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[A study on oxidative DNA damage and lipid peroxidation in patients with tuberculous pleurisy]
1Department of Respiratory Diseases, First Affiliated Hospital of Lanzhou Medical College, Lanzhou 730000, China.
Objective:
To explore the levels of mononuclear cell oxidative DNA damage and lipid peroxidation in patients with tuberculous pleurisy.
Methods:
The mononuclear cell DNA damages in pleural effusion and peripheral blood of 28 patients with tuberculous pleurisy and in peripheral blood of 25 healthy persons were detected by single cell gel electrophoresis (comet%). The levels of total antioxidative capacity (TAC) in supernatant of pleural effusion and blood plasma of 28 patients and in blood plasma of 25 healthy persons were measured by o-phenanthroline colorimetric analysis. The contents of malondialdehyde (MDA) of blood plasma from 28 patients and from 25 healthy persons were measured by thiobarbituric acid colorimetric analysis. The differences between groups were analyzed by t test.
Results:
The comet percentage of mononuclear cells in pleural effusion from patients with tuberculous pleurisy was (41.3 +/- 14.5)%, which was significantly higher than that in the peripheral blood (21.2 +/- 4.2)% (P < 0.01); The level of TAC in supernatant of pleural effusion was (5 172 +/- 1 195) U/L, which was lower than that in the blood plasma (8 656 +/- 1 592) U/L (P < 0.01). There was a negative correlation between the comet percentage of mononuclear cells and the level of TAC (r = -0.425, P < 0.05) in pleural effusion. The comet percentage of mononuclear cells in peripheral blood and the content of MDA in blood plasma from patients were (21.2 +/- 4.2)% and (8.25 +/- 1.37) micro mol/L, which were significantly higher than those from the controls (8.9 +/- 3.7)% and (4.46 +/- 0.93) micro mol/L respectively (P < 0.01); The level of TAC in blood plasma was (8 656 +/- 1 592) U/L, which was lower than that from the controls (10 610 +/- 1 399) U/L (P < 0.01). There were negative correlations between the level of TAC in blood plasma and the comet percentage of mononuclear cells in peripheral blood or the content of MDA in blood plasma (r = -0.438, -0.413, P < 0.05), and there was a positive correlation between the comet percentage of mononuclear cells in peripheral blood and the content of MDA in blood plasma (r = 0.899, P < 0.01).
Conclusion:
There is oxidation/antioxidation imbalance in patients with tuberculous pleurisy, namely oxidative stress, with inadequate total antioxidative capacity, particularly in the diseased pleural cavity.
Insights
Tuberculous pleurisy patients exhibit oxidative stress, with higher DNA damage and lipid peroxidation. Their total antioxidative capacity is inadequate, especially within the pleural cavity, indicating an imbalance.
Area of Science:
- Biochemistry
- Immunology
- Molecular Biology
Context:
- Tuberculous pleurisy is an inflammatory condition affecting the pleura.
- Oxidative stress plays a role in various inflammatory diseases.
- Understanding oxidative stress markers can aid in disease management.
Purpose:
- To investigate mononuclear cell oxidative DNA damage and lipid peroxidation in tuberculous pleurisy.
- To assess total antioxidative capacity (TAC) in patients with tuberculous pleurisy.
- To correlate oxidative stress markers with disease status.
Summary:
- Patients with tuberculous pleurisy showed significantly higher mononuclear cell DNA damage (comet percentage) in pleural effusion compared to peripheral blood.
- Elevated levels of malondialdehyde (MDA), a marker of lipid peroxidation, were observed in patients' peripheral blood.
- Total antioxidative capacity (TAC) was significantly lower in both pleural effusion and blood plasma of patients compared to healthy controls, with a particularly pronounced reduction in the pleural cavity.
Impact:
- The findings reveal an oxidation-antioxidation imbalance, indicative of oxidative stress, in tuberculous pleurisy.
- Inadequate total antioxidative capacity, especially in the pleural cavity, is a key feature of the disease.
- This study highlights the potential of oxidative stress markers for understanding the pathophysiology of tuberculous pleurisy.
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