Combined efficacies of lipoic acid and meso-2,3-dimercaptosuccinic acid on lead-induced erythrocyte membrane lipid peroxidation and antioxidant status in rats

2003 ◽  
Vol 22 (4) ◽  
pp. 183-192 ◽  
Author(s):  
R Sivaprasad ◽  
M Nagaraj ◽  
P Varalakshmi
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Body Weight ◽  
Erythrocyte Membrane ◽  
Lipoic Acid ◽  
Combined Treatment ◽  
Membrane Lipid ◽  
Dimercaptosuccinic Acid ◽  
Membrane Lipid Peroxidation ◽  
Antioxidant Defence System

One of the most intriguing phenomenon observed during lead toxicity has been attributed to lead-induced oxidative stress. The combined effect of DL-a-lipoic acid (LA) and meso 2,3-dimercaptosuccinic acid (DMSA) on lead-induced alterations in selected parameters, which are indicators of oxidative stress in erythrocytes, have been studied. Lead acetate (Pb, 0.2%) was administered in drinking water for 5 weeks to induce toxicity. LA (25 mg/ kg body weight per day i.p.) and DMSA (20 mg/kg body weight per day i.p.) were administered individually and also in combination during week 6. Clinical evidence of toxic exposure was evident from the elevated blood lead levels (BPb) along with lowered levels of haemoglobin (Hb) and haematocrit (Ht). Lead-exposed animals showed enhanced membrane lipid peroxidation (LPO) in the erythrocytes. Damage to the erythrocyte membrane was evident from the decline in the activities of the trans-membrane enzymes, viz., Na1, K1 ATPase, Ca21 ATPase and Mg21 ATPase. Lead-exposed rats also suffered an onslaught on the antioxidant defence system witnessed by lowered activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and reduced glutathione (GSH). Serum glutamic-oxoloacetic transaminase (SGOT) and serum glutamic-pyruvic transaminase (SGPT) were also elevated in lead-exposed rats. Treatment with either LA or DMSA reversed the lead-induced biochemical disturbances encountered by the erythrocytes, but combined treatment with LA and DMSA was very effective in mitigating all the parameters indicative of oxidative stress.

Erythrocyte membrane lipid peroxidation and glycosylated hemoglobin in diabetes

Diabetes ◽  
1989 ◽  
Vol 38 (12) ◽  
pp. 1539-1543 ◽  
Author(s):  
S. K. Jain ◽  
R. McVie ◽  
J. Duett ◽  
J. J. Herbst
Keyword(s):  
Lipid Peroxidation ◽  
Erythrocyte Membrane ◽  
Glycosylated Hemoglobin ◽  
Membrane Lipid ◽  
Membrane Lipid Peroxidation

Erythrocyte Membrane Lipid Peroxidation and Glycosylated Hemoglobin in Diabetes

Diabetes ◽  
1989 ◽  
Vol 38 (12) ◽  
pp. 1539-1543 ◽  
Author(s):  
S. K. Jain ◽  
R. McVie ◽  
J. Duett ◽  
J. J. Herbst
Keyword(s):  
Lipid Peroxidation ◽  
Erythrocyte Membrane ◽  
Glycosylated Hemoglobin ◽  
Membrane Lipid ◽  
Membrane Lipid Peroxidation

scholarly journals Role of Membrane Lipid Peroxidation, Enzymatic and Non-enzymatic Antioxidative Systems in the Development of Chilling Injury in Japanese Plums

2012 ◽  
Vol 137 (6) ◽  
pp. 473-481 ◽  
Author(s):  
Sukhvinder Pal Singh ◽  
Zora Singh
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Cold Storage ◽  
Chilling Injury ◽  
Membrane Lipid ◽  
Enzymatic Antioxidants ◽  
Membrane Lipid Peroxidation ◽  
Stress Theory ◽  
Antioxidative Systems ◽  
Duration Of Storage

Chilling injury (CI) is a major postharvest constraint in the long-term cold storage, transportation, and distribution of japanese plums (Prunus salicina). The aim of the work was to explain the development and severity of CI in japanese plums based on the oxidative stress theory following time course analysis of enzymatic and non-enzymatic antioxidants. Changes in membrane lipid peroxidation and enzymatic and non-enzymatic antioxidative systems in japanese plum cultivar Blackamber were determined at weekly intervals during 5 weeks of cold storage at 0 °C and at 2-day intervals during poststorage simulated shelf conditions (21 ± 1 °C) for 8 days after each week of cold storage. Fruit respiration and ethylene production rates showed typical climacteric patterns after removal from cold storage and these rates were relatively high after 4 and 5 weeks compared with 0 to 3 weeks of storage. The CI symptoms first appeared after 3 weeks of cold storage after fruit had been transferred to simulated shelf conditions. The incidence and severity of CI intensified with increasing storage duration. The extent of lipid peroxidation indicated by concentration of thiobarbituric acid-reactive substances and membrane damage manifested as electrolyte leakage increased with increasing duration of storage and subsequent simulated shelf conditions. Membrane lipid peroxidation exhibited positive correlation with the severity of CI. Activities of primary antioxidant enzymes and the enzymes involved in the ascorbate–glutathione cycle were determined to explain the levels of reduced and oxidized forms of cellular redox buffers, ascorbate and glutathione. In response to chilling stress, antioxidative protection systems operated efficiently during the first 3 weeks of cold storage, but extended storage resulted in loss of ability to ameliorate increasing levels of oxidative stress. In this study, the comprehensive analyses of various metabolites and antioxidative systems explain the series of events involved in development of CI in japanese plums in support of the oxidative stress theory.

