[The oxidative DNA damage of monocytes and its in vitro repair by melatonin in patients with tuberculous pleurisy].

Objective: To explore the level of mononuclear cell oxidative DNA damage and the total antioxidative capacity (TAC) in patients with tuberculous pleurisy. To evaluate the in vitro repair effects of melatonin on mononuclear cell DNA damage in pleural effusion of the patients.

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 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 mononuclear cells from pleural effusions of 20 patients were treated by melatonin in vitro.

Results: The comet percentage of mononuclear cells in pleural effusion from patients with tuberculous pleurisy was (41.3 +/- 14.5)%, which was higher than in peripheral blood (21.2 +/- 4.2)%, P < 0.01. The level of TAC in supernatant of pleural effusion was (5.17 +/- 1.19) U/ml, which was lower than in blood plasma (8.66 +/- 1.59) U/ml, 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 from patients was (21.2 +/- 4.2)%, which was higher than from controls (8.9 +/- 3.7)%, P < 0.01. The level of TAC in blood plasma was (8.66 +/- 1.59) U/ml, which was lower than from the controls (10.61 +/- 1.39) U/ml, P < 0.01. After treatment with melatonin, the comet percentage of mononuclear cells in pleural effusion decreased from (40.8 +/- 9.3)% to (11.0 +/- 3.7)%, P < 0.01.

Conclusion: There are oxidative DNA damage and oxidation/antioxidation imbalance in patients with tuberculous pleurisy, particularly in the diseased pleural cavity. Melatonin can facilitate, probably by its antioxidative effects, the in vitro repair of the damaged DNA of mononuclear cells from pleural effusion of patients with tuberculous pleurisy.