Systemic complement activation, lung injury, and products of lipid peroxidation.

Ward, Peter A.; Till, Gerd O.; Hatherill, J. R.; Annesley, Thomas M.; Kunkel, Robin G.

doi:10.1172/jci112001

Cited by 213 publications

(79 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The plasma content of the lipid peroxidation products, as fluorescent lipids and conjugated dienes, was estimated according to Ward et al [25]. The concentration of free SH groups in the plasma was measured with DTNB at 412 nm [26].…”

Section: Other Biochemical Methodsmentioning

confidence: 99%

Blood glutathione redox status in gestational hypertension

Németh

Orvos

Boda

2001

Free Radical Biology and Medicine

View full text Add to dashboard Cite

Abstract-Gestational hypertension during the third trimester reflects an exaggerated maternal inflammatory response to pregnancy. We hypothesized that oxidative stress present even in normal pregnancy becomes uncompensated in hypertensive patients. A glucose-6-phosphate dehydrogenase (G6PD) activity sufficient to meet the increased reductive equivalent need of the cells is indispensable for defense against oxidative stress. The erythrocyte glutathione redox system was studied, where G6PD is the only NADPH source. The glutathione (GSH) redox status was measured both in vivo and after an in vitro oxidative challenge in pregnant women with gestational hypertension (n ϭ 19) vs. normotensive pregnant subjects (n ϭ 18) and controls (n ϭ 20). An erythrocyte GSH depletion with an increase in the oxidized form (GSSG) resulted in an elevated ratio GSSG/GSH (0.305 Ϯ 0.057; mean Ϯ SD) in hypertensive pregnant women vs. normotensive pregnant or control subjects (0.154 Ϯ 0.025; 0.168 Ϯ 0.073; p Ͻ .001). In hypertensive pregnant patients, a "GSH stability" decrease after an in vitro oxidative challenge suggested a reduced GSH recycling capacity resulting from an insufficient NADPH supply. The erythrocyte GSSG/GSH ratio may serve as an early and sensitive parameter of the oxidative imbalance and a relevant target for future clinical trials to control the effects of antioxidant treatment in women at increased risk of the pre-eclampsia syndrome.

show abstract

Section: Other Biochemical Methodsmentioning

confidence: 99%

Blood glutathione redox status in gestational hypertension

Németh

Orvos

Boda

2001

Free Radical Biology and Medicine

View full text Add to dashboard Cite

show abstract

“…Conjugated Dienes-The levels of conjugated dienes were analyzed by extraction of cells with heptane/isopropyl alcohol (2:1) and measured spectrophotometrically in heptane layer (27).…”

Section: Estimation Of Lipid Peroxidationmentioning

confidence: 99%

Modification in Oxidative Stress, Inflammation, and Lipoprotein Assembly in Response to Hepatocyte Nuclear Factor 4α Knockdown in Intestinal Epithelial Cells

Marcil

Seidman

Sinnett

et al. 2010

Journal of Biological Chemistry

View full text Add to dashboard Cite

show abstract

“…Lipids were extracted using 2:l chloroform:methanol; the samples were then dried under nitrogen, heptane was added, and absorbance read at 233 nm under UV light (after blanking with heptane) (25). All comparisons were performed between 02-exposed and air-exposed lungs from both age groups.…”

Section: Animalsmentioning

confidence: 99%

Failure of Premature Rabbits to Increase Antioxidant Enzymes During Hyperoxic Exposure: Increased Susceptibility to Pulmonary Oxygen Toxicity Compared with Term Rabbits

1991

View full text Add to dashboard Cite

ABSTRACI'. Although the prematurely born are known to have decreased baseline levels of protective antioxidant enzymes (Frank L, Sosenko IRS: J Pediatr 110:9 and 106, 1987), the ability to augment the baseline values during high O2 exposure is the key factor determining O2 tolerance versus O2 susceptibility. We have compared the pulmonary antioxidant enzyme responses of prematurely delivered rabbits (gestational d 29 of 32) and full-term rabbits to 48-72 h of hyperoxic exposure. We found that although full-term newborns exposed to >90% 0 2 consistently showed elevated superoxide dismutase, catalase, glutathione peroxidase, and glucose-6-phosphate dehydrogenase activities, the premature animals repeatedly failed to respond to hyperoxia with increased antioxidant enzyme activity levels. Consistent with the comparative antioxidant enzyme responses were the evidences of O2 toxicity in the two age groups. The prematurely born rabbits had significantly increased lung lavage protein content, lung conjugated diene levels, and more severe light microscopic lung pathology compared with the full-term animals during equal 0 2 exposure time. This first reported comparison of prematurely born versus full-term animal responses to hyperoxia might help to explain the clinical observation that the very prematurely born infant is excessively prone to the development of 02-induced lung injury and the progressive development of bronchopulmonary dysplasia. (Pediatr Res 29: 292-296,1991) Abbreviations SOD, superoxide dismutase CAT, catalase GP, glutathione peroxidase G-6-PD, glucose-6-phosphate dehydrogenase AOE, antioxidant enzyme BPD, bronchopulmonary dysplasia DSPC, disaturated phosphatidylcholine VLBW, very low birth weight VLBW premature infants have a distressingly high incidence of the chronic lung disease BPD. BPD is considered to be a multifactorial process, with hyperoxic ventilation being one of the clearly established causative factors ( 1-3).

show abstract

Systemic complement activation, lung injury, and products of lipid peroxidation.

Abstract: IntroductionPreviously we have demonstrated that systemic activation of the complement system after intravenous injection of cobra venom factor (CVF)

Cited by 213 publications

References 29 publications

Blood glutathione redox status in gestational hypertension

Blood glutathione redox status in gestational hypertension

Modification in Oxidative Stress, Inflammation, and Lipoprotein Assembly in Response to Hepatocyte Nuclear Factor 4α Knockdown in Intestinal Epithelial Cells

Failure of Premature Rabbits to Increase Antioxidant Enzymes During Hyperoxic Exposure: Increased Susceptibility to Pulmonary Oxygen Toxicity Compared with Term Rabbits

Contact Info

Product

Resources

About