Blood, toxicity

Florfenicol was believed to be more like thiamphenicol (XI), which appeared to be free of the blood toxicity problems associated with chloramphenicol. The toxicity of chloramphenicol was loosely linked to the presence of the nitro group. Nevertheless, Schering regarded Florfenicol as too risky to develop for human use, leaving the compound to be picked up by Schering s Animal Health Division for use as an animal antibiotic. 

Docampo R, Moreno SN, Gadelha FR, de Souza W, Cruz FS. Prevention of Chagas disease resulting from blood transfusion by treatment of blood toxicity and mode of action of gentian violet. Biomed Environ Sd 1988 1(4) 406-13. 

E.G. Buckley, J.A. Salisbury and R. Machemer, Is blood toxicity to the retina reversible, Surg Forum. 31 4W(1980). 

I6I C. Warfarin baits need contain only 0 025% active principle, and rats are killed after ingesting about 5 doses the bait can be left down and the risk of acute toxicity to man or domestic animals is not serious. In common with other coumarin derivatives, warfarin reduces the clotting power of blood and death is caused by haemorrhages initiated by any slight injury. Warfarin is a vitamin K antagonist, and large oral doses of the vitamin can be given as an antidote. 

Carbon disulphide. When working with this solvent, its toxicity (it is a blood and nerve poison) and particularly its high inflammability should be home in mind. Distillation of appreciable quantities of carbon disulphide should be carried out in a water bath at 55-65° it has been known to ignite from being overheated on a steam bath. 

The term chiral recognition refers to a process m which some chiral receptor or reagent interacts selectively with one of the enantiomers of a chiral molecule Very high levels of chiral recognition are common m biological processes (—) Nicotine for exam pie IS much more toxic than (+) nicotine and (+) adrenaline is more active than (—) adrenaline m constricting blood vessels (—) Thyroxine an ammo acid of the thyroid gland that speeds up metabolism is one of the most widely used of all prescription... 

Formaldehyde, HCHO, is a primary and necessary constituent of the first five synthetic adhesives in the listing. It is a simple organic chemical first identified during the latter half of the 1800s. Its irritating and toxic odor and preservative properties were known from the time of its early development. It is a ubiquitous chemical, formed naturally in small quantities by every process of incomplete combustion as well as in normal biologic processes. The human body has a natural formaldehyde level of about 3 lg/g, ie, 3 parts per million (ppm) in the blood at all times. 

Of the water-soluble vitamins, intakes of nicotinic acid [59-67-6] on the order of 10 to 30 times the recommended daily allowance (RE)A) have been shown to cause flushing, headache, nausea, and moderate lowering of semm cholesterol with concurrent increases in semm glucose. Toxic levels of foHc acid [59-30-3] are ca 20 mg/d in infants, and probably approach 400 mg/d in adults. The body seems able to tolerate very large intakes of ascorbic acid [50-81-7] (vitamin C) without iH effect, but levels in excess of 9 g/d have been reported to cause increases in urinary oxaHc acid excretion. Urinary and blood uric acid also rise as a result of high intakes of ascorbic acid, and these factors may increase the tendency for formation of kidney or bladder stones. AH other water-soluble vitamins possess an even wider margin of safety and present no practical problem (82). 

Several species of the moray eel (Gymnothorax) have caused toxic reactions, especially ki Japan. The toxic principle appears to be protekiaceous and is found predominately ki the blood but it may occur ki the flesh as well. Its exact stmcture remains somewhat uncertain. 

Adverse side effects of gold treatments include stomatitis, rash, and proteinuria. Complete blood counts and urinalysis should be performed before each or every other injection of gold compounds. Pmritic skin rash and stomatitis are more common adverse effects that may resolve, if therapy is withheld for a few weeks and then restarted cautiously at a lower dose. Oral gold causes less mucocutaneous, bone marrow, and renal toxicity than injectable gold, but more diarrhea and other gastrointestinal reactions appear. 

Hexa.cya.no Complexes. Ferrocyanide [13408-63 ] (hexakiscyanoferrate-(4—)), (Fe(CN) ) , is formed by reaction of iron(II) salts with excess aqueous cyanide. The reaction results in the release of 360 kJ/mol (86 kcal/mol) of heat. The thermodynamic stabiUty of the anion accounts for the success of the original method of synthesis, fusing nitrogenous animal residues (blood, horn, hides, etc) with iron and potassium carbonate. Chemical or electrolytic oxidation of the complex ion affords ferricyanide [13408-62-3] (hexakiscyanoferrate(3—)), [Fe(CN)g] , which has a formation constant that is larger by a factor of 10. However, hexakiscyanoferrate(3—) caimot be prepared by direct reaction of iron(III) and cyanide because significant amounts of iron(III) hydroxide also form. Hexacyanoferrate(4—) is quite inert and is nontoxic. In contrast, hexacyanoferrate(3—) is toxic because it is more labile and cyanide dissociates readily. Both complexes Hberate HCN upon addition of acids. 

The alimentary symptoms may be overshadowed by neuromuscular dysfunction, accompanied by signs of motor weakness that may progress to paralysis of the exterior muscles or the wrist (wrist drop), and less often, of the ankles (foot drop). Encephalopathy, the most serious result of lead poisoning, frequendy occurs in children as a result of pica, ie, ingestion of inorganic lead compounds in paint chips this rarely occurs in adults. Nephropathy has also been associated with chronic lead poisoning (147). The toxic effects of lead may be most pronounced on the developing fetus. Consequendy, women must be particulady cautious of lead exposure (148). The U.S. Center for Disease Control recommends a blood level of less than 10 p.m per 100 mL for children. 

Reviews on the occurrence, biochemical basis, and treatment of lead toxicity in children (11) and workers (3,12,13) have been pubhshed. Approximately 17% of all preschool children in the United States have blood lead levels >10 //g/dL. In inner city, low income minority children the prevalence of blood lead levels >10 //g/dL is 68%. It has been estimated that over two million American workers are at risk of exposure to lead as a result of their work. PubHc health surveillance data document that each year thousands of American workers occupationally exposed to lead develop signs and symptoms indicative of... 

Lead is toxic to the kidney, cardiovascular system, developiag red blood cells, and the nervous system. The toxicity of lead to the kidney is manifested by chronic nephropathy and appears to result from long-term, relatively high dose exposure to lead. It appears that the toxicity of lead to the kidney results from effects on the cells lining the proximal tubules. Lead inhibits the metaboHc activation of vitamin D in these cells, and induces the formation of dense lead—protein complexes, causing a progressive destmction of the proximal tubules (13). Lead has been impHcated in causing hypertension as a result of a direct action on vascular smooth muscle as well as the toxic effects on the kidneys (12,13). 

Lead is known to cause reproductive and developmental toxicity. Decreased sperm counts and abnormal sperm development have been reported in male workers heavily exposed to lead. Increased incidences of spontaneous abortion have been reported in female lead workers as well as in the wives of male lead workers (13). Lead crosses the placenta and has been found to cause irreversible neurologic impairment to the fetus at maternal blood levels as... 

Fig. 43. Schematic of a hoUow-fiber artificial kidney dialyser used to remove urea and other toxic metaboUtes from blood. Several million of these devices...

---