Entamoeba histolytica: production of nitric oxide and in situ activity of NADPH diaphorase in amebic liver abscess of hamsters

La Salle University, Filadelfia, Pennsylvania, United States
Parasitology Research (Impact Factor: 2.33). 02/2001; 87(1):49-56. DOI: 10.1007/s004360000287
Source: PubMed

ABSTRACT 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.

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    ABSTRACT: The molecular mechanisms by which Entamoeba histolytica causes amebic liver abscess (ALA) are still not fully understood. Amebic mechanisms of adherence and cytotoxic activity are pivotal for amebic survival but apparently do not directly cause liver abscess. Abundant evidence indicates that chronic inflammation (resulting from an inadequate immune response) is probably the main cause of ALA. Reports referring to inflammatory mechanisms of liver damage mention a repertoire of toxic molecules by the immune response (especially nitric oxide and reactive oxygen intermediates) and cytotoxic substances released by neutrophils and macrophages after being lysed by amoebas (e.g., defensins, complement, and proteases). Nevertheless, recent evidence downplays these mechanisms in abscess formation and emphasizes the importance of peroxynitrite (ONOO(-)). It seems that the defense mechanism of amoebas against ONOO(-), namely, the amebic thioredoxin system (including peroxiredoxin), is superior to that of mammals. The aim of the present text is to define the importance of ONOO(-) as the main agent of liver abscess formation during amebic invasion, and to explain the superior capacity of amoebas to defend themselves against this toxic agent through the peroxiredoxin and thioredoxin system.
    04/2014; 2014:324230. DOI:10.1155/2014/324230
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    ABSTRACT: Nitric oxide participation during amoebic liver abscess development. Nitric oxide participates in both physiological and pathophysiological functions, and it plays an important role in the mammalian immune system in killing or inhibiting the growth of many pathogens, including parasites, viruses and bacteria. En- tamoeba histolytica is a protozoan parasite that causes amoebiasis, which is characterized by intestinal damage and amoebic liver abscess development. The development of amoebic liver abscess in hamsters is similar to that in humans, whereas mice are resistant to amoebic liver abscess development due to an increase in nitric oxide produc- tion. Unlike in mice, amoebic liver abscess development in hamsters is due to an excess in nitric oxide production or possibly to a greater susceptibility of the hamster to damage caused by nitric oxide. Therefore, it could be important to elucidate if, in humans, an excess in nitric oxide production favors amoebic liver abscess development.
    Medicina 04/2007; 67(2):167-176. · 0.42 Impact Factor
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    ABSTRACT: The immunocompetence handicap hypothesis (ICHH) proposes that testosterone enhances the expression of sexual traits but suppresses immune function. However, studies to test the hypothesis have shown mixed results. Alternatively, sexual traits, immune function, and parasite susceptibility may be mediated by the stress hormone corticosterone. Here, we report an experimental test of the ICHH that included the manipulation of both testosterone and parasites in male laboratory mice (Mus musculus L., 1758). We conducted a factorial experiment, injecting each individual mouse with testosterone or not and infecting them with the nematode parasite Trichinella spiralis (Owen, 1835) or not. As predicted, testosterone enhanced the scent attractiveness of male mice, whereas parasite infection reduced it, but only in male mice not injected with testosterone. However, we found no evidence that corticosterone is involved in mediating the effects of testosterone. These results confirm that maintaining high testosterone levels entails the cost of increased parasite abundance. This study provides direct evidence supporting the ICHH.
    Canadian Journal of Zoology 09/2014; 92(9). DOI:10.1139/cjz-2014-0093 · 1.35 Impact Factor

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