Marçal L E, Rehder J, Newburger P E, Condino-Neto A
Departamento de Pediatria e Centro de Investigação em Pediatria, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, Campinas, SP, Brasil.
Braz J Med Biol Res. 2004 Nov;37(11):1607-13. doi: 10.1590/s0100-879x2004001100003. Epub 2004 Oct 26.
Asthma is an inflammatory condition characterized by the involvement of several mediators, including reactive oxygen species. The aim of the present study was to investigate the superoxide release and cellular glutathione peroxidase (cGPx) activity in peripheral blood granulocytes and monocytes from children and adolescents with atopic asthma. Forty-four patients were selected and classified as having intermittent or persistent asthma (mild, moderate or severe). The spontaneous or phorbol myristate acetate (PMA, 30 nM)-induced superoxide release by granulocytes and monocytes was determined at 0, 5, 15, and 25 min. cGPx activity was assayed spectrophotometrically. The spontaneous superoxide release by granulocytes from patients with mild (N = 15), moderate (N = 12) or severe (N = 6) asthma was higher at 25 min compared to healthy individuals (N = 28, P < 0.05, Duncan test). The PMA-induced superoxide release by granulocytes from patients with moderate (N = 12) or severe (N = 6) asthma was higher at 15 and 25 min compared to healthy individuals (N = 28, P < 0.05 in both times of incubation, Duncan test). The spontaneous or PMA-induced superoxide release by monocytes from asthmatic patients was similar to healthy individuals (P > 0.05 in all times of incubation, Duncan test). cGPx activity of granulocytes and monocytes from patients with persistent asthma (N = 20) was also similar to healthy individuals (N = 10, P > 0.05, Kruskal-Wallis test). We conclude that, under specific circumstances, granulocytes from children with persistent asthma present a higher respiratory burst activity compared to healthy individuals. These findings indicate a risk of oxidative stress, phagocyte auto-oxidation, and the subsequent release of intracellular toxic oxidants and enzymes, leading to additional inflammation and lung damage in asthmatic children.
哮喘是一种炎症性疾病,其特征是涉及多种介质,包括活性氧。本研究的目的是调查患有特应性哮喘的儿童和青少年外周血粒细胞和单核细胞中的超氧化物释放及细胞谷胱甘肽过氧化物酶(cGPx)活性。选取了44例患者,并将其分类为患有间歇性或持续性哮喘(轻度、中度或重度)。在0、5、15和25分钟时测定粒细胞和单核细胞自发或佛波酯(PMA,30 nM)诱导的超氧化物释放。用分光光度法测定cGPx活性。与健康个体(N = 28,P < 0.05,Duncan检验)相比,轻度(N = 15)、中度(N = 12)或重度(N = 6)哮喘患者的粒细胞在25分钟时自发超氧化物释放更高。与健康个体(N = 28,两次孵育时P均 < 0.05,Duncan检验)相比,中度(N = 12)或重度(N = 6)哮喘患者的粒细胞在15和25分钟时PMA诱导的超氧化物释放更高。哮喘患者单核细胞自发或PMA诱导的超氧化物释放与健康个体相似(所有孵育时间P > 0.05,Duncan检验)。持续性哮喘患者(N = 20)的粒细胞和单核细胞的cGPx活性也与健康个体(N = 10,P > 0.05,Kruskal-Wallis检验)相似。我们得出结论,在特定情况下,患有持续性哮喘的儿童的粒细胞与健康个体相比呈现出更高的呼吸爆发活性。这些发现表明存在氧化应激、吞噬细胞自氧化以及随后细胞内有毒氧化剂和酶释放的风险,从而导致哮喘儿童出现额外的炎症和肺损伤。