scholarly journals K+-Linked Release of Oxidized Glutathione Induced by tert-Butyl Hydroperoxide in Perfused Rat Liver Is Independent of Lipid Peroxidation and Cell Death.

1994 ◽  
Vol 65 (3) ◽  
pp. 183-191 ◽  
Author(s):  
Masanobu Ozaki ◽  
Shouko Aoki ◽  
Yasusuke Masuda
Keyword(s):  
Lipid Peroxidation ◽  
Cell Death ◽  
Rat Liver ◽  
Perfused Rat Liver ◽  
Oxidized Glutathione ◽  
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 Effects of Epigallocatechin Gallate on Tert-Butyl Hydroperoxide-Induced Mitochondrial Dysfunction in Rat Liver Mitochondria and Hepatocytes

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Vojtech Mezera ◽  
Rene Endlicher ◽  
Otto Kucera ◽  
Ondrej Sobotka ◽  
Zdenek Drahota ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Rat Liver ◽  
Epigallocatechin Gallate ◽  
Rat Hepatocytes ◽  
Liver Mitochondria ◽  
Rat Liver Mitochondria ◽  
Retention Capacity ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Tert Butyl Hydroperoxide

Epigallocatechin gallate (EGCG) is a green tea antioxidant with adverse effects on rat liver mitochondria and hepatocytes at high doses. Here, we assessed whether low doses of EGCG would protect these systems from damage induced by tert-butyl hydroperoxide (tBHP). Rat liver mitochondria or permeabilized rat hepatocytes were pretreated with EGCG and then exposed to tBHP. Oxygen consumption, mitochondrial membrane potential (MMP), and mitochondrial retention capacity for calcium were measured. First, 50 μM EGCG or 0.25 mM tBHP alone increased State 4 Complex I-driven respiration, thus demonstrating uncoupling effects; tBHP also inhibited State 3 ADP-stimulated respiration. Then, the coexposure to 0.25 mM tBHP and 50 μM EGCG induced a trend of further decline in the respiratory control ratio beyond that observed upon tBHP exposure alone. EGCG had no effect on MMP and no effect, in concentrations up to 50 μM, on mitochondrial calcium retention capacity. tBHP led to a decline in both MMP and mitochondrial retention capacity for calcium; these effects were not changed by pretreatment with EGCG. In addition, EGCG dose-dependently enhanced hydrogen peroxide formation in a cell- and mitochondria-free medium.Conclusion. Moderate nontoxic doses of EGCG were not able to protect rat liver mitochondria and hepatocytes from tBHP-induced mitochondrial dysfunction.

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