Ascorbic acid prevents lipid peroxidation and oxidative damage of proteins in guinea pig extrahepatic tissue microsomes

1995 ◽  
Vol 142 (1) ◽  
pp. 71-78 ◽  
Author(s):  
Chinmay K. Mukhopadhyay ◽  
Mrinal K. Ghosh ◽  
Indu B. Chatterjee
Keyword(s):  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Guinea Pig ◽  
Oxidative Damage ◽  
Extrahepatic Tissue

scholarly journals Inhibition of lipid peroxidation by the iron-binding protein lactoferrin

1981 ◽  
Vol 199 (1) ◽  
pp. 259-261 ◽  
Author(s):  
John M. C. Gutteridge ◽  
Suzanne K. Paterson ◽  
Anthony W. Segal ◽  
Barry Halliwell
Keyword(s):  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Oxidative Damage ◽  
Metal Ion ◽  
Binding Protein ◽  
Iron Binding ◽  
Iron Binding Protein

Lactoferrin containing physiological amounts of iron is an inhibitor of lipid peroxidation induced by iron(III) salts and ascorbic acid. It might therefore help to protect neutrophils, inflammatory foci and secretions from metal-ion-dependent oxidative damage.

scholarly journals Effect of Ascorbic Acid on Antioxidant Defense Systems and Lipid Peroxidation in Guinea Pig

1989 ◽  
Vol 6 (1) ◽  
pp. 21-27 ◽  
Author(s):  
Ashwani KOUL ◽  
Krishan L. KHANDUJA ◽  
Indu B. KOUL ◽  
Mahesh P. GUPTA ◽  
Sabhiya MAJID ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Guinea Pig ◽  
Antioxidant Defense ◽  
Defense Systems ◽  
Antioxidant Defense Systems

Protective effect of ascorbic acid against lipid peroxidation and oxidative damage in cardiac microsomes

1993 ◽  
Vol 126 (1) ◽  
pp. 69-75 ◽  
Author(s):  
Mau Mukhopadhyay ◽  
Chinmay K. Mukhopadhyay ◽  
Indu B. Chatterjee
Keyword(s):  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Oxidative Damage ◽  
Protective Effect

Melatonin reduces high levels of lipid peroxidation induced by potassium iodate in porcine thyroid

2019 ◽  
pp. 1-7 ◽  
Author(s):  
Paulina Iwan ◽  
Jan Stepniak ◽  
Malgorzata Karbownik-Lewinska
Keyword(s):  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Membrane Lipids ◽  
Chemical Properties ◽  
Iodine Concentration ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Protective Effects ◽  
Potassium Iodate ◽  
Hormone Synthesis

Abstract. Iodine is essential for thyroid hormone synthesis. Under normal iodine supply, calculated physiological iodine concentration in the thyroid is approx. 9 mM. Either potassium iodide (KI) or potassium iodate (KIO3) are used in iodine prophylaxis. KI is confirmed as absolutely safe. KIO3 possesses chemical properties suggesting its potential toxicity. Melatonin (N-acetyl-5-methoxytryptamine) is an effective antioxidant and free radical scavenger. Study aims: to evaluate potential protective effects of melatonin against oxidative damage to membrane lipids (lipid peroxidation, LPO) induced by KI or KIO3 in porcine thyroid. Homogenates of twenty four (24) thyroids were incubated in presence of either KI or KIO3 without/with melatonin (5 mM). As melatonin was not effective against KI-induced LPO, in the next step only KIO3 was used. Homogenates were incubated in presence of KIO3 (200; 100; 50; 25; 20; 15; 10; 7.5; 5.0; 2.5; 1.25 mM) without/with melatonin or 17ß-estradiol. Five experiments were performed with different concentrations of melatonin (5.0; 2.5; 1.25; 1.0; 0.625 mM) and one with 17ß-estradiol (1.0 mM). Malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA) concentration (LPO index) was measured spectrophotometrically. KIO3 increased LPO with the strongest damaging effect (MDA + 4-HDA level: ≈1.28 nmol/mg protein, p < 0.05) revealed at concentrations of around 15 mM, thus corresponding to physiological iodine concentrations in the thyroid. Melatonin reduced LPO (MDA + 4-HDA levels: from ≈0.97 to ≈0,76 and from ≈0,64 to ≈0,49 nmol/mg protein, p < 0.05) induced by KIO3 at concentrations of 10 mM or 7.5 mM. Conclusion: Melatonin can reduce very strong oxidative damage to membrane lipids caused by KIO3 used in doses resulting in physiological iodine concentrations in the thyroid.

