MDA In Lung Tissue Research Articles

Mitochondrial injury induced by nanosized titanium dioxide in A549 cells and rats

The nanosized titanium dioxide (nano-TiO2) is an important nanoscale compound applied in many different fields because of its superior performance. Here, an anatase nano-TiO2 showed cytotoxicity in a dosage-dependent manner, which was in accordance with changes of A549 cell ultrastructure, A549 cell viability and intracellular ATP level. The lungs of rats treated with single intratracheal instillation of nano-TiO2 were injured, which was demonstrated by changes of alveolar epithelial cell ultrastructure, lung tissue pathology and lung tissue MDA level. The results of this study indicated that nano-TiO2 should be related to the generation of intracellular reactive oxygen species (ROS), which injured mitochondria and prevented the synthesis of ATP. The cells were approaching to apoptosis eventually. In macroscopic view, the lungs inevitably suffered.

Tempol, a membrane-permeable radical scavenger, ameliorates lipopolysaccharide-induced acute lung injury in mice: A key role for superoxide anion

Acute lung injury or acute respiratory distress syndrome is a serious clinical problem with high mortality. Oxidative stress was found to play a major role in mediating lung injury and antioxidants have been shown to be effective in attenuating acute lung injury. In this study, we determine the effects of tempol, a membrane-permeable radical scavenger, in lipopolysaccharide (LPS)-induced acute lung injury and the underlying mechanism. Acute lung injury was induced by intraperitoneal injection of LPS (1 mg/kg) and mice were treated with tempol 30 min before injection of LPS. One hour later, bronchoalveolar lavage fluid was collected and subjected to estimation of total and differential cell counts as well as the proinflammatory cytokines; tumor necrosis factor-alpha(TNF-α), interleukin-1beta(IL-1β) and interferon-gamma (IFN-γ). Lung tissue damage was confirmed by histopathological changes and by immunohistochemical analysis of myeloperoxidase (MPO). Moreover, lipid peroxidation, reduced glutathione (GSH) and nitric oxide (NO) were investigated in the lung tissue. Pretreatment with tempol produced significant attenuation of LPS-induced lung injury as well as inhibition of LPS mediated increase in MPO immunostaining, MDA and NO levels in lung tissue. Elevated cytokines levels in both bronchoalveolar lavage fluid and lung tissue homogenates of acute lung injury mice were significantly decreased after administration of tempol. These findings confirmed significant protection by tempol against LPS-induced acute lung injury and that superoxide anion scavenging appears to be a potential target for new potential therapy in pulmonary disorders.

Therapeutic effects and mechanism of saikosaponin-d in mice with bleomycin-induced pulmonary fibrosis

To study the therapeutic effects and mechanism of saikosaponin-d (SSd) in mice with bleomycin (BLM)-induced pulmonary fibrosis. According to the random number table, 180 mice were randomly divided into 5 groups. Four groups were pulmonary fibrosis models. Fibrosis model mice were established by intratracheal injection of bleomycin (5 mgxkg(-1)). They were BLM, DXM, SSd and SSd + DXM groups (n = 40 each). At 1 hour post-modeling, DXM, SSd and SSd + DXM groups were injected ip with dexamethasone (DXM, 5 mgxkg(-1)xd(-1), 0.1 ml), SSd (1.8 mgxkg(-1)xd(-1), 0.18 ml), DXM + SSd (0.28 ml) respectively qd until Day 28. BLM group was similarly dosed with normal saline. In addition, a normal control group (NC group, n = 20) treated likewise. The mice were anesthetized and sacrificed at Days 3, 7, 14, 28 for harvests of serum and lung tissue samples. The conventional histopathological changes of lung tissue were observed. Except for NC group, modeling groups of mice were used to observe the natural survival rate. Such indices as superoxide dismutase (SOD) and malonaldehyde (MDA) were examined both in lung tissue and serum samples. And hydroxyproline (HYP) was tested only in lung tissue. SSd could markedly increase the survival rate (80.0% in SSd and SSd + DXM groups vs 50.0% in BLM group, P < 0.05) and reduce alveolitis and fibrosis in mice. In comparison with BLM group, the levels of HYP of three treatment groups (DXM, SSd and SSd + DXM) in lung tissue was significantly lower (P < 0.05) at Days 14 and 28. The levels of MDA both in serum and lung tissue were significantly lower at Days 3, 7 and 14 (P < 0.05). The serum level of SOD was significantly higher at Days 3, 7 and 14 while the level of SOD in lung tissue was significantly higher at Days 3 and 7 (P < 0.05, P < 0.01). SSd has marked therapeutic effects upon bleomycin-induced pulmonary fibrosis in mice. And the mechanism may be associated with its anti-lipid peroxidation effect.

