Combined administration of taurine and meso 2,3–dimercaptosuccinic acid in the treatment of chronic lead intoxication in rats

2004 ◽  
Vol 23 (4) ◽  
pp. 157-166 ◽  
Author(s):  
S JS Flora ◽  
Manisha Pande ◽  
Smrati Bhadauria ◽  
G M Kannan
Keyword(s):  
Oxidative Stress ◽  
Soft Tissues ◽  
Aminolevulinic Acid ◽  
Thiobarbituric Acid ◽  
Concomitant Administration ◽  
Significant Inhibition ◽  
Male Rats ◽  
Lead Intoxication ◽  
Zinc Protoporphyrin ◽  
Thiobarbituric Acid Reactive Substance

The present study describes the dose–dependent effect of taurine, an amino acid and a known antioxidant, either alone or in combination with meso 2,3–dimercaptosucci–nic acid (DMSA) in the treatment of subchronic lead intoxication in male rats. The effects of these treatments in influencing the lead–induced alterations in haem synthesis, hepatic, renal or brain oxidative stress and lead concentration from soft tissues were investigated. Exposure to lead produced a significant inhibition of blood–aminolevulinic acid dehydratase (ALAD) activity, reduction in glutathione (GSH) and an increase in zinc protoporphyrin (ZPP) suggesting an altered haem synthesis pathway. Only DMSA was able to increase the activity of ALAD, while both taurine and DMSA were able to significantly increase GSH level towards normal. Animals treated with taurine significantly reduced the alterations in some of the biochemical parameters indicative of oxidative stress. Thiobarbituric acid reactive substance (TBARS) levels reduced significantly in liver, kidney and red blood cells, while GSH level increased. Activity of superoxide dismutase (SOD) also showed an increase in blood and brain in animals treated with taurine. The data also provided a promising role of taurine during chelation of lead by potentiating the depletion of blood, liver and brain lead compared to DMSA alone. It can thus be concluded from the study that concomitant administration of an antioxidant could play a significant and important role in abating a number of toxic effects of lead when administered along with the thiol chelators.

scholarly journals Protective Effects of Selenium, Calcium, and Magnesium Against Arsenic-Induced Oxidative Stress in Male Rats

2010 ◽  
Vol 61 (2) ◽  
pp. 153-159 ◽  
Author(s):  
Deepti Srivastava ◽  
Ramlingam Subramanian ◽  
Datta Madamwar ◽  
Swaran Flora
Keyword(s):  
Oxidative Stress ◽  
Aminolevulinic Acid ◽  
Inorganic Arsenic ◽  
Concomitant Administration ◽  
Environmental Pollutant ◽  
Male Rats ◽  
Protective Effects ◽  
Essential Trace Elements ◽  
Calcium And Magnesium ◽  
Potent Carcinogen

Protective Effects of Selenium, Calcium, and Magnesium Against Arsenic-Induced Oxidative Stress in Male RatsInorganic arsenic is a potent carcinogen and environmental pollutant. More than one hundred million people are reported to be exposed to elevated concentrations of arsenic mainly via drinking water. Essential trace elements can affect toxicity of metals by interacting with metals at the primary site of action and can also modify the body's response to toxic metals by altering their metabolism and transport. This study investigates the effects of concomitant administration of selenium, magnesium, and calcium with arsenic on blood biochemistry and oxidative stress. Selenium was the most effective in reducing arsenic-induced inhibition of blood δ-aminolevulinic acid dehydratase (ALAD) activity and liver oxidative stress. Calcium and magnesium also showed favourable effects on haematological and other biochemical parameters. Because selenium was the most effective, it should be added to chelation therapy to achieve the best protective effects against arsenic poisoning in humans.

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome

2011 ◽  
Vol 14 (3) ◽  
pp. 443-448 ◽  
Author(s):  
N. Kurhalyuk ◽  
H. Tkachenko ◽  
K. Pałczyńska
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Brown Trout ◽  
Salmo Trutta ◽  
Thiobarbituric Acid ◽  
Control Group ◽  
Thiobarbituric Acid Reactive Substance ◽  
Tbars Level ◽  
Reactive Substance ◽  
Brown Trout Salmo Trutta

Resistance of erythrocytes from Brown trout (Salmo trutta m. trutta L.) affected by ulcerative dermal necrosis syndrome In the present work we evaluated the effect of ulcerative dermal necrosis (UDN) syndrome on resistance of erythrocytes to haemolytic agents and lipid peroxidation level in the blood from brown trout (Salmo trutta m. trutta L.). Results showed that lipid peroxidation increased in erythrocytes, as evidenced by high thiobarbituric acid reactive substance (TBARS) levels. Compared to control group, the resistance of erythrocytes to haemolytic agents was significantly lower in UDN-positive fish. Besides, UDN increased the percent of hemolysated erythrocytes subjected to the hydrochloric acid, urea and hydrogen peroxide. Results showed that UDN led to an oxidative stress in erythrocytes able to induce enhanced lipid peroxidation level, as suggested by TBARS level and decrease of erythrocytes resistance to haemolytic agents.

