Myeloperoxidase (MPO), Possible Biomarker in Heart Failure

The justification for choosing and this enzyme marker to investigate the variation in serum concentration is supported by at least two arguments: cytokine myeloperoxidase at the level of the hypocritical myocardium, with or without contractile deficiency, can be secreted by any type of component or resident in the myocardium In cardiac failure, one of the forms that responds to the oxidative stress existing in the disease is MPO secretion that occurs early after some authors even during Class I contractile myocardial deficiency (NYHA classification).

Improvement of the chemical inhibition phenotyping assay by cross-reactivity correction

Background:The fraction of an absorbed drug metabolized by the different hepatic cytochrome P450 (CYP) enzymes, relative to total hepatic CYP metabolism (Methods:To overcome this drawback, the cross-reactivities exhibited by six chemical inhibitors (furafylline, montelukast, sulfaphenazole, ticlopidine, quinidine and ketoconazole) were quantified using specific CYP enzyme marker reactions. The determined cross-reactivities were used to correct theResults:UncorrectedConclusions:Correcting

α-glutathione s-transferase (α-GST) release, an early indicator of carbon tetrachloride hepatotoxicity in the rat

1 The use of the cytoplasmic enzyme, alpha glutathione s-transferase (α-GST) as an early index of carbon tetrachloride (CCl4) toxicity in the rat was investigated and compared with a standard enzyme marker, aspartate aminotransferase (AST). The hepatotoxic effects of CCl 4 in the rat were determined in a time and dose-response study. 2 Following CCl 4 exposure, α-GST release was shown to be an earlier and more sensitive biomarker of hepatotoxicity than AST. 3 Significant increases in α-GST were detected 2 h after CCl4 exposure. Using the enzyme marker AST, this early hepatotoxic injury went undetected. At 6 and 16 h, α-GST was also a more sensitive indicator of hepatotoxicity than AST. 4 α-GST release was significantly increased at a dose of 5 μl/kg, the lowest concentration of CCl4 administered and clearly responded in a dose-dependent manner with increasing doses of CCl4. In contrast, release of AST did not reach statistical significance until a dose of 25 μl/kg. 5 Thus, these findings indicate that α-GST is a more sensitive and more accurate reflector of CCl4 induced hepatotoxicity than AST.