Malaria is a significant public health problem in more than 100 countries and causes an estimated 200 million new infections every year. Despite the significant effort to eradicate this dangerous disease, lack of complete knowledge of its physiopathology compromises the success in this enterprise. In this paper we review oxidative stress mechanisms involved in the disease and discuss the potential benefits of antioxidant supplementation as an adjuvant antimalarial strategy.

The risk of chronic diseases such as Alzheimer's disease is growing as a result of the continuous increasing average life span of the world population, a syndrome characterized by the presence of intraneural neurofibrillary tangles and senile plaques composed mainly by beta-amyloid protein, changes that may cause a number of progressive disorders in the elderly, causing, in its most advanced stage, difficulty in performing normal daily activities, among other manifestations. Therefore, it is important to understand the underlying pathogenic mechanisms of this syndrome. Nevertheless, despite intensive effort to access the physiopathological pathways of the disease, it remains poorly understood. In that context, some hypotheses have arisen, including the recent oxidative stress hypothesis, theory supported by the involvement of oxidative stress in aging, and the vulnerability of neurons to oxidative attack. In the present revision, oxidative changes and redox mechanisms in Alzheimer's disease will be further stressed, as well as the grounds for antioxidant supplementation as adjuvant therapy for the disease will be addressed.

Parkinson’s disease (PD) occurs in approximately 1% of the population over 65 years of age and has become increasingly more common with advances in age. The number of individuals older than 60 years has been increasing in modern societies, as well as life expectancy in developing countries; therefore, PD may pose an impact on the economic, social, and health structures of these countries. Oxidative stress is highlighted as an important factor in the genesis of PD, involving several enzymes and signaling molecules in the underlying mechanisms of the disease. This review presents updated data on the involvement of oxidative stress in the disease, as well as the use of antioxidant supplements in its therapy.

A statistically significant increase in methemoglobinemia was observed following oral therapy with primaquine, with no clinical manifestations, and independent of sex and the qualitative expression of glucose-6-phosphate dehydrogenase.

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.