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Vitamin poisoning

Arnrich, 1978). Marie and See (1954) have described the symptoms of acute vitamin poisoning in children, vomiting, drowsiness, and bulging of the fontanelle. Table 1 documents that adults tend to complain of severe headaches, vertigo, abdominal pain, vomiting. [Pg.174]

Covalent synthesis of complex molecules involves the reactive assembly of many atoms into subunits with aid of reagents and estabUshed as well as innovative reaction pathways. These subunits are then subjected to various reactions that will assemble the target molecule. These reaction schemes involve the protection of certain sensitive parts of the molecule while other parts are being reacted. Very complex molecules can be synthesized in this manner. A prime example of the success of this approach is the total synthesis of palytoxin, a poisonous substance found in marine soft corals (35). Other complex molecules synthesized by sequential addition of atoms and blocks of atoms include vitamin potentially anticancer KH-1 adenocarcinoma antigen,... [Pg.206]

The hver of sharks and other oily fishes sometimes accumulate toxic levels of vitamin A, and cases of acute poisoning have been reported both among Eskimos and the Japanese. [Pg.481]

Shipping vitamin D in crystalline or resin form should be done in containers marked appropriately to indicate the material is toxic by DOT standards. Its proper DOT labeling is DOT Hazard Class 6.1, poisonous. Waste material should be burned or placed in an appropriate landfill. [Pg.132]

Approximately 200 kg/yr of Vitamin formulations are also marketed as rat poisons. The metaboUtes of vitamin and synthetic derivatives are... [Pg.140]

The isoprene-derived molecule whose structure is shown here is known alternately as Coumarin and warfarin. By the former name, it is a widely prescribed anticoagulant. By the latter name, it is a component of rodent poisons. How can the same chemical species be used for such disparate purposes The key to both uses lies in its ability to act as an antagonist of vitamin K in the body. [Pg.254]

Check parathyroid hormone (PTH), vitamin D and precursors, magnesium, and phosphate levels ° Pharmacological causes of decreased ionized calcium may include excess infusions of citrate, EDTA, lactate, fluoride poisoning, foscarnet, cinacalcet, bisphosphates, or unrelated increase in serum phosphate or decrease in serum magnesium levels... [Pg.161]

While the human body can remove an excess of any water-soluble vitamin, excesses of fat-soluble vitamins are more serious. Early arctic explorers discovered that the Inuit regarded seal liver and polar bear liver as taboo and must not be eaten. Those explorers who ignored this advice risked retinol poisoning as the livers of both these species are rich in retinol (vitamin A) that can not be excreted. The effects of retinol poisoning are extremely unpleasant. It is for this reason that fortification with fat-soluble vitamins is not likely to be undertaken. [Pg.46]

Acute toxicity of paraquat in the domestic chicken was highly responsive to nutritional selenium status and not to Vitamin E status. As little as 0.01 mg Se/kg ration protected 8-day-old chicks against acute paraquat poisoning (Combs and Peterson 1983). Paraquat administered to chickens by way of diet was less toxic than the same amount administered in drinking water (Fletcher 1967). [Pg.1175]

Treatment — Patients should be decontaminated immediately prior to treatment using the decontamination method presented in Section 7.3.3. The Lilly Cyanide Antidote Kit contains amyl nitrite, sodium nitrite, and sodium thiosulfate. Dimeth-ylaminophenol, cobalt-edetate, or vitamin B12a are alternative antidotes for cyanide poisoning.5... [Pg.87]

The metabolism of cyanide has been studied in animals. The proposed metabolic pathways shown in Figure 2-3 are (1) the major pathway, conversion to thiocyanate by either rhodanese or 3-mercapto-pyruvate sulfur transferase (2) conversion to 2-aminothiazoline-4-carboxylic acid (Wood and Cooley 1956) (3) incorporation into a 1-carbon metabolic pool (Boxer and Richards 1952) or (4) combining with hydroxocobalamin to form cyanocobalamin (vitamin B12) (Ansell and Lewis 1970). Thiocyanate has been shown to account for 60-80% of an administered cyanide dose (Blakley and Coop 1949 Wood and Cooley 1956) while 2-aminothiazoline-4-carboxylic acid accounts for about 15% of the dose (Wood and Cooley 1956). The conversion of cyanide to thiocyanate was first demonstrated in 1894. Conversion of cyanide to thiocyanate is enhanced when cyanide poisoning is treated by intravenous administration of a sulfur donor (Smith 1996 Way 1984). The sulfur donor must have a sulfane sulfur, a sulfur bonded to another sulfur (e.g., sodium thiosulfate). During conversion by rhodanese, a sulfur atom is transferred from the donor to the enzyme, forming a persulfide intermediate. The persulfide sulfur is then transferred... [Pg.74]

MushettCW, Kelley KL, Boxer GE, etal. 1952. Antidotal efficacy of vitamin B12 (hydroxo-cobalamin) in experimental cyanide poisoning. Proc Soc Exp Biol Med 81 234-247. [Pg.261]

Vitamin Bg deficiency, iron deficiency, and lead poisoning all can cause anemia. These three conditions are summarized and compared in Ihble 1-17-6. [Pg.254]


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See also in sourсe #XX -- [ Pg.183 ]

See also in sourсe #XX -- [ Pg.306 ]




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