scholarly journals Allylic Oxidations Catalyzed by Dirhodium Caprolactamate via Aqueoustert-Butyl Hydroperoxide: The Role of thetert-Butylperoxy Radical

2009 ◽  
Vol 74 (2) ◽  
pp. 730-738 ◽  
Author(s):  
Emily C. McLaughlin ◽  
Hojae Choi ◽  
Kan Wang ◽  
Grace Chiou ◽  
Michael P. Doyle
Keyword(s):  
Butyl Hydroperoxide ◽  
Dirhodium Caprolactamate

The Fe(III)-catalyzed functionalization of saturated hydrocarbons by tert-butyl hydroperoxide: Mechanistic studies on the role of dioxygen

1992 ◽  
Vol 33 (38) ◽  
pp. 5473-5476 ◽  
Author(s):  
Derek H.R. Barton ◽  
Stéphane D. Bévière ◽  
Warinthorn Chavasiri ◽  
Darío Doller ◽  
Bin Hu
Keyword(s):  
Mechanistic Studies ◽  
Saturated Hydrocarbons ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Tert Butyl Hydroperoxide

Glutathione protects against exogenous oxidant injury to rabbit renal proximal tubules

1988 ◽  
Vol 255 (5) ◽  
pp. F874-F884
Author(s):  
J. M. Messana ◽  
D. A. Cieslinski ◽  
R. P. O'Connor ◽  
H. D. Humes
Keyword(s):  
Oxidant Stress ◽  
Glutathione Depletion ◽  
Plasma Membrane Permeability ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Cation Homeostasis ◽  
Tert Butyl Hydroperoxide ◽  
Organ Systems ◽  
Nonprotein Thiols

Glutathione, comprising a major portion of cellular nonprotein thiols, plays a central role in a diverse group of cell metabolic functions. Glutathione and related enzyme systems have been shown to protect against both toxin and oxidant-induced injury in several organ systems. The role of glutathione in protecting renal epithelia against oxidant stress has not been investigated previously. We report here the response of enriched, isolated rabbit renal proximal tubule segments to oxidant stress induced by tert-butyl hydroperoxide. In addition, the effects of glutathione depletion by various biochemical means and of exogenous glutathione supplementation on the response of tubule segments to tert-butyl hydroperoxide exposure are described. Depletion of cell glutathione by several distinct methods potentiates oxidant-induced injury. Augmentation of cellular glutathione affords significant protection against exogenous oxidant stress. The protective effect of glutathione may reside in its ability, in conjunction with glutathione peroxidase, to arrest the propagation of lipid peroxidation and, therefore, to minimize alterations in plasma membrane permeability. The results of this study do not exclude the possibility that glutathione prevents tert-butyl hydroperoxide induced oxidation of critical sulfhydryl groups of catalytic or structural proteins associated with control of cell cation homeostasis. These results confirm the important role of glutathione in protecting renal tubular epithelia against oxidant stress.

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.

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