World Journal of
Pharmaceutical and Life Sciences

( An ISO 9001:2015 Certified International Journal )

An International Peer Reviewed Journal for Pharmaceutical and Life Sciences
An Official Publication of Society for Advance Healthcare Research (Reg. No. : 01/01/01/31674/16)
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*Ohadoma S. C., Lawal B. A. S., Udoh Ekaette S. and Eban L. K.


The hexose monophosphate pathway also called the pentose phosphate pathway occurs in the cytosol of a cell, and includes two irreversible oxidative reactions, followed by a seriesof reversible sugar–phosphate interconversions (Larry, 2015). No adenosine triphosphate(ATP) is directly consumed or produced in this cycle, instead two reduced nicotinamide adenine dinucleotide phosphates(NADPHs) are produced for each glucose 6-phosphate molecule entering the oxidativepart of the pathway (Larry, 2015). The rate and direction of the reversible reactions of the pentosephosphate pathway are determined by the supply of and demand for intermediates of the cycle(Chayen et al.,1986; LeBlanc, 2008; Larry, 2015). The pathway provides a major portion of the body’s NADPH, which functions as biochemical reductant. It also produces ribose 5-phosphate, required for the biosynthesis of nucleotides, and provides a mechanism for the metabolic use of 5-carbonsugars obtained from the diet or the degradation of structural carbohydrates (Larry, 2015).The oxidative portion of the pentose phosphate pathway consists of three reactions that lead to the formation of ribulose 5-phosphate, CO2, and two molecules of NADPH for each molecule of glucose 6-phosphate oxidized (Lehninger et al., 2008; Larry 2015). This portion of the pathway isparticularly important in the liver, lactating mammary glands, and adipose tissue, whichare active in the NADPH-dependent biosynthesis of fatty acids.Also in the testes,ovaries, placenta, and adrenal cortex, which are active in the NADPH-dependentbiosynthesis of steroid hormones; and in red blood cells, whichrequire NADPH to keep glutathione reduced (Larry, 2015).Thus NADPH production is regulated by the relative levels of NADP and NADPH, which alter the activity of glucose-6-phosphate dehydrogenase enzyme (Lehninger et al., 2008). All of the HMP enzymes after the 6-phosphogluconate dehydrogenase step are fully reversible. These enzymes allow for the synthesis of ribose-5-phosphate from the glycolytic intermediates fructose-6-phosphate and glyceraldehyde-3-phosphate, and the conversion of ribose-5-phosphate into glycolytic intermediates (Lehninger et al., 2008; Larry, 2015). NADPH (and therefore the hexose monophosphate pathway) is part of the mechanism that red blood cells use to prevent oxygen-mediated damage to their membranes and proteins, and to maintain haemoglobin in the oxidation state required for oxygen transport (Larry, 2015). Experimental studies by Chayen et al., 1986, showed thatHMP activity is also high in mature RBCs, the lens and cornea, all of which need NADPH for reduced glutathione production; which in turn protects them from oxidative damage. An erythrocytic deficiency in Glucose-6-Phosphate deficiency can cause an increase in the concentration of methemoglobin, which is a decrease in the amount of reduced glutathione, an increase in hydrogen peroxide (H2O2), and increased fragility of red blood cell membranes (LeBlanc , 2008; Larry, 2015). The net result is haemolysis, which can be exacerbated when patients are given excessive amounts of oxidizing agent drugs such as Aspirin or sulfonamide antibiotics. On the other hand, a relative deficiency of Glucose-6-Phosphate in erythrocytes may protect some persons from certain parasitic infestations (e.g., falciparum malaria), since the parasites that cause this disease require NADPH for its survival cycle (LeBlanc,2008; Larry, 2015).

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