Enhancement of intracellular glutathione protects endothelial cells against oxidant damage

Tsan, Min‐Fu; Danis, Ellen H.; Vecchio, P. J. Del; Rosano, Carmen L.

doi:10.1016/s0006-291x(85)80154-6

Cited by 102 publications

(34 citation statements)

References 19 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Buthionine sulfoximine (BSO), an agent which depletes intracellular glutathione (mainly GSH) [22], was used to test the hypothesis that lowering glutathione concentration would cause endothelial dysfunction, specifically a loss of barrier function. The permeability response to BSO incubated with the cells for 48 h is shown in Figure 4.…”

Section: Resultsmentioning

confidence: 99%

Effect of advanced glycation end products on oxidative stress in endothelial cells in culture: a warning on the use of cells studied in serum-free media

et al. 2001

View full text Add to dashboard Cite

A common cardiovascular complication of diabetes is an increase in the vascular escape rate of albumin, generally interpreted as an increase in microvascular permeability [1±3]. One of the more recent theories to explain this endothelial dysfunction focuses on the accumulation in blood and tissues of the advanced glycation end products (AGEs) formed from protein modification by glucose [4]. The AGE hypothesis holds that chronic diabetes-accelerated chemical modification of proteins, lipids and other molecules by reducing sugars alters their structure and function, inducing cellular Diabetologia (2001) Abstract Aims/hypothesis. Alterations in vascular permeability and oxidative stress are characteristics of endothelial dysfunction in diabetic vascular disease. Since AGE-proteins have been hypothesized to mediate these effects, we studied the effects of AGE-bovine serum albumin on endothelial monolayer permeability and intracellular glutathione. Methods. AGE-BSA was prepared by incubating BSA for 30 days at 37 C with 0.5 mol/l glucose and 0.2 mol/l phosphate buffer, pH 7.4. Permeability to fluorescently labelled BSA was assessed in a bovine pulmonary artery endothelial cell monolayer preparation. Glutathione was measured by an enzymatic assay. Results. AGE-BSA concentrations greater than 3 to 4 mmol/l produced maximal increases in permeability (6±8 times basal) within 3 to 4 h of incubation with the cells. This effect persisted for at least 48 h. However, BSA incubated in the absence of glucose produced similar effects. Dialysis of the AGE-BSA showed that low molecular weight components contained the permeability-increasing activity. Phosphate buffer used to prepare the AGE-BSA, at concentrations equivalent to those present in phosphate-buffered saline and in the AGE preparation (~5 mmol/l), produced similar permeability increases at equivalent incubation times. Metal chelators (0.5 mmol/l) or inclusion of fetal bovine serum (10±20 %) blocked these permeability increases. These increases in permeability were associated with a decrease in endothelial glutathione, both inhibited by 10 mmol/l N-acetylcysteine, and a loss of cell-tocell and cell-to-matrix adhesion molecules. Conclusion/interpretation. Trace amounts of redoxactive metal ions in biological buffers could induce oxidative stress and alterations in cellular functions attributed to AGE-proteins in vitro. It is important to use metal-free phosphate and bicarbonate buffers in studies on cell biology in vitro, especially in serum-free media. [Diabetologia (2001

show abstract

Section: Resultsmentioning

confidence: 99%

Effect of advanced glycation end products on oxidative stress in endothelial cells in culture: a warning on the use of cells studied in serum-free media

et al. 2001

View full text Add to dashboard Cite

show abstract

“…It has been emphasized that such damage results from the oxidative stress caused by the oxygen metabolites released by PMN (1-6), particularly H202 (4)(5)(6). Even in vivo, endothelial cells may be exposed to oxidants, for example, at sites of inflammation, where PMN are recruited and activated, or when PMN are activated intravascularly, as in the adult respiratory distress syndrome (ARDS) (7,8).…”

Section: Introductionmentioning

confidence: 99%

Neutrophil-endothelial cell interaction. Evidence for and mechanisms of the self-protection of bovine microvascular endothelial cells from hydrogen peroxide-induced oxidative stress.

Dobrina¹,

Patriarca²

1986

J. Clin. Invest.

View full text Add to dashboard Cite

MethodsBovine microvascular endothelial cells (MEC) were able to degrade the H202 generated by phorbol myristate acetate-activated bovine neutrophils or by glucose oxidase with a maximal capacity of 4.0±1.2 (SD) nmol/10' cells/min, corresponding to the H202 released by about 3 X 10' neutrophils. H202 degradation occurred via the glutathione redox cycle and catalase. Degradation via the glutathione redox cycle was coupled with a marked stimulation of the hexose monophosphate shunt activity. The effect of H202 on ethidium bromide exclusion and on succinate oxidation was studied. Neither parameter was altered when MEC were exposed to H202 produced at rates within their degradative capacity. As soon as this was exceeded, impairment of both functions occurred. It is concluded that endothelial cells can protect themselves from H20rinduced i 'ury in a well-defined range of environmental H202 concentrations by actively degrading the peroxide.

show abstract

“…To determine whether oxidative stress was involved in HKainduced apoptosis, we assessed the effect of GSH on this process, 50 using a proliferation assay to determine relative numbers of viable endothelial cells remaining after exposure to HKa in the absence or presence of GSH. GSH (150 g/mL) inhibited HKa-induced endothelial-cell apoptosis on all ECM proteins (except collagen, on which no apoptosis occurred; Figure 3B).…”

Section: Hka-induced Ros Generation Is Necessary For Apoptosis and Ismentioning

confidence: 99%

“…To assess the effects of HKa on intracellular redox status, we measured the levels of GSH, an important intracellular antioxidant, 50,[54][55][56] in control and HKa-treated endothelial cells. Exposure of proliferating endothelial cells cultured on gelatin to HKa led to a rapid fall in intracellular GSH, which was not observed in untreated endothelial cells or in cells undergoing apoptosis after exposure to 2-methoxyestradiol ( Figure 5A).…”

Section: Hka Exposure Decreases Intracellular Gsh Content and Causes mentioning

confidence: 99%

Endothelial-cell apoptosis induced by cleaved high-molecular-weight kininogen (HKa) is matrix dependent and requires the generation of reactive oxygen species

Sun

McCrae

2006

Blood

View full text Add to dashboard Cite

Enhancement of intracellular glutathione protects endothelial cells against oxidant damage

Cited by 102 publications

References 19 publications

Effect of advanced glycation end products on oxidative stress in endothelial cells in culture: a warning on the use of cells studied in serum-free media

Effect of advanced glycation end products on oxidative stress in endothelial cells in culture: a warning on the use of cells studied in serum-free media

Neutrophil-endothelial cell interaction. Evidence for and mechanisms of the self-protection of bovine microvascular endothelial cells from hydrogen peroxide-induced oxidative stress.

Endothelial-cell apoptosis induced by cleaved high-molecular-weight kininogen (HKa) is matrix dependent and requires the generation of reactive oxygen species

Contact Info

Product

Resources

About