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Lung cell apoptosis

Two studies have implicated a role of ASMase in pathological conditions that involve lung cell apoptosis (i) S. Uhlig and collaborators (Goggel et al.,... [Pg.504]

Schwarze PE, Johnsen NM, Samuelsen JT, Thrane EV, Lund K, Lag M, Ref-snes M, Kongerud J, Becher R, Boe J, Holme JA, Wiger R (1996) The use of isolated lung cells in in vitro pulmonary toxicology Studies of DNA damage, apoptosis and alteration of gene expression. Cent Eur J Public Health 4 Suppl 6-10. [Pg.255]

A study using a rat model of sepsis induced by cecal ligation and perforation (CLP) showed that PMXB hemoperfusion performed 24 hours after the CLP procedure reduced plasminogen activator inhibitor -1 expression in the lung, and apoptosis in renal tubular cells (Ito et al., 2009). [Pg.331]

Lau, A. T.,He, Q. Y., Chiu,J. F. (2004). A proteome analysis of the arse-nite response in cultured lung cells Evidence for in vitro oxidative stress-induced apoptosis. The Biochemical Journal, 382, 641-650. [Pg.564]

For example, emodin, Fig. (4) is an active component from the root and rhizome of Rheum palmatum L. that has been reported to exhibit antitumor effects, but the mechanism is not known. Several studies demonstrated that emodin induces cell apoptosis in human lung squamous carcinoma cell line... [Pg.307]

Shen, H.M., Zhang, Z., Zhang, Q.F., and Ong, C.N., Reactive oxygen species and caspase activation mediate silica-induced apoptosis in alveolar macrophages. Am. J. Physiol. Lung Cell. Mol. Physiol, 280, LI0-17, 2001. [Pg.70]

Hetland RB, Cassee FR, Refsnes M et al (2004) Release of inflammatory cytokines, cell toxicity and apoptosis in epithelial lung cells after exposure to ambient air particles of different size fractions. Toxicol In Vitro 18 203-212... [Pg.447]

Cho NH, Choi YP, Moon DS, Kim H, Kang S, Ding O, et al. Induction of cell apoptosis in non-small cell lung cancer cells by cyclin Al small interfering RNA. Cancer Sci 2006 97 1082-1092. [Pg.439]

Kerby GS, Cottin V, Accurso FJ, Hoffmann F, Chan ED, Fadok V, Riches DWH. Hyperosmolarity down-regulates p42 and Akt activation and augments apoptosis in macrophages. Implications for early pulmonary inflammation in cystic fibrosis. Am J Physiol Lung Cell Mol Physiol 2001 283 L188. [Pg.144]

Oleic acid—attempt to reproduce lung injury from lipid embolism Endothelial cell necrosis Endotoxin (EPS)—endothelial cell apoptosis... [Pg.284]

Isolated rat type II lung cells were more sensitive than Clara cells to cadmium-induced apoptosis and cell viability (LIg et al. 2002). On exposure to 10 jUmol/1 cadmium acetate, the levels of the apoptosis-modulating proteins p53 and Bax were increased at 2 h and 5-12 h, respectively. The expression of p53 preceded the expression of Bax and the apoptotic process. The exposure to 10/ nol/l cadmium acetate did not significantly increase the formation of cellular reactive oxygen species. However, after the exposure to a high concentration of cadmium acetate (100/anol/1), a 30% increase of the reactive oxygen species level was observed. Catalase, superoxide dismutase, dimethyl sulphoxide, or tetramethylthiourea did not protect against cadmium-induced apoptosis. [Pg.223]

To determine whether 4-hydroxynonenal could account for the acute effects of ozone on human alveolar macrophages, Hamilton jr. et al. (1998) exposed healthy, non-smoking volunteers to 0.4 ppm ozone or air for 1 h with exercise (each subject served as his/her own control). Six hours after ozone exposure, cells obtained by airway lavage were examined for apoptotic cell injury, presence of 4-hydroxynonenal adducts, and expression of stress proteins. Significant apoptosis was evident in airway lung cells after ozone exposure. Western analysis demonstrated an increase in a 32-kDa 4-hydroxynonenal protein adduct and a number of stress proteins, viz., 72-kDa heat shock protein and ferritin, in alveolar macrophages after ozone exposure. All these effects could be replicated by in vitro exposure of alveolar macrophages to 4-hydroxy-nonenal. [Pg.331]

DATS on cultured human neoplastic lung cells (A549), and they also found that the growth inhibition is also related to the increase in the intracellular Ca " and the apoptosis. [Pg.436]

Aoshiba K, Tamaoki J, Nagai A. Acute cigarette smoke exposure induces apoptosis of alveolar macrophages. Am J Physiol Lung Cell Mol Physiol 2001 281(6) L1392-L1401. [Pg.284]


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