Phosphate remineralization

Nitrate versus phosphate concentrations at 2500 m in the (a) Atlantic, (b) Indian, and (c) Pacific Oceans. Dissolved oxygen versus phosphate concentrations at 2500 m in the (d) Atlantic, (e) Indian, and (f) Pacific Oceans. The slopes of these lines represent the proportions by which these constituent concentrations are altered by the remineralization of POM in the deep sea. These data are replotted from Figure 10.1. Source From Conkright, M. E., et al. (2002). World Ocean Atlas 2001, Volume 4 Nutrients, NOAA Atlas NESDIS 52,... 

Because phosphate is released during remineralization with no decrease in O2, the A02/AP0 produced via denitrification should be lower than that predicted by the aerobic respiration of Redfield-Richards planktonic detritus. To reach the suboxic conditions required for denitrification requires the aerobic respiration of a considerable amount of POM and, hence, release of phosphate. Thus, A02/AP0 ratios less than 138 are most likely to be found in waters with high phosphate concentrations. The prevalence of denitrification in deep waters is suggested by their low (14.7) average N-to-P ratio (Figure 8.3). Areas where the OMZ are pronoimced, such as coastal upwelling areas, have particularly low N-to-P ratios as shown in Figure 10.7. 

As illustrated in Figure 10.8, surfece-water phosphate and nitrate concentrations are uniformly low at aU latitudes below 45°. In contrast, high-latitude surface waters are characterized by much higher concentrations. This causes the phosphate concentration in new NADW to range from 0.7 to 0.9 pM and 1.8 to 2.0 pM in AABW. As the water masses sink and travel through the ocean basins, their phosphate concentrations increase as sinking POM is remineralized. Thus, the phosphate concentration at any... 

Assuming Redfield-Richards behavior, i.e., the aerobic respiration of planktonic detritus, the concentration of remineralized phosphate can be estimated from AOU/138. 

Preformed phosphate represents an important component of the dissolved phosphate reservoir. This is seen in the relatively low ratio of remineralized to preformed phosphate, which ranges from 0.36 to 0.70. Based on the Broecker Box model presented in Chapter 9, only about 1% of the phosphate escapes from the ocean on any given mixing cycle to become buried in the sediments. So to a first approximation, only 36 to 70% of the phosphate in a deepwater mass originates from remineralization. (The wide range in percentage reflects geographic variability related to the age of the water... 

Phosphate is remineralized during the oxidation of organic matter and dissolution of hard parts, such as bones and teeth, that are composed of the minerals hydroxyapatite and fluoroapatite. Unlike the other products of remineralization, pore-water phosphate concentrations are regulated only by mineral solubility, such as through vivianite (iron phosphate) and francolite (carbonate fluoroapatite). Redox reactions are not significant because phosphorus exists nearly entirely in the h-5 oxidation state. 

The iron-based redox cycle depicted in Figure 18.9 provides an effective preconcentrating step for phosphorus by trapping remineralized phosphate in oxic sediments. The conversion of phosphorus from POM to Fe(lll)OOH to CFA is referred to as sink switching. Overall this process acts to convert phosphorus from unstable particulate phases (POM to Fe(lll)OOH) into a stable particulate phase (CFA) that acts to permanently remove bioavailable phosphorus from the ocean. This is pretty important because most of the particulate phosphate delivered to the seafloor is reminer-alized. Without a trapping mechanism, the remineralized phosphate would diffuse back into the bottom waters of the ocean, greatly reducing the burial efficiency of phosphorus. 

Matthews, J. L., Martin, J. H., Kennedy III, J. W., and Collins, E. J. An ultrastructural study of calcium and phosphate deposition and exchange in tissues. In Hard tissue growth, repair and remineralization (eds. K. Elliott and D. W. Fitzsimons), pp. 187-211. Amster-dam-London-New York Elsevier-Excerpta Medica-North-Holland 1973. 

