PARENT SESSION
MA2 Chemical, Biological and Combined Methods for the Detection of Pollutants.
to ,
Session Chair: Diego Santiago Laguna

(011) Induced acute lung injury and inflammation in lungs of experimental model inhaling nickel sulfate: Differential gene expression and histopathology study.

Mallakin, Ali¹, McDowell, Susan², Toney-Early, Kenya¹, waltz, Susan¹, Leikauf, George², Degen, Sandra¹, ^{1 2}

ABSTRACT- The human gene that encodes for a protein with a structure similar to hepatocyte growth factor (HGF) has been isolated and characterized. This protein has been called HGF-like protein or HGFL. The cell surface receptor for HGFL has been found to be the Ron tyrosine kinase receptor; a member of the c-Met proto-oncogene family. The aims were to assess the acute lung injury by determining pulmonary histopathology, inflammation, gene expression and survival time with selected strains of mice exposed continuously to NiSO4 aerosol. In order to take advantage of the deficiency of Ron in the experimental mice, studies with control and knockout mice have been performed to ascertain the role of this tyrosine kinase in normal and challenged liver and lung functions. Overall, a gradual rise in mortality for both control and experimental mice was observed with increasing duration of exposure. Results revealed an increase in inflammatory response in experimental mice upon exposure to nickel sulfate, leading in generation of pulmonary edema as well as significant elevation of systemic nitric oxide. Histopathology results revealed that there is an aberrant histological response in organs of experimental mice. Edema, inflammation and perivascular swelling in lungs and focal tubular necrosis in kidneys of experimental animals after two days nickel exposure were significant. Less lung injury was observed in control mice as indicated by the reduce in the number of neutrophils and alveolar perivascular swelling. Gene expression and microarray studies are in progress which reveal the expression patterns of genes associated with acute lung injury in relationship to each other and relation to genes which have not been associated with acute lung injury. This assessment of gene expression will determine the importance of genetic factors contributing to lung injury.

Key words: Microarray, Nickel exposure, Toxicity, Acute lung injury