Abstract
Menaquinone is essential in electron transport and ATP generation in all Gram-positive, and anaerobically respiring Gram-negative bacteria. By inhibiting menaquinone production in target organisms, bactericidal action can be achieved irrespective of the organisms' growth phase. This pathway is absent in human cells, as menaquinone is obtained only through the diet. This paper provides a succinct review of major advancements, where present, at all enzymatic steps of the biosynthetic pathway of menaquinone. Structure–activity relationships are evaluated, as well as results translating these relationships to growth inhibition studies.
Highlights
Menaquinone is essential in electron transport and ATP generation in all Gram-positive, and anaerobically respiring Gram-negative bacteria
Menaquinone (MK, 1) (Fig. 1) plays an important role in electron transport in all Gram-positive, and anaerobically respiring Gram-negative bacteria.[1,2,3,4,5,6]. It is the primary form of electron transport between NADH dehydrogenase II, succinate dehydrogenase, cytochrome bc[1] complex, as well as nitrate and fumarate reductase enzymes, which are present in the bacterial cell membrane
The synthesis of 1 by bacteria is a seven-step process (Scheme 1) which starts with chorismate (3), a branch-point intermediate supplied by the shikimate pathway.[1,2,6,13,14,15]
Summary
Menaquinone (MK, 1) (Fig. 1) plays an important role in electron transport in all Gram-positive, and anaerobically respiring Gram-negative bacteria.[1,2,3,4,5,6] It is the primary form of electron transport between NADH dehydrogenase II, succinate dehydrogenase, cytochrome bc[1] complex, as well as nitrate and fumarate reductase enzymes, which are present in the bacterial cell membrane In these steps, MK (1) is reduced by two electrons to produce menaquinol (MKH2 (2)) and shuttles these electrons to an acceptor in the step of the chain.[7] This substrate oxidation process provides the energy needed to maintain the proton gradient and potential energy used by the F0F1ATPase complex to convert ADP into ATP. MK's (1) role in humans is not completely understood, it is hypothesised that 1 is utilised to produce clotting factors if phylloquinone (vitamin K1) is unavailable.[10,11,12]
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