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82 Dehydrogenases

**Author details** 

Serhat Elcicek

**9. References** 

Adil M. Allahverdiyev, Malahat Bagirova,

Rabia Cakir Koc, Sezen Canim Ates, Serap Yesilkir Baydar, Serkan Yaman, Emrah Sefik Abamor and Olga Nehir Oztel

*Department of Bioengineering, Firat University, Elazig, Turkey* 

*Department of Bioengineering, Yildiz Technical University, Istanbul, Turkey* 

*Department of Bioengineering, Yildiz Technical University, Istanbul, Turkey* 

(1967) Standardization of procedures for the study of glucose-6-phosphate dehydrogenase. Report of a WHO Scientific Group. *World Health Organ Tech Rep Ser* Vol.366(No.:1-53. (Betke K, Brewer GJ, Kirkman HN, Luzzatto L,Motulsky AC, Ramot B, and Siniscalco M 1967) Standardization of procedures for the study of glucose-6-phosphate

One of them is that G6PD deficiency provides partial protection from malaria infections, especially for falciparum infections. In several studies, it was demonstrated that risk of contracting malaria in patients that have G6PD deficiency decreased at a rate of 46 to 58%. On the other hand, using antimalarial drugs can cause life-threatening hemolytic anemia in patients with G6PD deficiency. Since G6PD deficiency does not provide exact protection, these patients still have a risk of contracting malaria. However, using primaquine, which is the only radical cure of Plasmodium infections, can induce more severe hemolysis by generating oxyhemoglobin, GSH depletion and Heinz bodies and enhancing oxidative attack. This threatens the lives of patients with G6PD deficiency. Hence, patients with malaria should be screened for their tendency to G6PD deficiency before their treatment with antimalarial drugs. Common methods that are used for diagnosing G6PD deficiency are unreliable. Even worse is that it is very difficult to distinguish heterozygously-deficient patients from healthy individuals. Additionally, current methods cannot accurately indicate hemolysis, even though they give information about activity of the enzyme. Also, these methods do not determine primaquine sensitivity in patients with G6PD deficiency every time. However, the method that we developed provides the determination of primaquine sensitivity in patients with G6PD deficiency *in vitro* independently from the variants of G6PD deficiency. The principle of the method is based on the quantitative detection of hemolysis by incubation of erythrocytes obtained from G6PD-deficient patients with primaquine in low hematocrit while rotating the culture in a hybridization oven for 2 hours at 37°C. By considering primaquine-induced hemolysis in patients with G6PD deficiency, it can be determined whether these patients may be treated with primaquine or not. The advantages of this method are that it can determine the primaquine-sensitivity in patients with G6PD deficiency before treatment with primaquine. Using this method not only on G6PD deficiency patients but also on patients that suffer from other diseases that may cause

primaquine-induced hemolysis constitutes another advantage of the method.


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**Chapter 5** 

© 2012 Naik et al., licensee InTech. This is an open access chapter distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

and reproduction in any medium, provided the original work is properly cited.

© 2012 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution,

**Role and Function** 

P. Naik, S. Prasad and L. Cucullo

http://dx.doi.org/10.5772/48338

**1. Introduction** 

brain disorders.

**of Dehydrogenases in CNS** 

Additional information is available at the end of the chapter

**and Blood-Brain Barrier Pathophysiology** 

Dehydrogenase (DHO) is one of the most common types of enzyme that is crucial in oxidation reactions. This enzyme oxidizes its specific substrate by a redox reaction in which one or more hydrides (H−) are transferred to an electron acceptor. Apart from energetics and ATP formation, DHOs are associated with both catabolic and anabolic pathways linked to normal functioning and homeostasis. In this chapter, we will cover different aspects of the major DHOs that play a role in the regulation of brain and bloodbrain barrier (BBB) physiology starting from their role in bioenergetic metabolism. In born errors in metabolism (IEM) due to genetic deficiency in a single specific DHO have strong neurological implications. We will be covering some examples of such IEMs in this chapter. Furthermore, aging processes can impair the function or activity of DHOs. Recent studies show convincing evidence associating altered DHO activity with the pathogenesis and progression of several neurological disorders such as Alzheimer's and Parkinson's disease. Whether they are contributors to the etiology of the disease or symptomatic manifestation of these complex neurological disorders is still debatable; however, this link between DHOs and neurological disorders cannot be overlooked and will be further discussed in this chapter. We will also cover neuronal signaling, neurotransmitter release and degradation emphasizing localized region-specific expression of some brain DHOs in these processes. It is not possible to cover the detailed cerebral physiology and function in this chapter; however to summarize we will discuss the different types of DHOs in central nervous system (CNS) and BBB physiology, their key enzymatic action, their function in crucial metabolic pathways, and thus how their altered activity or expression can be linked to the underlying pathogenesis of various

