Effects of membrane lipid peroxidation by tert butyl hydroperoxide on the sodium current in isolated feline ventricular myocytes

1994 ◽  
Vol 9 (5) ◽  
pp. 227-234 ◽  
Author(s):  
Takahiro Uchida ◽  
Masao Nishimura ◽  
Tomoaki Saeki ◽  
Yoshio Watanabe
Keyword(s):  
Lipid Peroxidation ◽  
Ventricular Myocytes ◽  
Sodium Current ◽  
Membrane Lipid ◽  
Membrane Lipid Peroxidation ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Tert Butyl Hydroperoxide

scholarly journals tert-Butyl Hydroperoxide (tBHP)-Induced Lipid Peroxidation and Embryonic Defects Resemble Glucose-6-Phosphate Dehydrogenase (G6PD) Deficiency in C. elegans

2020 ◽  
Vol 21 (22) ◽  
pp. 8688
Author(s):  
Hung-Chi Yang ◽  
Hsiang Yu ◽  
Tian-Hsiang Ma ◽  
Wen-Ye Tjong ◽  
Arnold Stern ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
G6pd Deficiency ◽  
Short Term ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
C Elegans ◽  
Tert Butyl Hydroperoxide ◽  
Calcium Independent Phospholipase A2 ◽  
Glucose 6 Phosphate Dehydrogenase

G6PD is required for embryonic development in animals, as severe G6PD deficiency is lethal to mice, zebrafish and nematode. Lipid peroxidation is linked to membrane-associated embryonic defects in Caenorhabditis elegans (C. elegans). However, the direct link between lipid peroxidation and embryonic lethality has not been established. The aim of this study was to delineate the role of lipid peroxidation in gspd-1-knockdown (ortholog of g6pd) C. elegans during reproduction. tert-butyl hydroperoxide (tBHP) was used as an exogenous inducer. Short-term tBHP administration reduced brood size and enhanced germ cell death in C. elegans. The altered phenotypes caused by tBHP resembled GSPD-1 deficiency in C. elegans. Mechanistically, tBHP-induced malondialdehyde (MDA) production and stimulated calcium-independent phospholipase A2 (iPLA) activity, leading to disturbed oogenesis and embryogenesis. The current study provides strong evidence to support the notion that enhanced lipid peroxidation in G6PD deficiency promotes death of germ cells and impairs embryogenesis in C. elegans.

scholarly journals Protective Effect of Natural and Synthetic Anthocyanins against Tert-butyl-hydroperoxide-induced Oxidative Damages in Normal and β-thalassemic Major Human Erythrocytes In Vitro

2020 ◽  
Vol 17 (1) ◽  
pp. 38-47
Author(s):  
Naïma Charif ◽  
Nassima Mokhtari-Soulimane ◽  
Sabri Cherrak ◽  
Hafida Merzouk ◽  
Mourad Elhabiri
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Thalassemia Major ◽  
Dpph Assay ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Oxidative Damages ◽  
Blood Disorder ◽  
Tert Butyl Hydroperoxide

Background: Even though β-thalassemia major is a genetic blood disorder, the damages endured by erythrocytes are mediated in part by oxidative stress. Antioxidants such as anthocyanins are capable to prevent the pro-oxidant effects induced by reactive oxygen species (ROS). Objective: This study aims to evaluate the in vitro preventive effects of one natural and two synthetic anthocyanins on normal and β-thalassemic erythrocytes on which toxicity has been induced by the free radical generator: tert-butyl-hydroperoxide TBHP. Methods: Erythrocytes isolated from fasting blood samples of healthy and β-thalassemic major individuals were treated either with TBHP alone or with TBHP after being pre-incubated with anthocyanins. Cell viability, reduced glutathione (GSH) and malondialdehyde (MDA) contents were measured after 90 minutes of incubation. In parallel, the antiradical scavenging capacities of the investigated anthocyanins were also estimated by using the 2,2-DiPhenyl-1-PicrylHydrazyl (DPPH•) assay. Results: The results clearly demonstrate that the treatment of erythrocytes with TBHP induces hemolysis along with marked redox state alteration (lipid peroxidation concomitant to GSH depletion) in both normal and β-thalassemia erythrocytes. During the pre-treatment with anthocyanins, erythrocytes become more resistant to oxidative impairments. Cyanin chloride and 6,7,3’,4’- tetrahydroxyflavylium chloride effectively prevent from TBHP-induced: hemolysis, lipid peroxidation and GSH depletion in normal and thalassemic erythrocytes, while 3’4’-dihdroxy-7-methoxyflavylium chloride had a lesser effect on MDA levels with thalassemic erythrocytes. These results are in agreement with those derived from the DPPH• assay. Conclusion: Our study contributes with important insights that tested anthocyanins may exert relevant potential in the alleviation of oxidative stress, especially the one affecting β-thalassemia erythrocytes.

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