Chronic hypoxia and glutathione-dependent detoxication in rat small intestine

1996 ◽  
Vol 270 (4) ◽  
pp. G725-G729 ◽  
Author(s):  
T. S. LeGrand ◽  
T. Y. Aw
Keyword(s):  
Oxidative Stress ◽  
Chronic Hypoxia ◽  
Thiobarbituric Acid ◽  
Redox System ◽  
Thiobarbituric Acid Reactive Substance ◽  
Sprague Dawley ◽  
Distal Intestine ◽  
Key Enzyme ◽  
Cysteine Synthetase ◽  
Glucose 6 Phosphate Dehydrogenase

It has previously been found that chronic O2 deficiency decreases activity of the enzymes of the glutathione (GSH) redox system in the liver. To study the effects of O2 deficiency on intestinal detoxication capacity, pair-fed (16 g food/day) Sprague-Dawley rats were exposed to air (20.9% O2; n = 4) or 10% O2 (n = 4) for 10 days. Animals were killed, and intestinal mucosal homogenate (20% wt/vol) was obtained and assayed for activities of glucose-6-phosphate dehydrogenase (G6PD), GSH peroxidase (GSHPx), GSH disulfide reductase (GSSGRd), and gamma-glutamyl cysteine synthetase (gamma-GCS). Hypoxia decreases activities of GSHPx, GSSGRd, and gamma-GCS by approximately 50%, which suggests compromised detoxication. A proximal-to-distal reduction in enzymatic capacity indicates impairment of detoxication may be more pronounced in the distal intestine. G6PD, a key enzyme in NADPH production, remains unchanged. Urinary malondialdehyde was also monitored. Hypoxic rats exhibited a threefold increase in thiobarbituric acid-reactive substance, consistent with a generalized oxidative stress in these animals. Taken together, the results indicate that chronic hypoxia promotes tissue oxidative stress and impairs the ability of the enterocyte to metabolize ingested oxidants.

scholarly journals Opposing Effects of Oxygen Regulation on Kallistatin Expression: Kallistatin as a Novel Mediator of Oxygen-Induced HIF-1-eNOS-NO Pathway

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
Julie Chao ◽  
Youming Guo ◽  
Pengfei Li ◽  
Lee Chao
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Animal Models ◽  
Hypoxia Inducible Factor ◽  
Thiobarbituric Acid ◽  
Organ Injury ◽  
Thiobarbituric Acid Reactive Substance ◽  
Bacterial Killing ◽  
Antioxidant Genes ◽  
Pkc Activation

Oxidative stress has both detrimental and beneficial effects. Kallistatin, a key component of circulation, protects against vascular and organ injury. Serum kallistatin levels are reduced in patients and animal models with hypertension, diabetes, obesity, and cancer. Reduction of kallistatin levels is inversely associated with elevated thiobarbituric acid-reactive substance. Kallistatin therapy attenuates oxidative stress and increases endothelial nitric oxide synthase (eNOS) and NO levels in animal models. However, kallistatin administration increases reactive oxygen species formation in immune cells and bacterial killing activity in septic mice. High oxygen inhibits kallistatin expression via activating the JNK-FOXO1 pathway in endothelial cells. Conversely, mild oxygen/hyperoxia stimulates kallistatin, eNOS, and hypoxia-inducible factor-1 (HIF-1) expression in endothelial cells and in the kidney of normal mice. Likewise, kallistatin stimulates eNOS and HIF-1, and kallistatin antisense RNA abolishes oxygen-induced eNOS and HIF-1 expression, indicating a role of kallistatin in mediating mild oxygen’s stimulation on antioxidant genes. Protein kinase C (PKC) activation mediates HIF-1-induced eNOS synthesis in response to hyperoxia/exercise; thus, mild oxygen through PKC activation stimulates kallistatin-mediated HIF-1 and eNOS synthesis. In summary, oxidative stress induces down- or upregulation of kallistatin expression, depending on oxygen concentration, and kallistatin plays a novel role in mediating oxygen/exercise-induced HIF-1-eNOS-NO pathway.

