In lead poisoning

Ercal N University of Missouri, Rolla, MO The adjunctive use of NAC to enhance the effectiveness of chelation-oriented therapies in lead poisoning National Institute of Environmental Health Sciences... [Pg.360]

Chisolm JJ Jr, Harrison HC, Eberlein WR, et al. 1955. Aminoaciduria, hypophosphatemia, and rickets in lead poisoning Study of a case. Am J Dis Child 89 159-168. [Pg.502]

Goldberg AM, Meredith PA, Miller S, et al. 1978. Hepatic drug metabolism and heme biosynthesis in lead-poisoned rats. Br J Pharmacol 62 529-536. [Pg.526]

Hermes-Lima M, Pereira B, Bechara EJH. 1991. Are free radicals involved in lead poisoning Xenobiotica 21 1085-1090. [Pg.532]

Kline TS. 1960. Myocardial changes in lead poisoning. Am J Dis Child 99 48-54. [Pg.539]

Maranelli G, Apostoli P. 1987. Assessment of renal function in lead poisoned workers. Occup Environ Chem Hazards 344-348. [Pg.547]

Millar JA, Cummings RLC, Battistini V, et al. 1970. Lead and delta-aminolevulinic acid dehydratase levels in mentally retarded children and in lead-poisoning in suckling rats. Lancet 2 695-698. [Pg.550]

Hunter, B. and G. Wobeser. 1980. Encephalopathy and peripheral neuropathy in lead-poisoned mallard ducks. [Pg.333]

For the treatment of poisoning, a selective antidote (which antagonises the action) may be given e.g., nalorphine and naloxone in case of morphine poisoning, atropine in case of anticholinergic drugs, dimercaprol in mercury and penicillamine in lead poisoning, etc. [Pg.50]

It is primarily indicated in lead poisoning. It is also useful in iron, zinc, copper, manganese and radioactive metal but not mercury poisoning. [Pg.397]

Formation of porphobilinogen The dehydration of two molecules of ALA to form porphobilinogen by 8-aminolevulinic acid dehydrase is extremely sensitive to inhibition by heavy metal ions (see Figure 21.3, and p. 279). This inhibition is, in part, responsible for the elevation in ALA and the anemia seen in lead poisoning. [Pg.277]

Detoxication of Metals. Pectins or pectin derivatives have been proposed as antidotes for heavy metal poisoning for nearly 200 years. Kertesz (9) has reviewed the early work in this area. Pectin complexes lead so strongly as to quantitatively remove it from solution. Absorption 6f lead, arsenic, and selenium by several animal species has been reduced by pectin- or apple-containing diets. Use of pectin as a prophylactic agent in lead poisoning continues to be of interest. Bondarev (88) recently reported an increase in excretion and a decrease in bone accumulation of lead when rats fed 6 mg/day of lead also received 72-432 mg/day of low ester pectin. Paskins-Hurlburt et al. (89) achieved an 87% decrease in lead absorption by pectate fed rats. These studies bear out the early observations of Fellenburg (see 9, p. 572), who concluded that pectin of decreased ester content would have an enhanced ability to complex metals. [Pg.123]

B-7) (B-7) Pyrimidine S -nucleotidase deficiency. RNA, in this condition, can not be completely degrad in maturing red blood cells. The nucleotides of uridine and cytidine accumulate. This is associated with a hemolytic anemia. In lead poisoning, lead inhibits 5 -nucleotidase and a1.< o mav result in an atieojia. In both... [Pg.59]

The principle toxicity of EDTA relates to the metal chelate, especially in lead poisoning. Lead may be released from the chelate in the kidneys, and then the lead may affect the tubules and glomeruli of the kidneys. [Pg.958]

EDTA Backup in lead poisoning, then for rarer toxicities (Cd, Cr, Co, Mn, Zn)... [Pg.299]

Glyceraldehyde-3-phosphate dehydrogenase, an enzyme in the glycolytic pathway (Chapter 8), is inactivated by alkylation with iodoacetate. Enzymes that use sulfhydryl groups to form covalent bonds with metal cofactors are often irreversibly inhibited by heavy metals (e.g., mercury and lead). The anemia in lead poisoning is caused in part because of lead binding to a sulfhydryl group of fer-rochelatase. Ferrochelatase catalyzes the insertion of Fe2+ into heme. [Pg.179]

Mendelsohn AL, Dreyer BP, Fierman AH, et al Low-level lead exposure and cognitive development in early childhood. J Dev Behav Pediatr 20 425-431, 1999 Milar CR, Schroeder SR, Mushak P, et al Failure to find hyperactivity in preschool children with moderately elevated lead burden. J Pediatr Psychol 6 85-95,1981 Millar JA, Battistini V, Cumming RL, et al Lead and delta-aminolevulinic acid dehydratase levels in mentally retarded children and in lead-poisoned suckling rats. Lancet 2 695-698, 1970... [Pg.143]

Wilson V, Thomson ML, and Dent, CE. Amino-aciduria in lead poisoning. A case in childhood. Lancet 1953 66-68. [Pg.503]

Lead is a nephrotoxin, so in lead poisoning renal function is usually severely compromised and hypertension is a cardinal feature. Perinatal exposure to lead can give rise to hypertension in later life. When large groups of patients with relatively low... [Pg.156]

ALA dehydratase, which contains zinc, and ferrochelatase are inactivated by lead. Thus, in lead poisoning, 8-ALA and protoporphyrin IX accumulate, and the production of heme is decreased. Anemia results from a lack of hemoglobin, and energy production decreases because of the lack of cytochromes for the electron transport chain. [Pg.811]

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