats. Lipid-soluble fluorophores in spleen were lowest in vitamin E-supplemented rats not fed copper and highest in copper-fed, vitamin E-deficient rats.

Topics: Animals; Body Weight; Copper; Fluorescence; Lipid Peroxides; Male; Pentanes; Rats; Rats, Inbred Strains; Spleen; Thiobarbiturates; Vitamin E