Changes in lipid peroxidation during pregnancy and after delivery in rats: effect of pinealectomy

Reproduction ◽  
2000 ◽  
pp. 143-149 ◽  
Author(s):  
RM Sainz ◽  
RJ Reiter ◽  
JC Mayo ◽  
J Cabrera ◽  
DX Tan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Energy Demand ◽  
Physiological State ◽  
High Energy ◽  
Free Radical Scavengers ◽  
Radical Scavengers ◽  
Oxygen Requirement ◽  
Pregnant Rats

Pregnancy is a physiological state accompanied by a high energy demand of many bodily functions and an increased oxygen requirement. Because of the increased intake and utilization of oxygen, increased levels of oxidative stress would be expected. In the present study, the degree of lipid peroxidation was examined in different tissues from non-pregnant and pregnant rats after the delivery of their young. Melatonin and other indole metabolites are known to be direct free radical scavengers and indirect antioxidants. Thus the effect of pinealectomy at 1 month before pregnancy on the accumulation of lipid damage was investigated in non-pregnant and pregnant rats after the delivery of their young. Malonaldehyde and 4-hydroxyalkenal concentrations were measured in the lung, uterus, liver, brain, kidney, thymus and spleen from intact and pinealectomized pregnant rats soon after birth of their young and at 14 and 21 days after delivery. The same parameters were also evaluated in intact and pinealectomized non-pregnant rats. Shortly after delivery, lipid oxidative damage was increased in lung, uterus, brain, kidney and thymus of the mothers. No differences were detected in liver and spleen. Pinealectomy enhanced this effect in the uterus and lung. It is concluded that during pregnancy high levels of oxidative stress induce an increase in oxidative damage to lipids, which in some cases is inhibited by the antioxidative actions of pineal indoles.

Mechanisms of Nickel-Induced Cell Damage in Allergic Contact Dermatitis and Nutritional Intervention Strategies

2020 ◽  
Vol 20 (7) ◽  
pp. 1010-1014 ◽  
Author(s):  
Dana Filatova ◽  
Christine Cherpak
Keyword(s):  
Lipid Peroxidation ◽  
Contact Dermatitis ◽  
Oxidative Damage ◽  
Allergic Contact Dermatitis ◽  
Cell Damage ◽  
Consumer Products ◽  
The Body ◽  
Cellular Damage ◽  
Nutritional Interventions ◽  
Allergic Contact

Background: Hypersensitivity to nickel is a very common cause of allergic contact dermatitis since this metal is largely present in industrial and consumer products as well as in some commonly consumed foods, air, soil, and water. In nickel-sensitized individuals, a cell-mediated delayed hypersensitivity response results in contact to dermatitis due to mucous membranes coming in long-term contact with nickel-containing objects. This process involves the generation of reactive oxidative species and lipid peroxidation-induced oxidative damage. Immunologically, the involvement of T helper (h)-1 and Th-2 cells, as well as the reduced function of T regulatory cells, are of importance. The toxicity, mutagenicity, and carcinogenicity of nickel are attributed to the generation of reactive oxygen species and induction of oxidative damage via lipid peroxidation, which results in DNA damage. Objective: The aim of this research is to identify nutritionally actionable interventions that can intercept nickel-induced cell damage due to their antioxidant capacities. Conclusion: Nutritional interventions may be used to modulate immune dysregulation, thereby intercepting nickel-induced cellular damage. Among these nutritional interventions are a low-nickel diet and an antioxidant-rich diet that is sufficient in iron needed to minimize nickel absorption. These dietary approaches not only reduce the likelihood of nickel toxicity by minimizing nickel exposure but also help prevent oxidative damage by supplying the body with antioxidants that neutralize free radicals.

scholarly journals Total Antioxidant Capacity and Lipid Peroxidation Status in Cervical Cancer Patients Compared with Women Without Cervical Cancer in Bangladesh

2021 ◽  
Vol 19 (4) ◽  
Author(s):  
Taslima Nigar ◽  
Annekathryn Goodman ◽  
Shahana Pervin
Keyword(s):  
Oxidative Stress ◽  
Cervical Cancer ◽  
Lipid Peroxidation ◽  
Ascorbic Acid ◽  
Antioxidant Capacity ◽  
Cancer Patients ◽  
Total Antioxidant Capacity ◽  
Stress Index ◽  
Oxidative Stress Index ◽  
Total Antioxidant

Abstract Purpose Over the past several decades, research has suggested reactive oxygen species act as cofactors for cervical cancer development. The aim of this study is to evaluate the antioxidant and lipid peroxidation status in cervical cancer patients in Bangladesh. Methods From December 2017 to 2018, a cross-sectional observational study was conducted on 50 cervical cancer patients and 50 controls. Plasma levels of lipid peroxidation and total antioxidant capacity were measured. The Student’s t test was used for statistical analysis. P values less than 0.05 were taken as a level of significance. Results There was a significant reduction in total antioxidant levels in patients with cervical cancer, 972.77 ± 244.22 SD µmol equivalent to ascorbic acid/L, compared to normal controls, 1720.13 ± 150.81 SD µmol equivalent to ascorbic acid/L (P < 0.001). Levels of lipid peroxidation were found to be significantly higher in cervical cancer, 7.49 ± 2.13 SD µmol/L, than in women without cervical cancer, 3.28 ± 0.58 SD µmol/L (P < 0.001). The cervical cancer patients had significantly higher levels of oxidative stress index (0.83 ± 0.31) in comparison to controls (0.19 ± 0.04) (P < 0.001). Conclusion There was an increased oxidative stress index due to imbalance between lipid peroxidation generation and total antioxidant capacity in cervical cancer patients. Further studies are needed to explore the role of oxidative stress as a cofactor for cervical carcinogenesis.

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