ascorbic-acid and Parasitemia

This study investigated the effects of co-administration of a commercial juice rich in vitamin C (Vit C) on the antimalarial efficacy of artemether-lumefantrine (AL) in Plasmodium berghei-infected mice. Fifty Balb/c mice were infected with Plasmodium berghei NK65 strain from a donor mouse. Parasitemia was established after 72 h. Animals were grouped into 6 (n = 10) and treated daily for 3 days with normal saline, chloroquine, artemether-lumefantrine (AL), AL plus 50% commercial juice (CJ), and AL plus 50% Vit C supplementation in drinks ad libitum, respectively. Body weight, parasitemia levels, and mean survival time were determined. Tumor necrosis factor-alpha (TNF-α), interleukin 6 (IL-6), nitrite, malondialdehyde, reduced glutathione (GSH), catalase, and superoxide dismutase (SOD) were determined in the serum and liver tissues. Spleen histopathological changes were determined by H&E staining. Parasitemia was cleared by administration of AL and was not affected by Vit C and CJ supplementation. Vit C significantly prevented body weight reduction in AL-treated mice. CJ and Vit C supplementation to AL-treated mice significantly improved survival proportion compared with AL alone animals. Vit C and CJ supplementation significantly improved reduction of TNF-α, IL-6, and malondialdehyde, and increased GSH, CAT, and SOD in AL-treated mice. Spleen cell degeneration and presence of malaria pigment were reduced in AL-treated animals. The results suggest that ad libitum co-administration of commercial juice and vitamin C with artemether-lumefantrine does not impair its antimalarial efficacy but rather improved antioxidant and anti-inflammatory effects in mice.

Topics: Animals; Antimalarials; Artemether; Artemether, Lumefantrine Drug Combination; Ascorbic Acid; Interleukin-6; Malaria; Malondialdehyde; Mice; Parasitemia; Plasmodium berghei; Superoxide Dismutase; Tumor Necrosis Factor-alpha

Trypanosoma cruzi infection stimulates inflammatory mediators which cause oxidative stress, and the use of antioxidants can minimize the sequelae of Chagas disease. In order to evaluate the efficacy of vitamin C in minimizing oxidative damage in Chagas disease, we orally administered ascorbic acid to Swiss mice infected with 5.0 × 10

Topics: Acute Disease; Animals; Antioxidants; Ascorbic Acid; Bilirubin; Chagas Disease; Chronic Disease; Disease Models, Animal; Inflammation; Iron; Male; Mice; Nitric Oxide; Oxidative Stress; Parasitemia; Peroxynitrous Acid; Trypanosoma cruzi

Drugs currently used for the treatment of Chagas' disease, nifurtimox and benznidazole, have a limited effectiveness and toxic side effects. With the aim of finding new therapeutic approaches, in vitro and in vivo anti-Trypanosoma cruzi activity of vitamin C alone and combined with benznidazole were investigated.. The trypanocidal activity on epimastigote and trypomastigote forms was evaluated by counting parasites in a Neubauer chamber after treatment with the compounds. For the amastigote stage, transgenic parasites expressing β-galactosidase were used and quantified by measuring the β-galactosidase activity. The cytotoxicity of compounds was tested on Vero cells. The redox state of the parasite was evaluated by determining the reduced thiol levels (spectrophotometric assay) and the intracellular oxidative state (by flow cytometry). The in vivo trypanocidal activity was evaluated on a murine model of Chagas' disease. The trypanocidal activity of vitamin C and benznidazole was similar for the three parasite forms. When combining both drugs, vitamin C did not induce any change in the antiparasitic activity of benznidazole on trypomastigotes; however, on mammal cells, vitamin C diminished the cytotoxicity degree of benznidazole. Two mechanisms of action may be postulated for vitamin C: a lethal pro-oxidant effect on the parasite when used alone, and an antioxidant effect, when combined with benznidazole. A similar behavior was observed on infected mice; i.e., parasite counts in infected mice treated with vitamin C were lower than that of the control group. Animals treated with benznidazole presented lower parasitemia levels, as compared with those treated with vitamin C alone. Again, vitamin C did not cause any effect on the antiparasitic profile of benznidazole. Even though a combined treatment was employed, the antioxidant effect of vitamin C on the host was evidenced; a 100% survival was observed and the weight loss occurring during the acute phase of the infection was reduced.. Based on these results, the combination of vitamin C with benznidazole could be considered as an alternative treatment for Chagas' disease. These preliminary results encourage further research to improve the treatment of Chagas' disease.

