KA (kojic acid) is a secondary metabolite isolated from Aspergillus fungi that has demonstrated skin whitening, antioxidant and antitumour properties among others. However, limited information is available regarding its effects on macrophages, the major cell involved in cell defence. The aim of the present study was to analyse whether KA affects functional properties related to macrophage activation, such as phagocytosis and spreading ability over a substrate. Treatment of resident macrophages with 50 μg/ml KA for 1 h induced both morphological and physiological alterations in cells. Immunofluorescence microscopy revealed enhanced cell spreading and an increase in cell surface exposure, associated with a rearrangement of microtubules, actin filaments and intermediate filaments. KA also potentiated phagocytosis by macrophages, as demonstrated by the increase in phagocytic activity towards yeast, when compared to untreated cells. KA increased the production of ROS (reactive oxygen species), but not NO (nitric oxide) production. Three tests were used to assess cell viability; MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide], NR (neutral red) uptake and PI (propidium iodide) exclusion test, which showed that macrophages maintain their viability following KA treatment. Results indicate that KA can modulate macrophage activation through cytoskeleton rearrangement, increase cell surface exposure, enhance the phagocytic process and ROS production. The study demonstrates a new role for KA as a macrophage activator.

Kojic acid (KA) is a fungal metabolite used as a topical treatment skin-whitening cosmetic agent for melasma in humans; however its potential as an anti-leishmanial agent is unknown. Chemotherapy is one of the most effective treatments for Leishmaniasis. However, the drugs available are expensive, invasive, require long-term treatment and have severe side effects. Thus, the development of new effective leishmanicidal agents is a necessity. In this study we investigated the anti-leishmanial effect of KA on L. amazonensis, following in vitro and in vivo infections. KA (50 μg/mL) was found to decrease the growth by 62% (IC50 34 μg/mL) and 79% (IC50 27.84 μg/mL) of promastigotes and amastigotes in vitro, respectively. Ultrastructural analysis of KA-treated amastigotes showed the presence of vesicles bodies into the flagellar pocket, and an intense intracellular vacuolization and swelling of the mitochondrion. During the in vitro interaction of parasites and the host cell, KA reverses the superoxide anions (O2 -) inhibitory mechanism promoted by parasite. In addition, 4 weeks after KA-topical formulation treatment of infected animals, a healing process was observed with a high production of collagen fibers and a decrease in parasite burden. Thus, these results demonstrated the great potential of KA as an anti-leishmanial compound.

A rapid molecular identification technique was applied on microbial microflora isolated from Brazilian cassava roots given a yeast profile presented in the samples analyzed. A total of 24 strain isolated from cassava were initially grouped and identified in five groups using restriction-fragment length polymorphism (RFLPs) of 5.8S-ITS rDNA region. Sequencing analysis of the domains D1 and D2 of the 26S rRNA gene or 5.8S rRNA-ITS region were used to identify different groups of yeasts. Representative colonies of yeasts of each group were isolated and identified as Debaromyces hansenii, Kodamaea ohmeri, Candida glabrata, C. haemulonii, and Pichia gullhermondii. It is hoped that these results will contribute toward selecting yeast from this microflora capable to degrade cassava starch in the near future.

Libidibia ferrea (juca) is a plant belonging to the Fabaceae (Leguminosae) family, whose antioxidant activity has been widely described in the literature. We evaluated this parameter of Aqueous ethanol extract (AE), ethyl acetate (ACO), chloroform (CLO) and hexane (HEX) extracts of L. ferrea. We then tested the most active extract for its toxicity and ability to inhibit migratory activity in the ACP02 gastric adenocarcinoma cell line in vitro. The AE and ACO extracts both had antioxidant activity, the AE extract showing greater potential. This may reflect that both extracts contained phenolic compounds. Although AE extract showed no cytotoxic, mutagenic or genotoxic effect, it altered cell morphology and migration activity. Analysis of apoptosis/necrosis indicated that this parameter does not appear to account for the apparent ability of AE to inhibit cancer cell migration. We speculate that the morphological changes in AE-treated cells could be due to cytoskeleton alterations related to the presence of myo-inositol in AE extract. Together, our results demonstrate this extract of L. ferrea can act as an exogenous antioxidant and might prove useful in efforts to fight secondary tumors.