Effects of Sulfur Dioxide Inhalation on Bronchoalveolar Lavage Fluid and Membrane Fluidity of Alveolar Macrophage in Rats


Article Preview

Sulfur dioxide (SO2) is a ubiquitous air pollutant which causes kinds of damage to human and other organisms. However, the effects and mechanisms on the plasma membrane when cells and tissues were exposed to SO2 were still unknown. The results herein showed a gradual reduction in body weight and dry lung weight for rats exposed to SO2. The wet lung weights were increased. The changes indicated SO2 inhalation caused pulmonary tissue permeability edema. Subscript textThe pulmonary permeability was increaseSubscript textSubscript textSubscript textd by the determination of protein contents in BALs and pulmonary permeability index (PPI). The intracellular proteins were penetrated into extracellular matrix. The total leukocytes in BALs of rats in each group exposed to SO2 were significantly increased, and the granulocytes were also increased significantly. However, the lymphocytes in BALs of rats exposed SO2 were to some extent different to the control groups. The activities of acid phosphatase (ACP), alkaline phosphatase (AKP) and lactic dehydrogenase (LDH) in BALs were increased to some extent. The results showed that the functions of plasma membrane were damaged with the damage of membrane structure, parts of the membrane bound enzymes and intracellular enzymes were released into BALs. The membrane fluidity in AM cells were significantly decreased by the determination of steady-state fluorescent polarization degree (P) and fluorescence microviscosity (η) of the AM.



Edited by:

Xiaochun Tang, Wei Zhong, Dachang Zhuang, Chunsheng Li and Yanyan Liu




Q. P. Du et al., "Effects of Sulfur Dioxide Inhalation on Bronchoalveolar Lavage Fluid and Membrane Fluidity of Alveolar Macrophage in Rats", Applied Mechanics and Materials, Vols. 295-298, pp. 594-598, 2013

Online since:

February 2013




[1] C. Thriel, M. Schäper, S. Kleinbeck, E. Kiesswetter, M. B. zkewicz, K. Golka, E. Nies, R.H. Monika, T. Brüning., Toxicology Letters, Volume 196(2010), P. 42.

DOI: https://doi.org/10.1016/j.toxlet.2010.03.031

[2] R.J. Li, Z.Q. Meng, J.F. Xie. Toxicology Letters, Volume 175, (2007), P. 71.

[3] O. H. Lowry, N. J. Rosenbrough, A. L. Far. J Biol Chem, Volume 193(1951), P. 265.

[4] L. Avallone, P. Lombardi, S. Florio, A. d'Angelo, E. Bogin. Eur J Clin Chem Clin Biochem. Volume 34(1996), P961.

[5] I. Koyama, T. Matsunaga, T. Harada, A. Kikuno, S. Hokari, T. Komoda. Clinical Biochemistry, Volume 37(2004), P. 688.

DOI: https://doi.org/10.1016/j.clinbiochem.2004.02.004

[6] A. Marczak. Bioelectrochemistry, Volume 74(2009), P. 236.

[7] U. Izagirre, P. Ruiz, I. Marigómez. . Biochemistry and Physiology Part C: Toxicology & Pharmacology, Volume 149( 2009) P. 587.

[8] M. Hasenberg, J. Behnsen, S. Krappmann, A. Brakhage, M. Gunzer. International Journal of Medical Microbiology, Volume 301( 2011), P. 436.

DOI: https://doi.org/10.1016/j.ijmm.2011.04.012

Fetching data from Crossref.
This may take some time to load.