Background:The fruits of Aronia melanocarpa (Michx.) Elliot is extremely rich in biologically active polyphenols.Objective:We studied the protective effect of A. melanocarpa fruit juice (AMFJ) in a model of amiodarone (AD)-induced pneumotoxicity in rats.Materials and Methods:AD was instilled intratracheally on days 0 and 2 (6.25 mg/kg). AMFJ (5 mL/kg and 10 mL/kg) was given orally from day 1 to days 2, 4, 9, and 10 to rats, which were sacrificed respectively on days 3, 5, 10, and 28 when biochemical, cytological, and immunological assays were performed.Results:AMFJ antagonized AD-induced increase of the lung weight coefficient. In bronchoalveolar lavage fluid, AD increased significantly the protein content, total cell count, polymorphonuclear cells, lymphocytes and the activity of lactate dehydrogenase, acid phosphatase and alkaline phosphatase on days 3 and 5. In AMFJ-treated rats these indices of direct toxic damage did not differ significantly from the control values. In lung tissue, AD induced oxidative stress measured by malondialdehyde content and fibrosis assessed by the hydroxyproline level. AMFJ prevented these effects of AD. In rat serum, AD caused a significant elevation of interleukin IL-6 on days 3 and 5, and a decrease of IL-10 on day 3. In AMFJ-treated rats, these indices of inflammation had values that did not differ significantly from the control ones.Conclusion:AMFJ could have a protective effect against AD-induced pulmonary toxicity as evidenced by the reduced signs of AD-induced direct toxic damage, oxidative stress, inflammation, and fibrosis.

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.

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Aim. To investigate the effects of MnTE-2-PyP on some markers of antioxidant defence system in asthma mice model. Material and Methods. The animals were divided into four groups: group 1, controls; group 2, injected with ovalbumin, group 3, treated with MnTE-2-PyP, and group 4, treated with ovalbumin and MnTE-2-PyP. The activities of superoxide dismutase, catalase, glutathione peroxidase and nonprotein sulfhydryl groups content (NPSH) were determined in lung homogenate. Results. The activities of superoxide dismutase and catalase in group 2 decreased significantly as compared to control group. The decrease of the same enzymes in group 4 was lower and significant as compared to group 2. Changes in the glutathione peroxidase activity showed a similar dynamics. The NPSH groups content decreased in group 2. In group 4 this decrease was relatively lower as compared to group 2. Conclusions. The application of MnTE-2-PyP mitigated the effects of oxidative stress in asthma mice model.