Phosphorus Physiological action

The physiological action of phosphorus.—Yellow phosphorus was formerly used largely in the preparation of lucifer matches, and the workman exposed to the fumes suffered from necrosis or rotting of the bones of the upper and particularly of the lower jaw—phossy-jaw. The use of red phosphorus and improved hygienic conditions have done much to minimize the risks of chronic phosphorus poisoning. 

Physiological Action.—Phosphorus in oil or emulsified in fat and chalk has been used in medicine, but appears to have no particular value. However, a preparation made by exposing finely divided iron to the vapours of smouldering phosphorus is useful as an application to wounds caused by corrosive concentrated carbolic acid. 

The myotic, toxic and other physiological properties of the dialkyl phosphorofluoridates, POF(O.R)2, have been fully described on pp. 42, 68 et seq. In 19444 we described an analogous compound of the phosphorofluoridite series, namely, diethyl phosphorofluoridite, PF(OEt)2. This could not be prepared by the action of sodium fluoride on the corresponding diethyl phosphorochloridite (the preparation of which is considered below). We obtained it, however, by the action of ethyl alcohol on phosphorus dichlorofluoride,... 

Hopf2 concludes that although insect nerve tissues produce substances that simulate acetylcholine and a cholinesterase which is inhibited by organo-phosphorus insecticides, these substances (in locusts at any rate) are not antagonized by atropine. Furthermore, tubocurarine does not poison insects, although it is active in warm-blooded animals and affects the neuromuscular junctions (see pp. 36, 37). In short, different physiological mechanisms appear to be at work in insects. In particular, it seems that acetylcholine, when injected into a variety of insects, has no marked toxic action. It seems then that, in some... 

Physiological Effects.—Phosphorus introduced into the etomaeh of animals acts as a cans tic poison. According to ORfila, the corrosion depends on the formation of phosphorous add, by the oxidation of phosphorus in the pulmonary canal, and the action of this acid upon the tissue with which it comes in contact. It is very rarely used in medicine, though it has been strongly recommended in oases attended with... 

Vitamin D, along with parathyroid hormone and calcitonin, plays a primary role in calcium and phosphorus homeostasis in the body. Intensive research efforts over the past several years have elucidated a role for vitamin D in many other physiological processes as well. The biological actions of this seco-steroid are mediated primarily through the action of its polar metabolite, 1,25-dihydroxy vitamin D3 (l,25(OH)2D3). There is emerging evidence that l,25(OH)2D3 has many more target tissues than those involved in its classical role in the control of mineral metabolism. In addition, some of the actions of l,25(OH)2D3 may be mediated by mechanisms other than the classical steroid-receptor interaction. In this chapter we will provide a brief overview of the multiple actions of vitamin D3 and the pleiotropic mechanisms by which these actions are accomplished. 

The parathyroid hormone regulates ionic calcium homeostasis in extracellular fluids by a direct action on the skeleton. It also promotes the renal excretion of phosphorus and produces other physiological effects which are not obviously related to its calcemic action. 

Phosphate balance in adults is almost always zero, in contrast to calcium balance, which is usually negative, because of the effective action of PTH on renal tubules to block Pi reabsorption. In late life, however, intestinal phosphate absorption decreases and the serum phosphate concentration declines. These physiological decrements may contribute to disease, especially to increased bone loss and osteopenia or more severe osteoporosis. Typically, these changes in Pi balance are also accompanied by similar changes in calcium balance. Too little dietary phosphorus and too little dietary calcium may be determinants of low bone mass and density and, hence, increased bone fragility. The usual scenario invoked to explain osteoporosis in old age, however, is that too little dietary calcium in the presence of adequate dietary phosphorus stimulates PTH release and bone loss (Figure 1). 

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