Degradation of oxidative stress-induced denatured albumin in rat liver endothelial cells

2005 ◽  
Vol 289 (3) ◽  
pp. C531-C542 ◽  
Author(s):  
Ryuji Bito ◽  
Sayaka Hino ◽  
Atsushi Baba ◽  
Miharu Tanaka ◽  
Haruka Watabe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Rat Liver ◽  
Laser Scanning ◽  
Thiobarbituric Acid ◽  
Serum Levels ◽  
Inhibitory Effect ◽  
Endocytic Pathway ◽  
Thiobarbituric Acid Reactive Substance ◽  
Liver Endothelial Cells

We previously identified conformationally denatured albumin (D2 and D3 albumin) in rats with endotoxicosis (Bito R, Shikano T, and Kawabata H. Biochim Biophys Acta 1646: 100–111, 2003). In the present study, we attempted first to confirm whether the denatured albumins generally increase in conditions of oxidative stress and second to characterize the degradative process of the denatured albumin using primary cultured rat liver endothelial cells. We used five models of oxidative stress, including endotoxicosis, ischemic heart disease, diabetes, acute inflammation, and aging, and found that serum concentrations of D3 albumin correlate with the serum levels of thiobarbituric acid-reactive substance ( R = 0.87), whereas the concentrations of D2 albumin are 0.52. Ligand blot analysis showed that the D3 albumin binds to gp18 and gp30, which are known endothelial scavenger receptors for chemically denatured albumin. Primary cultured rat liver endothelial cells degraded the FITC-D3 albumin, and the degradation rate decreased to ∼60% of control levels in response to anti-gp18 and anti-gp30 antibodies, respectively. An equimolar mixture of these antibodies produced an additive inhibitory effect on both uptake and degradation, resulting in levels ∼20% those of the control. Furthermore, filipin and digitonin, inhibitors of the caveolae-related endocytic pathway, reduced the FITC-D3 albumin uptake and degradation to <20%. Laser-scanning confocal microscopic observation supported these data regarding the uptake and degradation of D3 albumin. These results indicate that conformationally denatured D3 albumin occurs generally under oxidative stress and is degraded primarily via gp18- and gp30-mediated and caveolae-related endocytosis in liver endothelial cells.

Exercise-induced oxidative stress leads hemolysis in sedentary but not trained humans

2005 ◽  
Vol 99 (4) ◽  
pp. 1434-1441 ◽  
Author(s):  
Ümit Kemal Şentürk ◽  
Filiz Gündüz ◽  
Oktay Kuru ◽  
Günnur Koçer ◽  
Yaşar Gül Özkaya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Osmotic Fragility ◽  
Thiobarbituric Acid ◽  
Protein Carbonyl ◽  
Antioxidant Vitamin ◽  
Thiobarbituric Acid Reactive Substance ◽  
Protein Carbonyl Content ◽  
Trained Subjects ◽  
Exercise Induced ◽  
Sedentary Subjects

Intravascular hemolysis is one of the most emphasized mechanisms for destruction of erythrocytes during and after physical activity. Exercise-induced oxidative stress has been proposed among the different factors for explaining exercise-induced hemolysis. The validity of oxidative stress following exhaustive cycling exercise on erythrocyte damage was investigated in sedentary and trained subjects before and after antioxidant vitamin treatment (A, C, and E) for 2 mo. Exercise induced a significant increase in thiobarbituric acid-reactive substance and protein carbonyl content levels in sedentary subjects and resulted in an increase of osmotic fragility and decrease in deformability of erythrocytes, accompanied by signs for intravascular hemolysis (increase in plasma hemoglobin concentration and decrease in haptoglobulin levels). Administration of antioxidant vitamins for 2 mo prevented exercise-induced oxidative stress (thiobarbituric acid-reactive substance, protein carbonyl content) and deleterious effects of exhaustive exercise on erythrocytes in sedentary subjects. Trained subjects' erythrocyte responses to exercise were different from those of sedentary subjects before antioxidant vitamin treatment. Osmotic fragility and deformability of erythrocytes, plasma hemoglobin concentration, and haptoglobulin levels were not changed after exercise, although the increased oxidative stress was observed in trained subjects. After antioxidant vitamin treatment, functional and structural parameters of erythrocytes were not altered in the trained group, but exercise-induced oxidative stress was prevented. Increased percentage of young erythrocyte populations was determined in trained subjects by density separation of erythrocytes. These findings suggest that the exercise-induced oxidative stress may contribute to exercise-induced hemolysis in sedentary humans.

