Prior studies show that melatonin enhances the immune response. This study investigated the possible therapeutic effects of melatonin during the course of Trypanosoma cruzi infection. T. cruzi-infected male Wistar rats were orally treated with 5 mg/kg body weight/day of melatonin. Animals treated with melatonin showed a significant reduction in the number of blood trypomastigotes during the acute phase of infection compared with untreated animals (P<0.05). A significant increase in leucocytes numbers during the peak of parasitaemia was also observed (P<0.05). Moreover, both prior and concomitant treatment with melatonin increased interleukin-2 levels, especially 9 days postinfection (P<0.05). Histopathological observations of heart tissue revealed that melatonin administration also resulted in fewer and smaller amastigote burdens, and less inflammatory infiltrate and tissue disorganization, indicating a reduced parasitism of this tissue. These results show that melatonin is effective in controlling parasite replication and suggest that melatonin might serve as an effective therapeutic agent in the treatment of American trypanosomiasis.

No abstract

The extent of neuronal loss was studied in this work, in aged female Calomys callosus infected with the MORC-1 strain of Trypanosoma cruzi. Fifteen months after infection, one group of animals was immunosuppressed with cyclophosphamide (CY). Sections of the distal esophagus were collected and stained with cresyl violet. The neuron count was significantly different among groups, with enhanced neuronal loss in the infected group in comparison with the control aged noninfected group. Partial protection against neuronal destruction was observed in animals immunosuppressed with CY. The morphometry of the neuronal body displayed significant alterations concerning area, shape coefficient, and contour index that were statistically increased for the CY-infected group. These results indicate a protective role for CY against neuronal destruction.

The protective role of cyclophosphamide was studied in this work. Young male Calomys callosus were infected with Trypanosoma cruzi and allowed to age. Cyclophosphamide therapy was administered to animals during acute and late chronic phases of infection. Esophageal neurons were counted, displaying enhanced neuronal loss for the young and treated infected groups. For aged and cyclophosphamide treated animals, a protection was observed through a reduced loss of neurons as compared to the young and infected groups. Enhanced nitric oxide concentrations were observed for young animals as compared to aged counterparts. Splenocyte proliferation was reduced during the acute phase in comparison with those found in the chronic phase. Morphometry of neuronal body displayed a significant reduction concerning the area, perimeter, diameter and volume for aged animals as compared to young groups. These results indicate that the protective effects of cyclophosphamide together with process of neuroplasty of peripheral nervous system could lead to a protection against neuronal loss.

In this study, we verified the possible role of cyclophosphamide (CY) in protecting or not against neuronal losses in young and aged male Calomys callosus chronically infected with the MORC-1 strain of Trypanosoma cruzi through numerical quantification of neurons from the myenteric plexus of the colon and quantification of nitric-oxide concentration (NO) during the acute and chronic phase of infection. For this purpose, groups of young C. callosus were infected with the MORC-1 strain of T. cruzi. A group of infected animals received i.p. 0.2 mg/ml genuxal dissolved in distilled water treatment with CY. NO concentration in aged animals displayed reduced levels when compared to those found in young animals. No significant alterations in the number of neurons were observed in young animals, but for aged ones, a protective role of CY in reducing neuron loss was noted, in addition to enhancing the neuronal volume, area, and perimeter. These results suggest that CY administration, depending on the dose and time span, can act as a protective agent against neuronal losses.