Topics: Animals; Ascorbic Acid; Body Weight; Chagas Disease; Chlorocebus aethiops; Disease Models, Animal; Drug Interactions; Drug Therapy, Combination; Female; Mice, Inbred C3H; Nitroimidazoles; Parasite Load; Parasitemia; Survival Analysis; Treatment Outcome; Trypanocidal Agents; Trypanosoma cruzi; Vero Cells

The redox metabolism of the malaria parasite Plasmodium falciparum and its human host has been suggested to play a central role for parasite survival and clearance. A common approach to test hypotheses in redox research is to challenge or rescue cells with pro- and antioxidants. However, quantitative data on the susceptibility of infected erythrocytes towards standard redox agents is surprisingly scarce. Here we determined the IC

Topics: Acetylcysteine; Antioxidants; Ascorbic Acid; Benzothiazoles; Diamide; Diamines; Dithiothreitol; Dose-Response Relationship, Drug; Erythrocytes; Fluorescent Dyes; Host-Parasite Interactions; Humans; Hydrogen Peroxide; Inhibitory Concentration 50; Malaria, Falciparum; Organic Chemicals; Oxidants; Oxidation-Reduction; Oxidative Stress; Parasitemia; Plasmodium falciparum; Quinolines; tert-Butylhydroperoxide; Time Factors

To evaluate the efficacy of vitamin C in reducing the consequences generated by the production of free radicals in the acute and chronic phases of Chagas disease, two different doses of ascorbic acid were administered orally to 60 mice infected by Trypanosoma cruzi QM2 strain.. The animals were divided into six groups: G1, G2, and G3 for the acute phase study, and G'1, G'2, and G'3 for the chronic stage. The groups G1 and G'1 received 8.6 x 10⁻⁴ mg/g of vitamin C daily, whereas G2 and G'2 received 7.14 x 10⁻³ mg/g daily. The other groups, G3 and G'3, were considered placebos and received 10 µL of mineral water.. The study of the acute phase showed statistically significant differences between G1 and the other groups at various count days of the parasitemia evolution. The multiplying parasite was slower in G1 until the 11th day, but on the 22nd day it had greater parasitemia than in G2 and G3, and from the 36th day on, parasitemia stabilized at higher levels. However, when the histopathology of acute and chronic phases is considered, one does not note significant differences.. The administration of two different doses of vitamin C was not able to protect mice and to contain the oxidative stress caused by free radicals formed by the metabolism of oxygen (reactive oxygen species) and nitrogen (reactive nitrogen species).

Topics: Acute Disease; Animals; Antioxidants; Ascorbic Acid; Chagas Disease; Chronic Disease; Disease Models, Animal; Male; Mice; Parasitemia

The tissue changes that occur in Chagas disease are related to the degree of oxidative stress and antioxidant capacity of affected tissue. Studies with vitamin C supplementation did not develop oxidative damage caused by Chagas disease in the host, but other studies cite the use of peroxiredoxins ascorbate - dependent on T. cruzi to offer protection against immune reaction. Based on these propositions, thirty "Swiss" mice were infected with T. cruzi QM1 strain and treated with two different vitamin C doses in order to study the parasitemia evolution, histopathological changes and lipid peroxidation biomarkers during the acute phase of Chagas disease. The results showed that the parasite clearance was greater in animals fed with vitamin C overdose. There were no significant differences regarding the biomarkers of lipid peroxidation and inflammatory process or the increase of myocardium in animals treated with the recommended dosage. The largest amount of parasite growth towards the end of the acute phase suggests the benefit of high doses of vitamin C for trypomastigotes. The supplementation doesn't influence the production of free radicals or the number of amastigote nests in the acute phase of Chagas disease.

