Boron

Abstract

Boron is the only nonmetal in a family otherwise comprised of active metals, Group IlIA of the periodic table. As expected, boron exhibits bonding and structural characteristics intermediate to both. Like carbon (atomic number 6), boron (atomic number 5) has a tendency to form double bonds and macromolecules. In addition, there are several features that are more or less unique to boron and this group of elements. These include electron-deficient molecules (such as boron trifluoride) and bridge bonds (such as those in diborane, B2H6)' These tendencies have formed the basis for the many hypotheses attempting to predict the mode of action of boron as a nutrient essential to the metabolism of vascular plants (Section 17.2.1), as a toxicant to animals (Section 17.1.5), and for achieving boron accumulation in cancer cells (Section 17.1.8).In this chapter the biochemistry of boron is reviewed predominantly in vascular plants. The discussion is organized around those metabolic processes that boron nutrition repeatedly has been shown to influence: carbohydrate metabolism, hormone action, membrane structure and function, and nucleic acid biosynthesis.17.1.

Dietary boron as a physiological regulator of the normal inflammatory response: A review and current research progress

“…The source of the NADPH for the respiratory burst comes mainly from the reduction of NADP + in the pentose-phosphate (P-P) pathway, which is very active during the respiratory burst. In plants, one substrate of the P-P pathway, 6-phosphogluconate, is known to complex with boron, which thereby inhibits 6-phosphogluconate dehydrogenase (PGD), a key enzyme in the P-P pathway [12]. Thus a serious problem in boron-deficient plants is an increase in the amount of substrate metabolized via the P-P pathway, which gives rise to overabundant synthesis of phenolic compounds and subsequent death of plants in the subclass Dicotyledoneae [12].…”

“…In plants, one substrate of the P-P pathway, 6-phosphogluconate, is known to complex with boron, which thereby inhibits 6-phosphogluconate dehydrogenase (PGD), a key enzyme in the P-P pathway [12]. Thus a serious problem in boron-deficient plants is an increase in the amount of substrate metabolized via the P-P pathway, which gives rise to overabundant synthesis of phenolic compounds and subsequent death of plants in the subclass Dicotyledoneae [12]. It is reasonable to hypothesize that proper boron nutriture causes a simple reduction in leukocyte ROS generation through down-regulation of leukocyte PGD with subsequent alleviation of the arthritic symptoms.…”

Dietary Boron is a Physiological Regulator of the Normal Inflammatory Response

“…The primary electron donor for the reduction of oxygen during ROS generation is NADPH that comes mainly from reduction of in the pentose-phosphate (P-P) pathway (Klebanoff, 1988). In plants, a substrate in the P-P pathway, 6-phosphogluconate, complexes with boron, which thereby inhibits 6-phosphogluconate dehydrogenase (PGD) (Lovatt and Dugger, 1984). A serious problem in boron-deficient plants is increased substrate metabolism via the P-P pathway that ultimately causes plant death (Lovatt and Dugger, 1984).…”

“…In plants, a substrate in the P-P pathway, 6-phosphogluconate, complexes with boron, which thereby inhibits 6-phosphogluconate dehydrogenase (PGD) (Lovatt and Dugger, 1984). A serious problem in boron-deficient plants is increased substrate metabolism via the P-P pathway that ultimately causes plant death (Lovatt and Dugger, 1984). Therefore, it is reasonable to hypothesize that proper boron nutriture may cause a simple reduction in leukocyte ROS generation through down-regulation of leukocyte PGD with subsequent alleviation of arthritic symptoms.…”

The Biochemical Effects of Physiologic Amounts of Dietary Boron in Animal Nutrition Models

“…In plants, one substrate of the pentose-phosphate pathway, 6-phosphogluconate, is known to complex with boron, which thereby inhibits 6-phosphogluconate dehydrogenase. Thus, in borondeficient plants, there is an increase in the amount of substrate metabolized via the pentose-phosphate pathway, and a decrease in that metabolized via the Krebs cycle (30).…”