scholarly journals Exposure of precision-cut rat liver slices to ethanol accelerates fibrogenesis

2010 ◽  
Vol 299 (3) ◽  
pp. G661-G668 ◽  
Author(s):  
Courtney S. Schaffert ◽  
Michael J. Duryee ◽  
Robert G. Bennett ◽  
Amy L. DeVeney ◽  
Dean J. Tuma ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Cytokine Production ◽  
Smooth Muscle Actin ◽  
Thiobarbituric Acid ◽  
Ethanol Metabolism ◽  
Thiobarbituric Acid Reactive Substance ◽  
Ethanol Treatment ◽  
Liver Slices

Ethanol metabolism in the liver induces oxidative stress and altered cytokine production preceding myofibroblast activation and fibrogenic responses. The purpose of this study was to determine how ethanol affects the fibrogenic response in precision-cut liver slices (PCLS). PCLS were obtained from chow-fed male Wistar rats (200–300 g) and were cultured up to 96 h in medium, 25 mM ethanol, or 25 mM ethanol and 0.5 mM 4-methylpyrazole (4-MP), an inhibitor of ethanol metabolism. Slices from every time point (24, 48, 72, and 96 h) were examined for glutathione (GSH) levels, lipid peroxidation [thiobarbituric acid-reactive substance (TBARS) assay], cytokine production (ELISA and RT-PCR), and myofibroblast activation [immunoblotting and immunohistochemistry for smooth muscle actin (SMA) and collagen]. Treatment of PCLS with 25 mM ethanol induced significant oxidative stress within 24 h, including depletion of cellular GSH and increased lipid peroxidation compared with controls ( P < 0.05). Ethanol treatment also elicited a significant and sustained increase in interleukin-6 (IL-6) production ( P < 0.05). Importantly, ethanol treatment accelerates a fibrogenic response after 48 h, represented by significant increases in SMA and collagen 1α(I) production ( P < 0.05). These ethanol-induced effects were prevented by the addition of 4-MP. Ethanol metabolism induces oxidative stress (GSH depletion and increased lipid peroxidation) and sustained IL-6 expression in rat PCLS. These phenomena precede and coincide with myofibroblast activation, which occurs within 48 h of treatment. These results indicate the PCLS can be used as in vitro model for studying multicellular interactions during the early stages of ethanol-induced liver injury and fibrogenesis.

The effects of gasotransmitters inhibition on biochemical and haematological parameters and oxidative stress in propofol-anaesthetized Wistar male rats

2019 ◽  
Vol 97 (11) ◽  
pp. 1073-1079 ◽  
Author(s):  
M. Djuric ◽  
T. Nikolic Turnic ◽  
S. Kostic ◽  
S. Stankovic ◽  
K. Radonjic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Bolus Injection ◽  
Troponin T ◽  
Protoporphyrin Ix ◽  
Male Rats ◽  
High Density Lipoproteins ◽  
Zinc Protoporphyrin ◽  
Synthase Inhibitor ◽  
And Oxidative Stress ◽  
Wistar Male Rats

This study aimed to investigate the effects of propofol through evaluating its interaction with nitric oxide (NO), hydrogen sulfide (H2S), and carbon monoxide (CO). Wistar male rats were divided in 4 groups: (1) bolus injection of propofol (1% 10 mg/mL, 100 mg/kg bw, i.p.); (2) Nω-nitro-l-arginine methyl ester (L-NAME; NO synthase inhibitor, 60 mg/kg bw, i.p.) + bolus injection of propofol (1% 10 mg/mL, 100 mg/kg bw, i.p.); (3) DL-propargylglycine (DL-PAG; H2S synthase inhibitor, 50 mg/kg bw, i.p.) + bolus injection of propofol (1% 10 mg/mL, 100 mg/kg bw, i.p.); (4) zinc protoporphyrin IX (ZnPPIX; CO synthase inhibitor, 50 μmol/kg bw, i.p.) + bolus injection of propofol (1% 10 mg/mL, 100 mg/kg bw, i.p.). Increased levels of albumins, low-density lipoproteins, alkaline phosphatase, amylase, high-sensitivity Troponin T, and fibrinogen were found in L-NAME + propofol group. Platelet crit, platelet count, total cholesterol, and high-density lipoproteins were elevated in ZnPPIX + propofol group. Hydrogen peroxide was increased in all groups treated with gasotransmitters inhibitors. Reduced glutathione was reduced in all groups, superoxide dismutase activity only in L-NAME + propofol. The effect of propofol on various biochemical, haematological, and oxidative stress markers may be at least in part mediated through interaction with 3 estimated gasotransmitters.

