Nicotinamide deficiency

Nicotinamide deficiency leads to pellagra [pelle agra (Italian) = rough skin], which manifests itself in dermatitis (skin rash), pigmentation, a red and inflamed tongue, diarrhea, and weakness. People who consume large amounts of corn in an unbalanced diet are prone to develop the disease. 

Nicotinic acid Supplement nicotinamide deficiency, impaired absorption, increased requirements Therapy pellagra, vasomotoric headache, migraine, schizophrenia... 

Miller EG, Burns H (1984) N-nitrosodimethylamine carcinogenesis in nicotinamide-deficient rats. Cancer Res 44 1478-1482... 

At relatively high X-ray dose rates, the increase in aberration yield, namely dicentric and ring chromosomes (2 hit aberrations) is proportional to the square of the dose. Repair of chromosome breaks occurs within 4 hr after X-irradiation as measured by dose fractionation experiments (9). When a single radiation dose is fractionated into two smaller doses given 5 hr apart, there is time for breaks induced by the first dose to rejoin before the second dose is given. The yield of 2 hit aberrations observed in this case is the sum of the yields of each of the half doses rather than proportional to the total dose, i.e., four times the half dose (10). When, on the other hand, lymphocytes were cultured with 3AB (10), or in nicotinamide deficient medium (11) (thereby eliminating an essential precursor for polymer synthesis), the yield of chromosome dicentrics was proportional to the... 

Fig. 1. (left) Induction of SCE by benzamide in normal and nicotinamide deficient medium. Complete medium consists of nicotinamide-free RPMI-1640 plus 1 g/ml nicotinamide and 5% undialysed human serum. ( ), nicotinamide-free medium ( )nicotinamide added back to the medium. 

The neutral amino acids alanine, serine, threonine, asparagine, glutamine, valine, leucine, isoleucine, phenylalanine, tyrosine, tryptophan, histidine and citrulline share a common transporter at the luminal border of the epithelial cells in the renal tubuli and the epithelial cells in the small intestine [16]. In Hartnup disorder an impairment of this transporter leads to hyperexcretion of these neutral amino acids and to intestinal malabsorption. Excretion of tryptophan metabolites kynurenine and N-methyl-nico-tinamide is reduced. Plasma concentrations of the affected amino acids may be low normal or reduced. The inheritance is autosomal recessive. The hph2-deficient mouse has been postulated as a model for Hartnup disorder [17]. Affected persons may be asymptomatic, while some demonstrate pellagra-like photodermatitis or cerebellar ataxia due to a nicotinamide deficiency and respond well to the administration of nicotinamide [16]. 

An inborn error in which there is defective intestinal and renal transport of neutral amino acids, one of these being tryptophan. This amino acid is normally converted to the vitamin, nicotinamide. The clinical features of Hartnup disease are similar to the nicotinamide deficiency disease, pellagra, being due to the low amounts of tryptophan available for nicotinamide synthesis. The disease can be diagnosed by the presence of large amounts of indole compounds in the urine, which result from the action of gut bacteria on the unabsorbed dietary tryptophan. 

A metabolite of nicotinic acid which can be measured in urine to diagnose nicotinamide deficiency. It can be measured by its reaction with ketones to give a fluorescent compound. 

It can be converted by intestinal flora and probably by the tissues to the vitamin, nicotinamide. A dietary deficiency of tryptophan can therefore result in nicotinamide deficiency if dietary intake of nicotinamide is also low. Symptoms resembling those of nicotinamide deficiency can also occur in the inborn error, Hartnup disease, where body tryptophan levels are reduced due to diminished reabsorption of the amino acid from the renal tubules. 

Metabolism of Tryptophan. The catabolism of tryptophan is interesting since it leads to the biosynthesis of a vitamin, nicotinamide. It appears contradictory to state that a vitamin is formed by an organism, but nicotinamide deficiency can indeed be demonstrated only with the concurrent deficiency of vitamin Be. Tryptophan largely replaces the vitamin even in man. 

In 1913, Goldberger demonstrated that pellagra was due to a dietary deficiency. Pellagra had been eadier described by Thiery, who had coined the term mal de la rosa for this disease. Several decades later, Elvehjem and co-workers isolated nicotinamide from a Hver extract and identified it as a peUagra-preventing factor (1). 