In general, saliva (as well as plaque fluid) is supersaturated with respect to calcium-phosphate salts, and they prevent tendency to dissolve mineral crystals of teeth. Moreover, precipitation of calcium-phosphate salts that include hydroxyapatite may also occur (remineralization) in early lesions of tooth surfaces injured by acidic bacterial products (i.e., lactic acid). Salivary fluoride facilitates calcium-phosphate precipitation, and such crystals (i.e., fluorapatite) show lower acid solubility properties that lead to an increased caries preventive effect. The increase of pFI (i.e., buffer capacity and pH of saliva, as well as ureolysis in dental plaque) also facilitates crystal precipitation and remineralization (4, 13). 

Fluorine (F) and its metabolites are of importance in protecting teeth from caries. Fluorine is included in calcium hydroxyapatite, and it promotes the precipitation of calcium phosphate Ca(P03)2 and accelerates the remineralization. The necessary concentration of Fluorine added to drinking water to prevent caries is approximately 1 mg/L. Application of higher Fluorine concentrations (above 8 mg/L) leads to fluorosis. This is a disease that is characterized by a disturbance in the function of the thyroid gland. A long-term application of fluorine leads to intensive mineralization (possible precipitation of calcium sulfate), deformation of bones with possible accretion, and calcification of the connections. 

Remineralization of organic N and P results in increases in ammonium and phosphate below the sediment-water interface. The increase in alkalinity is also a result of the decomposition of organic matter either directly (as organic N is remineralized to NH ) or indirectly (as calcite dissolves in response to the release of CO2 associated with remineralization of organic C). In this sediment, the profiles of the redox-active species are not clearly separated. 

Schemehorn BR, Oiban JC, Wood GD, Fischer GM, Winston AE Remineralization by fluoride enhanced with calcium and phosphate ingredients. J Clin Dent 1999 10(1 Spec No) 13-16. 

Reynolds EC Remineralization of enamel subsurface lesions by casein phosphopeptide-stabilized calcium phosphate solutions. J Dent Res 1997 76 1587-1595. 

Mineralization is the precipitation of calcium phosphate, but biochemical mediation of this process is not fully understood. In this chapter, the chemistry underlying mineralization (Sect. 1) and the structures ofbones and teeth (Sect. 2) are described. Osteoblasts secrete osteoid matrix and matrix vesicles that transport type I collagen and calcium phosphate, respectively, to the matrix where they will mineralize. Secreted matrix vesicles take up calcium and phosphate until they burst and release the calcium phosphate, which then redissolves and remineralizes around the type I collagen (Sect. 3). Glycoproteins involved in correctly modeling bone and dentin, and the role of osteocalcin in limiting excessive bone growth is then discussed (Sect. 4). There follows a detailed description of enamel (E) mineralization and of the major proteins involved (Sect. 5) followed by two summaries the difference between enamel and bone mineralization, and the vitamins required for mineralization (Sect. 6). 

Bones are constantly dissolved by osteoclasts and remineralized by osteoblasts in response to mechanical forces. Osteoclasts possess an acidic compartment and pass demineralized bone products to the periosteum (Sect. 1). They develop in stress-induced bony microcracks and are activated by differentiation factors secreted by osteoblasts, especially after menopause. Menopausal osteoporosis is controlled by drugs that are a stable form of pyrophosphate (bisphosphonate) or cathepsin K inhibitors (Sect. 2). The calcium ion concentration of blood is raised by parathyroid hormone and a vitamin D derivative called calcitriol. Parathyroid hormone causes kidneys to excrete phosphate, retain calcium, and activate calcitriol production (Sect. 3). Calcitriol induces calcium transporter proteins in osteoclasts and intestinal epithelium, where they move calcium from bone or diet into blood (Sect. 4). The chapter concludes with a discussion of calcitonin which lowers blood calcium concentrations by reversing parathyroid hormone effects on the kidney and inhibiting osteoclast activity (Sect. 5). 

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