Pacheco-Yépez J, Campos-Rodríguez R, Shibayama M, Ventura-Juárez J, Serrano-Luna J, Tsutsumi V
Departamento de Patología Experimental, CINVESTAV-IPN, San Pedro Zacatenco, Mexico.
Parasitol Res. 2001 Jan;87(1):49-56. doi: 10.1007/s004360000287.
Entamoeba histolytica trophozoites were inoculated into the liver of hamsters and serum nitrate/nitrite levels [expressed as nitric oxide (NO) production] were determined at different times during amebic liver abscess (ALA) development. We also tested the effects of NO synthase (NOS) inhibitors such as N(G)-nitro-L-arginine methyl ester (L-NAME), aminoguanidine, and dexamethasone during ALA production. Since NOS activity has been correlated with expression of reduced nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd) in tissues, we performed histochemistry studies to determine the activity of the latter in livers infected with E. histolytica trophozoites. Production of NO in serum was directly proportional to the size of ALAs, and NOS inhibitors caused low levels of NO and smaller ALAs. Our data suggest that NO does not have any lytic effect on E. histolytica trophozoites and is therefore incapable of providing protection against the amebic liver infection. In addition, NADPHd activity was detected histochemically in hepatocytes and inflammatory cells associated with focal necrosis containing trophozoites. The positive reactivity observed in these parasites may be attributable to a close biochemical similarity of NADPHd to the NADPH:flavin oxidoreductase described in E. histolytica by other investigators.
将溶组织内阿米巴滋养体接种到仓鼠肝脏中,并在阿米巴肝脓肿(ALA)形成的不同时间测定血清硝酸盐/亚硝酸盐水平[以一氧化氮(NO)生成量表示]。我们还测试了NO合酶(NOS)抑制剂,如N(G)-硝基-L-精氨酸甲酯(L-NAME)、氨基胍和地塞米松在ALA形成过程中的作用。由于NOS活性与组织中还原型烟酰胺腺嘌呤二核苷酸磷酸黄递酶(NADPHd)的表达相关,我们进行了组织化学研究,以确定感染溶组织内阿米巴滋养体的肝脏中NADPHd的活性。血清中NO的生成量与ALA的大小成正比,NOS抑制剂导致NO水平降低和ALA变小。我们的数据表明,NO对溶组织内阿米巴滋养体没有任何溶解作用,因此无法提供针对阿米巴肝感染的保护。此外,在与含有滋养体的局灶性坏死相关的肝细胞和炎性细胞中,通过组织化学检测到了NADPHd活性。在这些寄生虫中观察到的阳性反应可能归因于NADPHd与其他研究者在溶组织内阿米巴中描述的NADPH:黄素氧化还原酶在生化上的密切相似性。