Under conditions of copper deficiency, some methanotrophs can express a cytosolic, soluble form of MMO (sMMO) (20-23), the properties of which form the focus of the present review. The sMMO system comprises three separate protein components which have all been purified to homogeneity (24,25). The hydroxylase component, a 251 kD protein, contains two copies each of three subunits in an a 82y2 configuration. The a subunit of the hydroxylase houses the dinuclear iron center (26) responsible for dioxygen activation and for substrate hydroxylation (27). The 38.6 kD reductase contains flavin adenine dinucleotide (FAD) and Fe2S2 cofactors (28), which enable it to relay electrons from reduced nicotinamide adenine dinucleotide (NADH) to the diiron center in the... 

Nicotinic acid, when given at the rate of several hundred milligrams a day, has pharmacological effects of which cerebral vasodilation is one. Nicotinamide does not have this effect, and hence the pharmacological effects of nicotinic acid probably do not involve simple replacement of a deficiency in an enzyme system. The fact that nicotinic acid itself in pharmacological doses appears to be of Implications for Advance in Psychiatry... 

Niacin, which refers to nicotinic acid and nicotinamide, is the metabolic precursor to three nicotinamide coenzymes. These are essential for the activity of a large number of enzymes catalyzing redox reactions. Pellagra is a niacin deficiency disease. 

Oxidation of nicotine with chromic acid led to the isolation of pyridine-3-carboxylic acid, which was given the trivial name nicotinic acid. We now find that nicotinic acid derivatives, especially nicotinamide, are biochemically important. Nicotinic acid (niacin) is termed vitamin B3, though nicotinamide is also included under the umbrella term vitamin B3 and is the preferred material for dietary supplements. It is common practice to enrich many foodstuffs, including bread, flour, corn, and rice products. Deficiency in nicotinamide leads to pellagra, which manifests itself in diarrhoea, dermatitis, and dementia. 

Nicotinate and nicotinamide, together referred to as niacin, are required for biosynthesis of the coenzymes nicotinamide adenine dinucleotide (NAD"") and nicotinamide adenine dinucleotide phosphate (NADP" ). These both serve in energy and nutrient metabolism as carriers of hydride ions (see pp. 32, 104). The animal organism is able to convert tryptophan into nicotinate, but only with a poor yield. Vitamin deficiency therefore only occurs when nicotinate, nicotinamide, and tryptophan are all simultaneously are lacking in the diet. It manifests in the form of skin damage (pellagra), digestive disturbances, and depression. 

Boron also appears to be involved in redox metabolism in cell membranes. Boron deficiency was shown to inhibit membrane H -ATPase isolated from plant roots, and H -ATPase-associated proton secretion is decreased in boron-deficient cell cultures [71]. Other studies show an effect of boron on membrane electron transport reactions and the stimulation of plasma reduced nicotinamide adenine dinucleotide (NADH) oxidase upon addition of boron to cell cultures [72, 73]. NADH oxidase in plasma membrane is believed to play a role in the reduction of ascorbate free radical to ascorbate [74]. One theory proposes that, by stimulating NADH oxidase to keep ascorbate reduced at the cell wall-membrane interface, the presence of boron is important in... 

Niacin (nicotinic acid, nicotinamide) has the active forms NAD and NADPH. It functions in electron transfer. A deficiency of niacin causes pellagra, which is characterized by der matitis, diarrhea, and dementia. There is no known toxicity for this vitamin. High doses of niacin are used to treat hyperlipidemia. 

Two vitamins, nicotinamide and pyridoxine (vitamin B6), are pyridine derivatives. Nicotinamide participates in two coenzymes, coenzyme I (65 R = H) which is known variously as nicotinamide adenine dinucleotide (NAD) or diphosphopyridine nucleotide (DPN), and coenzyme II (65 R = P03H2) also called triphosphopyridine nucleotide (TPN) or nicotinamide adenine dinucleotide phosphate (NADP). These are involved in many oxidation-reduction processes, the quaternized pyridine system acting as a hydrogen acceptor and hydrogen donor. Deficiency of nicotinamide causes pellagra, a disease associated with an inadequately supplemented maize diet. Nicotinic acid (niacin) and its amide are... 

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