Increased erythrocyte antioxidant status protects against smoking induced hemolysis in moderate smokers

2011 ◽  
Vol 30 (10) ◽  
pp. 1475-1481 ◽  
Author(s):  
Padmavathi Pannuru ◽  
Damodara Reddy Vaddi ◽  
Rameswara Reddy Kindinti ◽  
Nallanchakravarthula Varadacharyulu
Keyword(s):  
Lipid Peroxidation ◽  
Erythrocyte Membrane ◽  
Antioxidant Status ◽  
Reduced Glutathione ◽  
Membrane Lipid ◽  
Red Cell ◽  
Membrane Lipid Peroxidation ◽  
Free Radical Damage ◽  
Human Red Blood Cells ◽  
Nitrite Nitrate

Cigarette smoking is common in societies worldwide and has been identified as injurious to human health. Human red blood cells are important targets for electrophilic and oxidant foreign compounds. In the present study, the possible role of antioxidant status on smoking-induced erythrocyte hemolysis of smokers was studied. Erythrocyte superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activities, reduced glutathione (GSH) level, erythrocyte membrane lipid peroxidation, total cholesterol and phospholipids were determined. Further, nitrite/nitrate levels (NO2/NO3) in both plasma and erythrocyte lysate were measured. Results showed increased plasma and erythrocyte membrane lipid peroxidation and nitrite/nitrate levels in smokers. The activities of SOD, CAT and GPx were also increased with reduced glutathione (GSH) level in smokers. No significant change was observed in smokers red cell hemolysis and cholesterol/phospholipid (C/P) ratio compared to controls. Erythrocyte membrane lipid peroxidation was positively correlated with SOD ( r = 0.482, p < 0.01) and GPx ( r = 0.368, p < 0.018) in smokers. Increased levels of nitrite/nitrate and antioxidant status of erythrocytes might be playing a crucial role in protecting red cell from free radical damage induced by cigarette smoke.

scholarly journals Bitter Leaf (Vernonia Amygdalina) Modulates Nitrobenzene-Induced Renal Damage in Rats Via Suppression of Oxido-Inflammatory Activities

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Johnson Olaleye Oladele ◽  
Oyedotun Moses Oyeleke ◽  
Boyede Dele Olowookere ◽  
Oluwafeyisayo Doyinsola Babatope ◽  
Monisola Dorcas Olaniyan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Body Weight ◽  
Leaf Extract ◽  
Renal Damage ◽  
Kidney Diseases ◽  
Electrolyte Imbalance ◽  
Renal Diseases ◽  
Serum Electrolyte ◽  
Antioxidant Defence System

Abstract Renal diseases have been documented as one of the massive health challenges, ranked as the 12th most common cause of death globally. This study was carried out to assess the chemopreventive effects of Vernonia amydalina on nitrobenzene mediated renal damage in rats. Rats were exposed to 100 mg/kg body weight of nitrobenzene via oral administration and treated with 200 mg/kg body weight (BW) and 400 mg/kg BW of methanol leaf extract of Vernonia amydalina (MLVA) and Vitamin E for 14 consecutive days. Nitrobenzene significantly induced a renal injury with a significant increase in the serum levels of urea and creatinine with the concomitant altered serum electrolyte profile. Also, nitrobenzene mediated the oxidative stress and lipid peroxidation with a significant increase in the renal level of malondialdehyde (MDA), hydrogen peroxide (H2O2), with a concomitant decrease in the level of reduced glutathione (GSH), Catalase (CAT) and Superoxide dismutase (SOD). Furthermore, an inflammation was observed in the nitrobenzene-treated rats with the elevated level of nitric oxide (NO) and myeloperoxidase (MPO). However, the treatment with methanol leaf extract of Vernonia amydalina reversed all the nitrobenzene-associated renal damage, electrolyte imbalance, oxidative stress, lipid peroxidation, inflammation and altered antioxidant defence system. Taken together, methanol leaf extract of Vernonia amydalina offers protection which may be beneficial for the treatment and management of kidney diseases or other related disorders via enhancing the serum electrolyte homeostasis, protecting the structural integrity of the kidney, antioxidant, anti-inflammatory mechanisms.

scholarly journals Oxidative Stress of Vanadium-Mediated Oxygen Free Radical Generation Stimulated by Aluminium on Human Erythrocytes

1998 ◽  
Vol 35 (2) ◽  
pp. 254-260 ◽  
Author(s):  
M A M Abou-Seif
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Osmotic Fragility ◽  
Thiobarbituric Acid ◽  
Oxygen Free Radical ◽  
Membrane Lipid ◽  
Human Erythrocytes ◽  
Membrane Lipid Peroxidation ◽  
Radical Generation

It has been suggested that aluminium stimulates vanadium-mediated superoxide radical generation. The oxidative stress of generated superoxide radicals on antioxidant enzyme activity, oxidation of NADH and NADPH, membrane lipid peroxidation and osmotic fragility in human red blood cells (RBC) was investigated. RBC were incubated with varying concentrations of vanadium and aluminium ions at 37°C for 2 h. RBC incubated with vanadium ions showed significantly increased superoxide dismutase and catalase activities, and oxidized NADH and NADPH concentrations compared with control RBC preparations. Erythrocyte lipid peroxidation was assessed by measuring thiobarbituric acid reactivity. RBC incubated with elevated levels of vanadium showed significantly increased membrane lipid peroxidation when compared with control RBC; it increased further on addition of aluminium. A significant positive correlation was observed between the extent of vanadium induced membrane lipid peroxidation and the osmotic fragility of treated RBC. In the presence of vanadium, aluminium stimulates superoxide dismutase and catalase activities, NADH and NADPH oxidation and membrane lipid peroxidation, as well as increasing osmotic fragility of human erythrocytes. The stimulatory effect of aluminium was dependent on concentration. These results may have implications for the mechanism of toxicity of aluminium and vanadium in haemodialysis patients.

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