Abstract
Cyanotoxins present in the water for human use may yield serious health problems. We aimed to evaluate the effects of microcystin-LR (MC-LR) on lung mechanics, lung and liver histology and inflammation, and oxidative stress. Male Swiss mice (n=149) were randomly divided in 2 groups: control (CT) received sterile saline intratraqueally (i.t., 50 μL), and MC a sublethal dose of MC-LR (40 μg/kg, i.t.). CT (n=13), and MC mice were evaluated at 2 (n=16), 8 (n=13), 24 (n=24), 48 (n=15) e 96 h (n=17) after receiving MC-LR. In the remaining animals (CT=10 and MC=41) oxidative stress and damage were analyzed. Alveolar collapse increased in MC groups at 2, 8, 24 and 48 h compared to CT, accompanied by deterioration of lung mechanics on the same experimental time points, except for 24 h, when mechanics returned to baseline. The amount of polymorphonuclear cells and mieloperoxidase activity in lung augmented in all MC groups until 96 h, indicating a neutrophilic inflammatory cell infiltrate. Hepatic histology showed necrosis and hepatocyte disarrangement beginning at 8 h. Free MC-LR was detected in lung and liver homogenates, with a time-dependent toxin accumulation in liver. Antioxidative enzymes activities and thiobarbituric acid reactive substances were altered in MC-LR exposed animals. i.t. administration of MC-LR led to a biphasic compromise of pulmonary mechanics: an early deterioration (2 h and 8 h), normalization at 24 h, and a later worsening (48 h). Also, alveolar collapse, lung and liver inflammation, imbalance of antioxidants enzymes, and oxidative damage were identified. This work reinforces the airways as an important route of intoxication by MC-LR.
Supported by: PRONEX/FAPERJ, FAPERJ, CNPq, MCT
- © 2011 ERS