Topics: Acute Disease; Animals; Antioxidants; Ascorbic Acid; Chagas Disease; Dietary Supplements; Disease Models, Animal; Dose-Response Relationship, Drug; Lipid Peroxidation; Male; Mice; Parasitemia; Time Factors; Trypanosoma cruzi

The effects of aqueous extract of Hibiscus sabdariffa calyces on haematology and pathological changes in some selected organs during experimental Trypanosoma congolense infection of rats were investigated. Three groups of rats were intraperitoneally infected with T. congolense (Karu stock). One group was administered with the aqueous extract and another given a solution of vitamin C in drinking water; the remaining infected group was left untreated. Data from these groups were compared with those of two groups of healthy rats, one of which was similarly treated with the aqueous extract. The experiment was terminated three weeks, post-infection (pi). The uninfected and infected rats administered the extract consumed the equivalent of 9.94 mg - and 9.61 mg ascorbic acid / 100g / day during the experiment. Consumption of the extract significantly (p<0.01) retarded the rate of weight gain in both healthy and infected rats; even though the feed-intake was not significantly affected. After two weeks of infection the extract and vitamin C kept the parasitaemia significantly (p<0.01) lower than the untreated infected group. The anaemia in the untreated infected group was significantly (p<0.01) more severe than that of the corresponding extract- or vitamin-treated groups. Trypanosoma congolense infection caused significant (p<0.01) decreases in serum total proteins and albumin; serum and organ ascorbic acid as well as significant (p<0.01) elevation of serum alanine amino transferase levels in untreated rats. Consumption of the extract or vitamin C, however, prevented these disease-induced anomalies in the treated infected rats. Serum creatinine and urea levels were not affected by infection but the extract elevated these parameters significantly (p<0.01) above infection levels. It was concluded that consumption of the extract ameliorated the pathological changes in blood and organs of T. congolense-infected rats.

Topics: Anemia; Animals; Ascorbic Acid; Creatinine; Hematocrit; Hibiscus; Injections, Intraperitoneal; Kidney; Liver; Male; Parasitemia; Plant Extracts; Rats; Rats, Wistar; Trypanosoma congolense; Trypanosomiasis, African; Water

Rabbits infected with Trypanosoma brucei brucei (Basa isolate) were intraperitoneally administered with vitamins C and E at 100 mg/kg and 10 mg/kg body weight, respectively, from day 7 before infection to day 12 post-infection (p.i.). Another group of rabbits were similarly infected, but received no vitamin treatment. The uninfected (control) rabbits were either untreated or treated with vitamins like the infected group. Treatment of the infected animals did not affect the onset and level of parasitaemia. On day 12 p.i., the anaemia tended to be ameliorated, but insignificantly, by the treatment. The infection increased (p<0.05) serum urea and creatinine concentrations to similar levels in treated and untreated groups. However, the increase (p<0.05) in alanine and aspartate transaminases in the untreated infected animals was prevented in the treated infected ones. Therefore, it seemed that the treatment with antioxidant vitamins boosted their storage in hepatic cells, but not in erythrocytes and glomeruli, to annul any cellular injury due to infection. It is concluded that this may be an indirect evidence that the hepatic damage may be principally due to oxidative injury.

Topics: Alanine Transaminase; Anemia; Animals; Ascorbic Acid; Aspartate Aminotransferases; Creatine; Hematocrit; Injections, Intraperitoneal; Kidney; Liver; Male; Parasitemia; Rabbits; Trypanosoma brucei brucei; Trypanosomiasis, African; Urea; Vitamin E

Crithidia fasciculata was used to replace murine peritoneal wash cells as feeder cells for the adaptation of Plasmodium falciparum isolates to continuous culture in vitro, thus avoiding the need to sacrifice animals. Fourteen of 17 malaria parasite isolates in one study, and 12 of 12 isolates in a second study, were successfully adapted to continuous culture in the presence of C. fasciculata, while only 5 of 17 parallel control isolates in the first study, and 2 of 12 isolates in the second study, were adapted in the absence of any feeder cells. Biochemical assays were performed to investigate various hypotheses put forward to explain the mode of action of feeder cells. No effect of C. fasciculata feeder cells was observed on lactate removal, osmotic pressure, or glucose or amino acid content of the malaria culture media. This feeder cell system was shown to reduce the pH of the malaria culture medium. Neither this feeder system nor another system, murine peritoneal macrophages, had any effect on the cysteine content of the culture medium. C. fasciculata was shown to reduce the redox potential of the culture medium, as were other malaria growth enhancers including cysteine and glutathione. This effect on the redox potential of the culture medium is proposed to be a possible mode of action for the feeder cell systems studied.

Topics: Animals; Ascorbic Acid; Crithidia fasciculata; Culture Media; Cysteine; Glutathione; Humans; Hydrogen-Ion Concentration; Malaria, Falciparum; Osmotic Pressure; Oxidation-Reduction; Parasitemia; Plasmodium falciparum