Abstract
Rationale: Biological pollution caused by cyanotoxins leads to respiratory function impairment.
Aim: Study pulmonary mechanics, lung and liver histology in mice submitted to sublethal doses of microcystin-LR (MCLR) and evaluate whether the results depended on the doses.
Methods: Male Swiss mice were divided into 2 groups: CTRL (n=6) received distilled water intraperitoneally (ip, 100 mL) and TOX (n=30): injected with sublethal doses of MCLR (5, 10, 15, 20 and 25 μg/kg ip in 100 mL of distilled water). 24 h later pulmonary mechanics [static elastance (Est), viscoelastic component of elastance (ΔE), resistive (ΔP1), viscoelastic (ΔP2), and total (ΔPtot) pressures] were determined, and lungs and livers were prepared for histopathology. ANOVA was used to test differences among the groups.
Results: ΔP2, ΔE and ΔPtot were significantly higher than CTRL in all MCLR doses, but did not differ among them. Only TOX25 showed significantly higher Est and ΔP1 than CTRL. Alveolar collapse was higher in TOX10 (18.95%), TOX15 (17.56%), TOX20 (19.11%) and TOX25 (21.63%) than in CTRL (11.57%). The lung inflammatory cell content (cells/μm2) gradually increased: TOX10=2.90×10-3, TOX15=4.96×10-3, TOX20=5.46×10-3 and TOX25= 5.03×10-3 in relation to CTRL=1.41×10-3. All TOX mice showed a complete loss of liver architecture with hyalinization, steatosis, dilated sinusoidal spaces and a high degree of binucleated hepatocytes. Necrosis began in TOX15, whereas only TOX 25 showed inflammation.
Conclusion: MCLR impaired pulmonary mechanics, lung and liver histology. These findings depended on the degree of exposure.
Supported by: FAPERJ, CNPq, MCT
- © 2011 ERS
