Analysis of the redox status and its effect on the proliferation of Plasmodium falciparum in genetically different erythrocytes.

Author(s)

Kamila Anna Meissner

• Document type: Doctoral Thesis
• Press: São Paulo.
• Institution: Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB/SDI)
• Defense date: 2017-04-19

Examining board members

Carsten Wrenger; Jose Eduardo Krieger; Joachim Kurtz; Claudio Romero Farias Marinho

• Advisor: Carsten Wrenger

Abstract

Malaria, caused by Plasmodium spp., remains with more than 400.000 deaths annually one of the vastest diseases of our time. Plasmodium falciparum, is the most dangerous species leading to severe malaria. Nevertheless, there are some native resistances known like sickle cell trait or enzymopathies such as glucose-6-phosphate dehydrogenase deficiency. However, the protection mechanism is still unknown. Hypotheses like a better innate immune response or the increased oxidative stress inside the altered erythrocytes are discussed. This work is focusing on the oxidative defence system of P. falciparum using transgenically modified parasites cultured in wild-type and abnormal red blood cells. Elevated expression levels of different anti-oxidative systems in P. falciparum should give a deeper insight of the protection mechanism of the altered erythrocytes. In this work, we show the importance of the Glutathione-S-Transferase (GST) for the proliferation of the malaria pathogen in erythrocytes with glucose-6-phosphate dehydrogenase deficiency. This leads to the hypothesis that the increased ROS level in these red blood cells generating a high amount of xenobiotics within the parasite which results in cell death. (AU)

• FAPESP's process: 12/12807-3 - Analysis of the redox status and its effect on the proliferation of Plasmodium falciparum in genetically different erythrocytes
• Grantee: Kamila Anna Meissner
• Support Opportunities: Scholarships in Brazil - Doctorate