20Malaria still presents great epidemiologic importance by its high incidence in the 21 world and potential clinical severity. Plasmodium parasites are highly susceptible to 22 changes in the redox balance and the relationship between the redox state of the 23 parasite and host cells is very complex and involves nitric oxide (NO) synthesis. 24Thus, the present study is aimed at evaluating the effects of NO synthesis on the 25 redox status, parasitemia evolution and survival rate of Plasmodium berghei-26 infected mice. Two-hundred and twenty-five mice were infected with Plasmodium 27 berghei and submitted to the stimulation or inhibition of NO synthesis. The 28 stimulation of NO synthesis was performed through the administration of L-29 arginine, while its inhibition was made by the administration of dexamethasone.30 Inducible NO synthase (iNOS) inhibition by dexamethasone promoted an increase 31 in the survival rate of P. berghei-infected mice and data suggested the participation 32 of oxidative stress in brain as a result of plasmodial infection, as well as the 33 inhibition of brain NO synthesis, which promoted survival rate of almost 90% of the 34 animals until the 15 th day of infection, with possible direct interference of ischemia 35 and reperfusion syndrome, as seen by increased levels of uric acid. Inhibition of 36 iNOS caused a decrease of parasitemia and increased survival rate of infected 37 animals, suggesting that the synthesis of NO may stimulate a series of 38 compensatory redox effects that, if overstimulated, may be responsible for the 39 onset of severe forms of malaria. 40 Plasmodium berghei, Inducible nitric oxide synthase, parasitemia, survival rate. 42 43 93Moreover, in response to the infection, activated macrophages and 94 neutrophils act as the natural defense mechanism of the host organism and these 95 generate a large amount of free radicals by activation of respiratory burst, causing 96 an imbalance between the formation of oxidant species and the activity of 97 antioxidants. This imbalance triggers the oxidative stress, being an important 98 mechanism of human host in response to microbial infections that, in the case of 99 malaria, can lead to the death of parasites.
The present study aimed to evaluate the effects of dexamethasone on the redox status, parasitemia evolution, and survival rate of Plasmodium berghei-infected mice. Two-hundred and twenty-five mice were infected with Plasmodium berghei and subjected to stimulation or inhibition of NO synthesis. The stimulation of NO synthesis was performed through the administration of L-arginine, while its inhibition was made by the administration of dexamethasone. Inducible NO synthase (iNOS) inhibition by dexamethasone promoted an increase in the survival rate of P. berghei-infected mice, and the data suggested the participation of oxidative stress in the brain as a result of plasmodial infection, as well as the inhibition of brain NO synthesis, which promoted the survival rate of almost 90% of the animals until the 15th day of infection, with possible direct interference of ischemia and reperfusion syndrome, as seen by increased levels of uric acid. Inhibition of brain iNOS by dexamethasone caused a decrease in parasitemia and increased the survival rate of infected animals, suggesting that NO synthesis may stimulate a series of compensatory redox effects that, if overstimulated, may be responsible for the onset of severe forms of malaria.
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