Effects of Glutathione Depletion on Oxidant-Induced Endothelial Cell Injury

Gilmont, Robert R.; Dardano, Anthony N.; Young, Michael; Engle, Jennifer; Adamson, Belinda; Smith, David J.; Rees, Riley S.

doi:10.1006/jsre.1998.5328

Cited by 25 publications

(14 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Extensive cytoskeletal disruption and rearrangement was also shown to occur after endothelial cell exposure to H2O2 [37][38][39] . Endothelial shape changes have been observed to occur in experimental models of sepsis and several studies have reported these pathological changes upon endothelial cell exposure to H2O2 [30,[40][41][42][43] .…”

Section: Microcirculatory Dysfunctionmentioning

confidence: 99%

Metabolic theory of septic shock

Pravda¹

2014

WJCCM

View full text Add to dashboard Cite

Septic shock is a life threatening condition that can develop subsequent to infection. Mortality can reach as high as 80% with over 150000 deaths yearly in the United States alone. Septic shock causes progressive failure of vital homeostatic mechanisms culminating in immunosuppression, coagulopathy and microvascular dysfunction which can lead to refractory hypotension, organ failure and death. The hypermetabolic response that accompanies a systemic inflammatory reaction places high demands upon stored nutritional resources. A crucial element that can become depleted early during the progression to septic shock is glutathione. Glutathione is chiefly responsible for supplying reducing equivalents to neutralize hydrogen peroxide, a toxic oxidizing agent that is produced during normal metabolism. Without glutathione, hydrogen peroxide can rise to toxic levels in tissues and blood where it can cause severe oxidative injury to organs and to the microvasculature. Continued exposure can result in microvascular dysfunction, capillary leakage and septic shock. It is the aim of this paper to present evidence that elevated systemic levels of hydrogen peroxide are present in septic shock victims and that it significantly contributes to the development and progression of this frequently lethal condition.

show abstract

Section: Microcirculatory Dysfunctionmentioning

confidence: 99%

Metabolic theory of septic shock

Pravda¹

2014

WJCCM

View full text Add to dashboard Cite

show abstract

“…1989, 1995, Menger et al. 1997) and (ii) disruption of endothelial junctional integrity leading to the disruption of endothelial permeability barrier (Gilmont et al. 1998).…”

mentioning

confidence: 99%

Evidence for the role of cell stiffness in modulation of volume‐regulated anion channels

et al. 2006

View full text Add to dashboard Cite

show abstract

“…The GSH is an important component of the nonenzymatic antioxidant system that effectively protects cells against singlet oxygen ( 1 O 2 ), OH radical, and O 2 -radicals (47). Decreased levels of GSH could increase the injury associated with oxidative stress (48). It was reported that increasing the cellular GSH level could reduce IR injury (49).…”

Section: Discussionmentioning

confidence: 99%