A Via L-arginina óxido nítrico em plaquetas e hemácias de pacientes com anorexia nervosa

Abstract

The anorexia nervosa (AN) is an eating disorder with high morbi-mortality, that reaches mainly adolescents of the feminine sex. AN is characterized by a distortion of the corporal image that leading to alimentary restriction, and, consequently, loss of weight and diverse clinical complications such as a state of platelet increased aggregation. The nitric oxide (NO) is produced from the cationic amino acid L-arginine through an enzyme family named NO-synthase (NOS) and functions as a cardiovascular protector modulating many functions as endothelial relaxation and platelet activity. The objective of this thesis is to assess the L-arginine-NO pathway in AN, as well as to investigate the cycle of the urea, the platelet function, and the oxidative stress in patients with AN. The L-arginine transport, the production of cyclic guanosine monophosphate (cGMP), the activity and the expression of isoforms of NOS, iNOS and eNOS, the oxidative stress (formation of thiobarbituric acid-reactive substances TBARS and superoxide dismutase activity SOD), as well as the platelet function were assessed in platelets from patients with AN. In erythrocytes, the activity and expression of the NOS, the activity of arginase and the oxidative stress were investigated. Plasma amino acid levels and markers of oxidative stress in serum were also assessed. Our results have demonstrated that in AN the L-arginine influx by y+L system, the production of cGMP and activity of NOS are diminished in platelets in relation to controls. Yet in platelets from patients with AN, the expression of NOS isoforms as well as the platelet activity don t show altered. In erythrocytes from these patients, was seen reduced activity of NOS and raised function of arginase. The expression of NOS isoforms in erythrocytes were not affected by AN. The plasmatic concentration of L-arginine was diminished in AN patients. The TBARS formation in platelets, erythrocytes and serum, were not altered in patients with AN, while that the SOD activity was altered. Therefore, although of the low production of NO, the patients with AN presents an NO-independent compensatory cardioprotector mechanisms to be investigated. The discoveries presented in this study contribute for a better understanding of the physiopathology of AN.