Mechanisms involved in the protective effect of estradiol-17β on lipid peroxidation and DNA damage

1998 ◽  
Vol 274 (6) ◽  
pp. E1002-E1008 ◽  
Author(s):  
Stacey Ayres ◽  
William Abplanalp ◽  
James H. Liu ◽  
M. T. Ravi Subbiah
Keyword(s):  
Hydrogen Peroxide ◽  
Lipid Peroxidation ◽  
Dna Damage ◽  
Superoxide Radical ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Chain Propagation ◽  
Similar Degree ◽  
Estradiol 17Β ◽  
Ros Scavengers

Previous studies from our laboratory have shown that estrogens can protect against lipoprotein peroxidation and DNA damage. In this study, the mechanism of estradiol-17β (E2) action was investigated by comparing E2 with selective scavengers of reactive oxygen species (ROS) in terms of inhibition of 1) human low-density lipoprotein (LDL) peroxidation (measured by the diene conjugation method) and 2) DNA damage (measured by the formation of strand breaks in supercoiled OX-174 RFI DNA). In addition, the direct effect of E2 on the generation of individual ROS was also measured. By use of ROS scavengers, it was determined that lipoprotein peroxidation was predominantly due to superoxide (39%), with some contributions from hydrogen peroxide (23%) and peroxy (38%) radicals. E2 was a more effective inhibitor of peroxidation than all the ROS scavengers combined. In DNA damage, scavengers of hydrogen peroxide, hydroxyl, and superoxide radical offered significant protection (49–65%). E2 alone offered a similar degree of protection, and no additional effect was evident when it was combined with ROS scavengers. E2caused a significant reduction (37%) in the production of superoxide radical by bovine heart endothelial cells in culture but had no effect on the formation of either hydrogen peroxide or hydroxyl radicals. These studies show that 1) the protection offered by E2 in terms of lipid peroxidation could be due to its ability to inhibit generation of superoxide radical and prevent further chain propagation, and 2) in DNA damage protection, E2 mainly appears to inhibit chain propagation.

Melatonin Improves Lipid Profile and Ameliorates Lipid Peroxidation in Patients with Chronic Kidney Disease.

2018 ◽  
pp. 38-45
Keyword(s):  
Lipid Peroxidation ◽  
Placebo Group ◽  
Lipid Profile ◽  
Kidney Diseases ◽  
Oxidized Ldl ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Before And After ◽  
Inhibit Lipid Peroxidation ◽  
Controlled Clinical Study

Dyslipidemia and oxidative modifications of lipid are frequently associated in patients with chronic kidney diseases (CKD) and considered the most important risk factors for cardiovascular events. Melatonin is a well-known potent antioxidant and has beneficial effect on lipid metabolism. the study was designed to evaluate if Melatonin could improve lipid profile and ameliorates lipid peroxidation. This single blind placebo controlled clinical study carried out on 41 patients with CKD who were randomized into two groups, control groups (n=20) those who received placebo cap and melatonin group those who received 5mg melatonin (n=21). Lipid profile [total cholesterol (TC), triglyceride (TG), high-density lipoprotein (HDL-C), low-density lipoprotein (LDL-C)] and parameters of lipid peroxidation [oxidized LDL (oxLDL) and malondialdehyde (MDA) were measured before and after 12 weeks of the treatment. After 12 weeks of treatment, melatonin significantly increased HDL-C and decreased LDL-C compared to the initial value. The elevation in HDL-C and reduction in LDL-C were significantly different from that in placebo group. Also, both oxLDL and MDA levels significantly lowered by melatonin compared to the baseline and to the placebo group. Collectively, the results of our study showed that melatonin has advantageous effect on lipid profile and inhibit lipid peroxidation in patients with CKD.

Effect of Turmeric and Ginger on Lipid Profile in Male Rats Exposed to Oxidative Stress

2019 ◽  
Vol 10 (01) ◽  
Author(s):  
Eman A. Al-Rekabi ◽  
Dheyaa K. Alomer ◽  
Rana Talib Al-Muswie ◽  
Khalid G. Al-Fartosi
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Drinking Water ◽  
Lipid Profile ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Male Rats ◽  
Control Group ◽  
Very Low Density Lipoprotein ◽  
Low Density

The present study aimed to investigate the effect of turmeric and ginger on lipid profile of male rats exposed to oxidative stress induced by hydrogen peroxide H2O2 at a concentration of 1% given with consumed drinking water to male rats. Methods: 200 mg/kg from turmeric and ginger were used, and the animals were treatment for 30 days. Results: the results showed a significant increase in cholesterol, triglycerides, low density lipoprotein (LDL), very low density lipoprotein (VLDL), whereas it explained a significant decrease in high density lipoprotein (HDL) of male rats exposed to oxidative stress when compared with control group. the results showed a significant decrease in cholesterol, triglycerides, (LDL), (VLDL), whereas it explained a significant increase in (HDL) of rats treated with turmeric and ginger at dose 200 mg/kg when compared with male rats exposed to oxidative stress.

