Biochemical and metabolic response to nitrogen dioxide-induced endothelial injury

Journal Article · Thu Jan 01 04:00:00 EST 1987 · Research Report Health Effects Institue; (USA)

OSTI ID:5022239

Patel, J M; Block, E R ^[1]

---

1. Univ. of Florida, Gainesville (USA)

Nitrogen dioxide (NO2), a major oxidant constituent of vehicle emissions, is toxic to lung cells including endothelial cells. Since NO2 is a reactive free radical, one of the postulated mechanisms of NO2-induced pulmonary injury involves the peroxidation of membrane lipids. Therefore, this study evaluated the dose- and time-dependent effects of nitrogen dioxide exposure by measuring the biochemical and biophysical parameters, as well as the metabolic function, in porcine pulmonary artery and aortic endothelial cells in monolayer cultures. To evaluate the biochemical changes, the antioxidant enzyme GSH-reductase (GSH-red), GSH-peroxidase (GSH-per), and glucose-6-phosphate dehydrogenase (G6PDH) activities, as well as the lipid peroxide formation, glutathione (GSH) content, and lactate dehydrogenase (LDH) release were measured. Biophysical changes were measured by monitoring lipid fluidity in both the hydrophobic and hydrophilic regions of the plasma membrane. The uptake of 5-hydroxytryptamine (5-HT) was measured as a metabolic function of endothelial cells. Confluent porcine pulmonary artery and aortic endothelial cells were exposed to 3 or 5 ppm NO2 or air (control) for 3-24 hours. After 3-, 6-, or 12-hour exposures to 3 or 5 ppm NO2, the GSH-red and G6PDH activities, as well as the lipid peroxide formation and LDH release, were not different from those of controls in both pulmonary artery and aortic endothelial cells. Exposure of the cells to 3 or 5 ppm NO2 for 24 hours resulted in significant increases in GSH-red (p less than 0.05) and G6PDH activities in both cell types. Exposure to 5 ppm NO2 for 24 hours significantly (p less than 0.05) increased lipid peroxide formation and increased LDH release in both the pulmonary artery and aortic endothelial cells.

• OSTI ID: 5022239
• Journal Information: Research Report Health Effects Institue; (USA), Journal Name: Research Report Health Effects Institue; (USA) Vol. 9; ISSN RRHIE
• Country of Publication: United States
• Language: English

Related Subjects

560300* -- Chemicals Metabolism & Toxicology
63 RADIATION, THERMAL, AND OTHER ENVIRON. POLLUTANT EFFECTS ON LIVING ORGS. AND BIOL. MAT.
ANIMAL TISSUES
ANIMALS
AORTA
ARTERIES
AUTOMOBILES
BLOOD VESSELS
BODY
CARDIOVASCULAR SYSTEM
CELL CONSTITUENTS
CELL CULTURES
CELL MEMBRANES
CHALCOGENIDES
DOMESTIC ANIMALS
DOSE-RESPONSE RELATIONSHIPS
DRUGS
ENDOTHELIUM
ENZYME ACTIVITY
ENZYMES
EXHAUST GASES
FLUIDS
GASEOUS WASTES
GASES
GLUTATHIONE
LIPIDS
LUNGS
MAMMALS
MEMBRANES
METABOLISM
NITROGEN COMPOUNDS
NITROGEN DIOXIDE
NITROGEN OXIDES
ORGANIC COMPOUNDS
ORGANS
OXIDES
OXIDOREDUCTASES
OXYGEN COMPOUNDS
PATHOLOGICAL CHANGES
PEPTIDES
PEROXIDASES
POLYPEPTIDES
PROTEINS
RADIOPROTECTIVE SUBSTANCES
RESPIRATORY SYSTEM
SENSITIVITY
SWINE
TIME DEPENDENCE
TISSUES
TOXICITY
VEHICLES
VERTEBRATES
WASTES