scholarly journals The protective effect of vildagliptin in chronic experimental cyclosporine A-induced hepatotoxicity

2016 ◽  
Vol 94 (3) ◽  
pp. 251-256 ◽  
Author(s):  
Nagla A. El-Sherbeeny ◽  
Manar A. Nader
Keyword(s):  
Oxidative Stress ◽  
Nuclear Factor Kappa B ◽  
Thiobarbituric Acid ◽  
Serum Levels ◽  
Nuclear Extract ◽  
Thiobarbituric Acid Reactive Substance ◽  
Histopathological Changes ◽  
Dipeptidyl Peptidase 4 ◽  
Stress Markers ◽  
Apoptosis And Inflammation

The study examined the effect of dipeptidyl peptidase-4 (DPP-4) inhibitor, vildagliptin, in cyclosporine (CsA)-induced hepatotoxicity. Rats were divided into 4 groups treated for 28 days: control (vehicle), vildagliptin (10 mg/kg, orally), CsA (20 mg/kg, s.c.), and CsA-vildagliptin group. Liver function was assessed by measuring serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma glutamyltransferase (γGT), lactate dehydrogenase (LDH), and albumin, and histopathological changes of liver were examined. Oxidative stress markers were evaluated. Assessment of nuclear factor-kappa B (NF-κB) activity in hepatic nuclear extract, serum DPP-4, and expression of Bax and Bcl2 were also done. CsA-induced hepatotoxicity was evidenced by increase in serum levels of AST, ALT, and γGT; a decrease in serum albumin; and a significant alteration in hepatic architecture. Also, significant increase in thiobarbituric acid reactive substance (TBARS) and decrease in superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione (GSH) levels, increased expression Bax proteins with deceased expression of Bcl2, and increased hepatic activity of NF-κB and serum DPP-4 level were observed upon CsA treatment. Vildagliptin significantly improved all altered parameters induced by CsA administration. Vildagliptin has the potential to protect the liver against CsA-induced hepatotoxicity by reducing oxidative stress, DPP-4 activity, apoptosis, and inflammation.

scholarly journals Development of nutritional iron deficiency in growing male rats: haematological parameters, iron bioavailability and oxidative defence

2010 ◽  
Vol 105 (4) ◽  
pp. 517-525 ◽  
Author(s):  
María J. M. Alférez ◽  
Javier Díaz-Castro ◽  
Inmaculada López-Aliaga ◽  
María Rodríguez-Ferrer ◽  
Luis Javier Pérez-Sánchez ◽  
...  
Keyword(s):  
Thiobarbituric Acid ◽  
Iron Bioavailability ◽  
Male Rats ◽  
Haematological Parameters ◽  
Fe Deficiency ◽  
Albino Rats ◽  
Thiobarbituric Acid Reactive Substance ◽  
Sequence Of Events ◽  
Wistar Albino Rats ◽  
The Brain

Despite Fe deficiency having been widely studied, the sequence of events in its development still remains unclear. The aim of the present study was to elucidate the effects of nutritional Fe-deficiency development on haematological parameters, Fe bioavailability and the enzymes involved in oxidative defence in recently weaned male Wistar albino rats. Control (C) and Fe-deficient (ID) groups were fed the AIN-93 G diet with a normal Fe level (45 mg/kg diet) or with a low Fe level (5 mg/kg diet), respectively, for 20, 30 or 40 d. At day 20 serum Fe, serum ferritin and the saturation of transferrin decreased drastically, decreasing further in the course of Fe-deficiency development for the saturation of transferrin. The development of Fe deficiency did not affect plasma thiobarbituric acid-reactive substance production, or catalase (CAT) and glutathione peroxidase (GPx) activities in erythrocyte cytosol. Fe deficiency diminished hepatic Fe content and CAT and GPx activities in hepatic cytosol only at day the 20. However, in spite of the minor Fe deposits in the brain of ID rats, the CAT and GPx activities in the brain cytosolic fraction did not differ in any of the studied periods v. control rats. These results show that brain is a tissue that does not seem to depend on Fe levels for the maintenance of antioxidant defence mechanisms in the course of nutritional Fe deficiency.

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