Hemopexin Decreases Spontaneous Chemiluminescence of Cold Preserved Liver after Reperfusion

1998 ◽  
Vol 248 (3) ◽  
pp. 574-577 ◽  
Author(s):  
Clifford A. Brass ◽  
Stephan Immenschuh ◽  
De-Xiu Song ◽  
Heng H. Liem ◽  
Ursula Muller Eberhard
1998 ◽  
Vol 25 ◽  
pp. S66
Author(s):  
Homero Rubbo ◽  
Carlos Batthyány ◽  
Daniel Anselmi ◽  
Bruce A. Freeman ◽  
Rafael Radi

Author(s):  
O. V. Smirnova ◽  
A. A. Sinyakov ◽  
V. V. Tsukanov

Aim. A study of monocyte chemiluminescent activity at variant stages of gastric cancer.Materials and methods. The study enrolled 90 gastric cancer patients and 70 healthy donors. Spontaneous and induced chemiluminescence in monocytes was assessed for 90 min with a “BLM 3607” 36-channel chemiluminescence analyser (Russia). Opsonized zymosan-induced chemiluminescence enhancement was measured as a ratio of the areas under the induced vs. spontaneous chemiluminescence curves, the activation index. Statistical significance was estimated with the Mann—Whitney criterion (p < 0.05).Results. The maximal spontaneous monocyte chemiluminescence intensity significantly decreased in stage IV gastric cancer patients compared to the control cohort (p = 0.035). Time to maximum in spontaneous chemiluminescence increased in all gastric cancer patients vs. control (p = 0.001), and in stage IV gastric cancer vs. stage I patients (p = 0.043). The areas under a curve in spontaneous and induced monocyte chemiluminescence increased in all gastric cancer patients vs. control (p = 0.001), and in stage IV gastric cancer vs. stage I patients (p = 0.037). The activation index was higher in all gastric cancer cases compared to control (p = 0.001).Conclusion. All patients with gastric adenocarcinoma, irrespective of the stage, revealed changes in the monocyte chemiluminescence activity, i.e. a longer time to maximum in spontaneous chemiluminescence and larger area under the curve of spontaneous and induced chemiluminescence, the activation index. Maximal monocyte spontaneous chemiluminescence intensity diminished in stage IV gastric cancer compared to the control cohort. Immune activity reflected in monocyte chemiluminescence correlates with the stage of gastric adenocarcinoma.


Author(s):  
L. P. Kovalenko ◽  
R. V. Zhurikov ◽  
K. V. Korzhova ◽  
A. D. Durnev

The research of immunotoxicity of extended-release form of Afobazol was conducted on male CBA, C57BL/6 and F1 hybrids (CBA×C57BL/6) mice. Afobazol was administered per os for 14 days in doses of 12 mg/kg and 120 mg/kg. Control group received a placebo. Weight of thymus, spleen and popliteal lymph nodes was not affected by the extended-release form of Afobazol in doses of 12 mg/kg and 120 mg/kg in F1 hybrids (CBA×C57BL/6) mice compared to the control group (p> 0.05). Cellularity of thymus was significantly increased by the extended-release form of Afobazol in dose of 12 mg/kg (p< 0.01 vs control group). Administration of the extended-release form of Afobazol in doses of 12 mg/kg and 120 mg/kg decreased spontaneous chemiluminescence activity of peripheral blood lymphocytes in 2.0 and 2.2 times, in dose of 120 mg/kg level integral chemiluminescence response S was decreased in 2.4 times (p< 0.05 vs control group). Phagocytic activity of peritoneal macrophages and antibody production in F1 hybrids (CBA×C57BL/6) mice were not affected by administration of the extended-release form of Afobazol in doses of 12 mg/kg and 120 mg/kg (p > 0.05 vs control group). 14 days of the extended-release form of Afobazol in doses of 12 mg/kg and 120 mg/kg did not cause any significant change to intensity of delayed-type hypersensitivity reactions (p> 0.05 vs control group). The results of the study allow us to conclude that administration of the extended-release form Afobazol in the range of studied doses does not induce immunotoxicity.


1997 ◽  
Vol 272 (2) ◽  
pp. L262-L267 ◽  
Author(s):  
M. L. Barnard ◽  
B. Robertson ◽  
B. P. Watts ◽  
J. F. Turrens

Inhibition of nitric oxide (.NO) synthase by nitro-L-arginine (NLA) decreased baseline chemiluminescence in a dose-dependent fashion up to 78% at 300 microM NLA. This inhibition was prevented by pretreatment with 1 mM arginine. Similarly, addition of superoxide dismutase (SOD; 200 U/ml) to the perfusion buffer inhibited spontaneous light emission by 57%. Addition of NLA after SOD or vice versa did not inhibit light emission any further, suggesting that both .NO and O2.- were precursors of the same oxidant. Production of additional extracellular O2.- by neutrophils activated with phorbol 12-myristate 13-acetate increased light emission by >200%, but this increase was insensitive to NLA. Increasing the intracellular steady-state O2.- concentration by perfusion of control lungs with the Cu and Zn-containing SOD inhibitor diethyldithiocarbamate (1 mM) stimulated light emission up to fourfold, but this spontaneous chemiluminescence was also insensitive to NLA. In experiments using cultured endothelial cells supplemented with extracellular bovine serum albumin (BSA), 5 microM of the Ca2+ ionophore A-23187 (a stimulant of .NO synthase) stimulated chemiluminescence by 40%. This increase was again SOD and NLA sensitive. Addition of NLA after SOD or vice versa did not change light emission. These results suggest that the background chemiluminescence of isolated-perfused intact lungs may result from the constant release of small amounts of O2.- and .NO by endothelial cells into the capillary lumen, which in turn react with BSA in the perfusion buffer.


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