Pregnancy-associated plasma protein-A (PAPP-A) as a possible biomarker in patients with coronary artery disease.

BACKGROUND: Cardiovascular disease is the leading cause of death in the Western world, and a major cause of this disease is atherosclerosis. Research has demonstrated that pregnancy-associated plasma protein A (PAPP-A) plays a role in cardiovascular disease, as evidenced by the association between PAPP-A and severity of heart damage. AIM: The aim of this work was to investigate the correlation between PAPP-A concentrations in coronary and peripheral blood and certain clinicopathological factors and antioxidant enzyme activities in patients diagnosed with coronary artery disease. METHODS: For 65 patients, arterial blood was obtained by puncturing the femoral or radial artery, and coronary blood was obtained via percutaneous coronary intervention. PAPP-A, catalase (CAT), superoxide dismutase-1 (SOD-1), and superoxide dismutase-2 (SOD-2) levels were measured using spectrometric methods. RESULTS: Coronary PAPP-A levels were slightly higher than peripheral PAPP-A levels (81.25 ± 2.34 and 62 ± 3 ng/mL, respectively, P < 0.0001); these levels were correlated with each other (r = 0.6629, P < 0.001) but not with clinicopathological factors (P > 0.05). Coronary PAPP-A levels were significantly elevated among patients at risk for cardiovascular disease (P < 0.05). Antioxidant enzyme activities were significantly higher in coronary samples than in peripheral samples from subjects with ischemic cardiopathy secondary to atherosclerosis (P < 0.001). Neither coronary nor peripheral PAPP-A levels were correlated with antioxidant enzyme activities in patients with cardiopathy secondary to atherosclerosis (P > 0.05). CONCLUSIONS: PAPP-A levels could be used as biomarkers to identify patients at risk of coronary artery disease.

Modulation of the rat hepatic cytochrome P4501A subfamily using biotin supplementation.

Studies have found that biotin favors glucose and lipid metabolism, and medications containing biotin have been developed. Despite the use of biotin as a pharmacological agent, few studies have addressed toxicity aspects including the possible interaction with cytochrome P450 enzyme family. This study analyzed the effects of pharmacological doses of biotin on the expression and activity of the cytochrome P4501A subfamily involved in the metabolism of xenobiotics. Wistar rats were treated daily with biotin (2 mg/kg, i.p.), while the control groups were treated with saline. All of the rats were sacrificed by cervical dislocation after 1, 3, 5, or 7 days of treatment. CYP1A1 and CYP1A2 mRNAs were modified by biotin while enzyme activity and protein concentration were not affected. The lack of an effect of biotin on CYP1A activity was confirmed using other experimental strategies, including (i) cotreatment of the animals with biotin and a known CYP1A inducer; (ii) the addition of biotin to the reaction mixtures for the measurement of CYP1A1 and CYP1A2 activities; and (iii) the use of an S9 mixture that was prepared from control and biotin-treated rats to analyze the activation of benzo[a]pyrene (BaP) into mutagenic metabolites using the Ames test. The results suggest that biotin does not influence the CYP1A-mediated metabolism of xenobiotics.