Pneumotoxic effects of radioactive dust (RD) from a nuclear power plant in Kozloduy, Bulgaria.

BACKGROUND: Airborne radioactive particles isolated from the reactor halls of nuclear power plants are a potential risk to the respiratory system of the working staff. Such radioactive dust (RD) from the Nuclear Power Plant, Kozloduy, Bulgaria was investigated. METHODS: The RD was administered intratracheally to 60 male Wistar rats as an aqueous suspension and the biological effects are estimated, using sensitive biological markers in bronchoalveolar lavage fluid (BALF) and important parameters of the pulmonary antioxidant defense. RESULTS: The results obtained show that RD increases the total cell number, the activities of the lactate dehydrogenase and alkaline phosphatase as well as the protein content in BALF. The activities of superoxide dismutase and catalase in lung homogenate are decreased while activity of the glutathione peroxidase and the content of non-protein sulfhydrils is elevated. CONCLUSIONS: It is concluded that the RD causes transitory toxic effect on lung tissue and changes the correlation between the elements of the pulmonary antioxidative defense.

Antioxidant defense mechanisms in the lung toxicity of tri-n-butyl phosphate.

Pneumotoxic effects of the tri-n-butyl phosphate (TBP) are investigated on rats using biological markers in bronchoalveolar lavage fluid (BALF) and studying key antioxidant enzymes in lung homogenate. Each animal from the experimental group received intratracheally 5 microliters TBP (20% v/v in n-dodecane). Six rats from the control and treated groups are sacrificed on post-treatment days 1, 3, 7, 14, and 28. The lactate dehydrogenase activity, the total protein content and the total cell number in BALF are increased mainly on day 1 after the treatment. The activities of superoxide dismutase and catalase are decreased to day 7 and those of glutathione peroxidase and glutathione reductase on day 1 only. The malondialdehyde content is elevated to day 14. It is concluded that TBP causes moderate toxic injury of the lung parenchyma. The depression of the key antioxidant enzymes and the elevated lipid peroxidation are probably important mechanisms of the lung damage.

[The effect of the intratracheal administration of americium-241 on rat alveolar macrophages]. / Vliianie intratrakheal'nogo vvedeniia ameritsiia-241 na al'veoliarnye makrofagi krys.

In experiments in rats it was found that 241Am transitory decreases the total cell number and alveolar macrophage's percentage in bronchoalveolar lavage fluid (BALF): increases the macrophages size and nuclear size; and increases acid phosphatase and lactate dehydrogenase activities in BALF. It was suggested that 241Am causes and activation in the alveolar macrophages which probably appears as one of factors provoking lung injuries.

Enhancement of the pneumotoxic effect of cadmium acetate by ionizing radiation in the rat.

Experiments involving 120 male Wistar rats were performed to study the effect of treatment with cadmium acetate and external irradiation. A single 0.5 mg/kg body weight dose of cadmium acetate was administered intratracheally. Shortly thereafter, the animals received a single whole-body exposure to 4 Gy gamma rays (cesium source). Findings indicated the chemical elevated enzyme activities of lactate dehydrogenase (LDH), alkaline phosphatase (AlP), and acid phosphatase (AP), as well as protein content and percentage of neutrophils in bronchoalveolar lavage fluid (BALF); the percentage of alveolar macrophages was sharply reduced. Radiation alone produced no substantial changes in the parameters investigated. Treatment with both agents combined was found to result in a synergistic rise of LDH, AlP, and AP activities and protein content in BALF. It was concluded that the BALF biochemical markers used are reliable indicators for identifying the type of combined effect produced in the lungs by chemical agents and ionizing radiation.

Changes in antioxidant lung protection after single intra-tracheal cadmium acetate instillation in rats.

One-hundred male white rats were given a single intratracheal dose of 0, 5 mg kg-1 cadmium acetate. There was a fall in catalase (CAT) and superoxide dismutase (SOD) in lung homogenate throughout the 30 d after treatment. Non-protein sulphhydryl (NPSH) content, glucose-6-phosphate dehydrogenase (G-6-PD) and glutathione peroxidase (GP) were all increased from days 5 to 15. There was an increase in lactate dehydrogenase (LDH) and protein in bronchoalveolar lavage fluid (BALF) and in the relative weight of the lungs which provide evidence of severe toxic lesions of the lungs. Increased lipid peroxidation provoked by the reduced lung antioxidant protective capacity may be an important mechanism in the pulmonary damage caused by cadmium.