Biomarkers of oxidative stress and smoking in cancer patients Burlakova, Elena B; Zhizhina, Galina P; Gurevich, Svetlana M ...
Journal of Cancer Research and Therapeutics/Journal of cancer research and therapeutics,
01/2010, Letnik:
6, Številka:
1
Journal Article
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Context: Increased oxidative stress is a significant part of
pathogenesis of smoking-related cancer. Aim: The study aims to
investigate changes in antioxidant status induced by chronic cigarette
...smoking in cancer patients and healthy subjects. Setting and Design:
We examined the venous blood samples of 54 healthy subjects, both
smokers (25) and non-smokers and of 50 patients with smoking-related
cancer, both smokers (34) and non-smokers. Materials and Methods: We
measured the activities of five antioxidant (AO) enzymes: glutathione
peroxidase, glutathione transferase (GST), glutathione reductase,
superoxide dismutase and catalase in the blood of 50 cancer patients
and 54 healthy persons. Damage to cellular structures (level of malonic
dialdehyde, micro viscosity of erythrocyte membranes, number of
leukocyte DNA breaks) was determined. Statistical analysis of results
obtained was performed using conventional and multi-factorial
statistical methods. Results: Statistically significant increase in
GST activity and DNA breaks, but decrease of membranes micro viscosity
in cancer patients, compared with healthy subjects were obtained. In
the cancer patients, no influence of smoking on studied parameters was
found. Correlations of parameters within cancer patients and healthy
subjects group did not coincide with each other. Conclusions: Changes
of AO status parameters and oxidative damages in cell structures are
related to tumor processes indicating the augmentation of oxidative
stress in human blood. This study demonstrated potential applicability
of a statistical model based on the evaluated biomarkers of oxidative
stress to determine a smoking-induced harm of cancer incidence in
healthy subjects.
The main factor of Alzheimer disease (AD) is beta-amyloid peptide (Abeta). It is known to affect acetylcholinesterase (AChE) through lipid peroxidation (LPO) initiated with H2O2 which is formed as a ...result of Abeta activity. The direct action of H2O2 on the enzyme is also possible. For membrane bound AChE of erythrocytes we observed inhibition under H2O2 action which was replaced by activation at small H2O2 concentrations. At higher substrate concentrations the inversion of the effect came at smaller concentrations of H2O2. For soluble erythrocytic AChE inhibition took place (caused by Km increase). Soluble enzyme from Electric Eel revealed inhibition, which was not replaced by activation at any concentration of peroxide. Low H2O2 concentrations caused intensification of lipid peroxidation in microsomes. The magnitude of the changes in LPO rate was within the range of the changes, where LPO system fulfills the control function for cell metabolism. With the help of ESR technique of spin probes it was found the rigidization under H2O2 action of close to surface area of lipid bilayer in erythrocytic and brain cell membranes. Summing up we can say that H2O2 modifies membrane structure and activity of AChE. Whether or not it will contribute to AD pathogenesis or is the manifestation of compensatory processes-the possible subject of discussion and further investigation.
The main factor of Alzheimer disease (AD) is β-amyloid peptide (Aβ). It is known to affect acetylcholinesterase (AChE) through lipid peroxidation (LPO) initiated with H
2O
2 which is formed as a ...result of Aβ activity. The direct action of H
2O
2 on the enzyme is also possible.
For membrane bound AChE of erythrocytes we observed inhibition under H
2O
2 action which was replaced by activation at small H
2O
2 concentrations. At higher substrate concentrations the inversion of the effect came at smaller concentrations of H
2O
2. For soluble erythrocytic AChE inhibition took place (caused by
K
m increase). Soluble enzyme from Electric Eel revealed inhibition, which was not replaced by activation at any concentration of peroxide.
Low H
2O
2 concentrations caused intensification of lipid peroxidation in microsomes. The magnitude of the changes in LPO rate was within the range of the changes, where LPO system fulfills the control function for cell metabolism.
With the help of ESR technique of spin probes it was found the rigidization under H
2O
2 action of close to surface area of lipid bilayer in erythrocytic and brain cell membranes.
Summing up we can say that H
2O
2 modifies membrane structure and activity of AChE. Whether or not it will contribute to AD pathogenesis or is the manifestation of compensatory processes—the possible subject of discussion and further investigation.
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