scholarly journals Electronic and Tobacco Cigarettes Alter Polyunsaturated Fatty Acids and Oxidative Biomarkers

2021 ◽  
Author(s):  
Rajat Gupta ◽  
Yan Lin ◽  
Karla Luna ◽  
Anjali Logue ◽  
Alexander J Yoon ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Cardiovascular Risk ◽  
Polyunsaturated Fatty Acids ◽  
Low Density Lipoprotein ◽  
Plasma Concentrations ◽  
Multivariable Analysis ◽  
Plasma Lipid ◽  
Density Lipoprotein ◽  
Heme Oxygenase 1

Rationale: Chronic electronic cigarette (EC) users exhibit a higher susceptibility of low-density lipoprotein (LDL) to undergo oxidation as compared to non-user controls. However, there is a paucity of data regarding EC effects on lipid peroxidation in the blood and their relationship to cardiovascular risk. Objective: To test the hypothesis that chronic (≥1 year) EC use exerts intermediate effects on plasma lipid peroxidation and/or antioxidant defense compared to chronic tobacco cigarette (TC) smoking. Methods and Results: We enrolled EC-users (n=32), TC-smokers (n=29) and non-users (n=45), with mean ages of 28.3, 27.8 and 27.4 years, respectively. Plasma concentrations of free polyunsaturated fatty acids and oxidized metabolites were assessed by mass spectrometry. Total antioxidant capacity (TAC), concentrations of glutathione, bilirubin, heme oxygenase-1 (HO-1), and functional activity of paraoxonase1 (PON1) were determined by colorimetric and enzymatic assays. Multivariable analysis was performed using classification models for segregating participants based on biomarker profiles. Plasma arachidonic acid (AA) concentration was higher in TC-smokers but lower in EC-users, together with linoleic acid (LA) concentration, as compared to TC-smokers and non-users (p<0.05). Oxidized LA metabolites (9- and 13-hydroxyoctadecadienoic acid (HODE)) were lower in EC-users and TC-smokers as compared to non-users (p<0.001). Consistently, TAC and bilirubin were elevated in EC-users and TC-smokers as compared to non-users (p<0.05). Of interest, plasma HO-1 concentration was higher in TC-smokers as compared to non-users (p=0.01) with intermediate levels in EC-users. Multivariable analysis identified 5 biomarkers (13-HODE, LA, 9-HODE, 12-hydroxyeicosatetraenoic acid (HETE), AA) that discriminated EC-users from TC-smokers and non-users with an accuracy of 73.4%. Conclusions: Chronic use of EC induces common (i.e. lower 9- and/or 13-HODEs and higher TAC and bilirubin) as well as differential effects (i.e. altered AA and LA concentrations) to those induced by TC, along with intermediate plasma HO-1 concentration, suggesting that EC, likewise TC smoke, could impact cardiovascular risk.

Disassociation of oxidant-induced ATP depletion and DNA damage from early cytotoxicity in LLC-PK1 cells

1997 ◽  
Vol 272 (6) ◽  
pp. F729-F735 ◽  
Author(s):  
S. P. Andreoli ◽  
C. P. Mallett
Keyword(s):  
Hydrogen Peroxide ◽  
Lipid Peroxidation ◽  
Dna Damage ◽  
Oxidant Stress ◽  
Atp Depletion ◽  
Antioxidant Compounds ◽  
Tubular Epithelial Cells ◽  
Renal Tubular Epithelial Cells ◽  
Stressed Cells ◽  
Renal Tubular

To determine the mechanism(s) of oxidant-mediated cell lysis in renal tubular epithelial cells, we determined ATP depletion, DNA damage, lipid peroxidation, and cytotoxicity in LLC-PK1 cells exposed to 500 microM hydrogen peroxide for 1 h with and without inhibitors of lipid peroxidation including a lazaroid compound, 2-methylaminochroman (2-MAC), and Trolox, a vitamin E analog. ATP levels were determined by luciferin-luciferase, DNA damage by the alkaline unwinding technique, lipid peroxidation by the generation of malondialdehyde, and early cytotoxicity (5 h) by the release of 51Cr, whereas late cytotoxicity (24 h) was determined by release of [3H]leucine from prelabeled cells. Cells exposed to 500 microM hydrogen peroxide demonstrated significant (P < 0.01) ATP depletion, DNA damage, and lipid peroxidation, followed by cell death at 5 h. Concentrations of 0.1–25 microM 2-MAC or 25–500 microM Trolox each markedly and significantly (P < 0.01) inhibited lipid peroxidation and early cytotoxicity but had little to no effect on ATP depletion or DNA damage. Thus oxidant-stressed cells remained intact for several hours despite significant ATP depletion and DNA damage when lipid peroxidation was inhibited with the antioxidant compounds. At 24 h, 2-MAG and Trolox had lost their protective effect, suggesting that mechanisms other than lipid peroxidation play a role in later cytotoxicity. We conclude that ATP depletion and DNA damage are not the primary mediators of early cytotoxicity following oxidant stress, whereas lipid peroxidation plays an central role in mediating early cytotoxicity following oxidant injury.

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