Evaluation of the nitric oxide activity against Blastocystis hominis in vitro and in vivo

The effect of exogenous nitric oxide [NO] on growth, viability and ultra-structural of B. hominis was assessed in vitro by sodium nitrite [NaNO[2]] in 0.6 mM, 0.8 mM and 1 mM concentrations. The viability of B. hominis was identified using neutral red stain. The role of NO as an endogenous oxidant was assessed by identifying its level in cecum tissue, ileum tissue, blood and stool elutes of mice infected with B. hominis symptomatic human isolates using reactive nitrogen assay compared to control. In vitro study revealed that NaNO[2] inhibited the growth and decreased viability of B. hominis with minimal lethal concentration dose 1 mM on the 4[th] day while, minimal effects were detected with 0.6 and 0.8 mM. Transmission electron microscopy study proved that apoptotic-like features were observed in growing axenic culture of B. hominis upon exposure to NaNO[2]. These changes were not only found on the vacuolar [central body] form but also they were detected on granular, multi-vacuolar and cyst forms. In vivo study proved that high levels of NO were found in infected mice compared to low changes in control group. The high levels were in cecum tissue particularly. The mean levels of NO among infected mice were 211.8 +/- 20.7 micro M in cecum, 90.4 +/- 11.6 micro M in ileum, 60.1 +/- 4.7 micro M in blood and 63.6 +/- 7.3 micro M in stool elutes while, the mean levels of NO in control mice were 70.2 +/- 3.1 in cecum, 67.8 +/- 4.7 micro M in ileum, 30.9 +/- 4.2 micro M in blood and 28.1 +/- 2.9 micro M in stool elutes. The differences were statistically highly significant. NO-donor drugs proved useful in treatment and increase the host resistance to B. hominis

Effect of exogenous adminstration of anti-oxidants on Blastocystis hominis in vivo

The effect of exogenous administration of antioxidant [Anttox] on the course of B. hominis in experimentally infected mice was studied. B. hominis isolates were obtained from 10 gastrointestinal symptomatic adult patients. Three groups of 30 infected mice [3/isolate] were used. GI was untreated infected, GII was treated by antox for 4 weeks after infection diagnosis [treatment strategy], and GIII antox treated by antox for 4 weeks before infection [prophylactic strategy]. Mild pathological changes were detected on 13.4%, 19.9% and 86.8% of mice in Gs I, II and III, respectively. Moderate pathological changes were found in 29.9%, 26.6% and 6.6% of mice in Gs I, II and III, respectively. While, the majority of severe pathological changes were in Gs I and II [56.7% and 53.5%] as compared to GIII [6.6%]. Meanwhile, 86.8% of mice in GIII had B. hominis forms >10/high power field compared to 3.3% in Gs I and II, respectively. Although 19.8% of mice in GII were positive for B. hominis by direct smear, no growth resulted in vitro and all the forms were non-viable by using neutral red stain. All the differences were statistically significant. So, antioxidant exacerbated B. hominis intensity but it decreased the pathological changes