An experiment study of lung ischemia-reperfusion injury of pulmonary surgery in rabbit model.

The blocking of pulmonary vessels, including the blocking of pulmonary artery and pulmonary circulation, is always applied in the surgical treatment of locally advanced no-small cell lung cancer. However, the blocking of pulmonary vessels will induce lung ischemia-reperfusion injury (LIRI). The aim of this study is to establish pulmonary vessels blocking model in rabbit and to investigate the LIRI in pulmonary surgery. 114 New Zealand rabbits were randomly divided into 3 groups: group I, control group; group II, block left pulmonary artery; group III, block left pulmonary artery and vein. After the time of opening chest (group I), 1 h ischemia and 1 h, 2 h, 4 h, 6 h, 24 h reperfusion, the changes of arterial oxygen partial pressure in left pulmonary vein (PaO2) and the content of MDA in left lung tissue were observed. Then the water content of left lung and pathological study was recorded. Homodynamic parameters were stable in all 3 groups. There were significant differences in PaO2, MDA and wet/dry ratio of the lung tissue between I and other two groups at the time of 1 h ischemia and 1 h, 2 h, 4 h, 6 h reperfusion (P <0.05 and P < 0.01), but there was no significant difference between group II and group III (P >0.05), and there was no significant difference among the three groups after 24 h reperfusion (P >0.05). Pathological study revealed that similar injury changes happened between group II and group III, and the obvious injury happened at the time of 4 h reperfusion. At the time of 6 h reperfusion pathological changes in both group II and group III began to recover, and completely recover after 24 h reperfusion. The lung ischemic-reperfusion injury caused by blocking pulmonary artery is similar to that caused by blocking pulmonary artery and veins. It is safe to previously block pulmonary vessels within 1 h during pulmonary surgery.

Effect of Endotoxin and a Burn Injury on Lung and Liver Lipid Peroxidation and Catalase Activity

Both endotoxin and a burn alone produce oxidant-induced tissue lipid peroxidation. The endotoxin response is due in large part to hydrogen peroxide. The combination of endotoxin after a burn results in an increased liver, but not lung, oxidant injury. Our purpose was to determine whether the burn oxidant injury inactivated endogenous liver tissue catalase, thereby amplifying a subsequent H2O2 insult. Twenty-six adult sheep were studied. Twelve sheep had a 15% TBS burn. Tissue catalase activity, measured in lung and liver 3 days postburn, was significantly decreased from a control of 3.58 +/- 1.8 and 193 +/- 63, respectively, to 1.72 +/- 0.63 and 148 +/- 33 k(sec-1)/0.5 gram tissue. The addition of endotoxin 3 days postburn resulted in an increase in liver malondialdehyde, MDA, a measure of lipid peroxidation, from a control of 110 +/- 80 to 450 +/- 54 nmol/gram tissue. This value was significantly greater than the 210 +/- 80 nmol/gram tissue seen after endotoxin alone. Lung tissue MDA with burn and endotoxin was 65 +/- 8 compared to 42 +/- 7 for control and 80 +/- 6 nmol/gram for endotoxin alone. We conclude that a decrease in liver catalase activity occurs after a burn. The decrease corresponds to an accentuated oxidant-induced lipid peroxidation after an added endotoxin insult where H2O2 is known to be an etiologic agent. The catalase activity also decreases in postburn lung, but accentuated lung damage was not seen, indicating a variable tissue response from the burn-induced decrease in antioxidant activity.(ABSTRACT TRUNCATED AT 250 WORDS)