Dithiothreitol tetraacetate S-acetyl esterase activity in different liver subcellular fractions and its potential role in the ester-mediated prevention of oxidative stress induced cell damage.
M. Montalto de Mecca, G.D. Castro, Castro Ja
Abstract
M. Montalto de Mecca, G.D. Castro, Castro Ja
Abstract
The liver was previously shown to be able to hydrolyze dithiothreitol tetraacetate (DTTAC) to dithiothreitol (DTT) via a DTTAC-S-acetyl esterase (DTTACEST). In the present studies the intracellular distribution of DTTACEST activity and its characteristics are reported. Enzyme specific activity was: microsomes > > mitochondria > > nuclei and was absent in the cytosolic fraction. The Km of the DTTACEST in each fraction was: mitochondria > microsomes > nuclei and the Vmax was microsomes > mitochondria > nuclei. The results were analyzed in relation to the previously established antioxidative stress and free radical trapping properties of DTTAC and DTT and the preventive effects exerted by DTTAC against carbon tetrachloride induced liver necrosis or cancer.
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The liver was previously shown to be able to hydrolyze dithiothreitol tetraacetate (DTTAC) to dithiothreitol (DTT) via a DTTAC-S-acetyl esterase (DTTACEST). In the present studies the intracellular distribution of DTTACEST activity and its characteristics are reported. Enzyme specific activity was: microsomes > > mitochondria > > nuclei and was absent in the cytosolic fraction. The Km of the DTTACEST in each fraction was: mitochondria > microsomes > nuclei and the Vmax was microsomes > mitochondria > nuclei. The results were analyzed in relation to the previously established antioxidative stress and free radical trapping properties of DTTAC and DTT and the preventive effects exerted by DTTAC against carbon tetrachloride induced liver necrosis or cancer.
Key concepts: Dithiothreitol, Microsome, Mitochondrion, Cytosol, Chemistry, Intracellular, Biochemistry, Oxidative stress