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Cytosolic factors which affect microsomal lipid peroxidation in lung and liver.
Wright-JR; Colby-HD; Miles-PR
Arch Biochem Biophys 1981 Feb; 206(2):296-304
The effects of lung cytosol on pulmonary microsomal lipid peroxidation (LP) were investigated along with effects of liver cytosol on hepatic microsomal LP, the cytosolic concentrations of substances which may affect microsomal LP, and the relative contributions of these substances to the observed effects of cytosol on LP. Male Sprague-Dawley-rats were used for this study. Pulmonary and hepatic cytosol had significant, but different, effects on lung and liver microsomal LP, due primarily to ascorbate and glutathione. Both enzymatic and nonenzymatic lung microsomal LP were inhibited by lung cytosol whereas liver cytosol stimulated hepatic microsomal LP and enhanced iron stimulated LP but had no effect on NADPH induced liver microsomal LP. These effects may be significant in the intact cell. The two cytosols differed in composition but ascorbate was found in about equal concentrations in both and was primarily responsible for the effects on LP in both lung and liver microsomes. The small amount of inhibition in lung tissue not attributable to ascorbate probably was caused by the glutathione-peroxidase system or by protein in the cytosol. Additional testing showed lung cytosol stimulated LP in liver microsomes and liver cytosol inhibited both enzymatic and nonenzymatic LP in lung microsomes, further demonstrating that ascorbate had different effects in lung and liver. The authors suggest that ascorbate may be important in protecting pulmonary tissue against the harmful effects of LP.
NIOSH-Author; Laboratory-animals; Liver-microsomal-enzymes; Enzyme-activity; Lipids; Lung-tissue; Peroxidases
Issue of Publication
Archives of Biochemistry and Biophysics
Page last reviewed: May 5, 2020
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