PRACA POGLĄDOWA
Wybrane problemy związane ze środowiskowym narażeniem na metale ciężkie a terapia chelatująca
 
Więcej
Ukryj
1
Department of Internal Medicine and Hypertension Wroclaw University of Medicine Head: prof. Ryszard Andrzejak, MD, PhD
AUTOR DO KORESPONDENCJI
Anna Skoczynska   

Wrocław University of Medicine Pasteur 4, PL 50-367 Wrocław, Poland
 
Med Srod. 2010;13(3):62–67
SŁOWA KLUCZOWE
STRESZCZENIE ARTYKUŁU
Wstęp:
Istotnym aspektem przewlekłej ekspozycji na działanie metali ciężkich jest ich udział w patogenezie chorób o znaczeniu społecznym (nadciśnienia tętniczego, miażdżycy, chorób neuro-degeneracyjnych). W tym kontekście niezbędne są nowe strategie profilaktyczne i terapeutyczne. Osoby z rozpoznaniem przewlekłego zatrucia metalami ciężkimi zazwyczaj wymagają stosowania chelatorów w celu zwiększenia mobilizacji metali z tkanek i eliminacji ich z moczem. Ostre zatrucie metalami toksycznymi może być trudne do zdiagnozowania, szczególnie powstałe przypadkowo lub w celach samobójczych. Po zidentyfikowaniu czynnika sprawczego, pacjenci także wymagają chelatowania.

Cel:
Przedstawienie wybranych problemów związanych z toksycznością metali ciężkich i przegląd terapii farmakologicznych stosowanych u osób z objawami zatrucia.

Materiał i metody:
Przegląd piśmiennictwa i opinii ekspertów

Wyniki/wnioski:
Chelatowanie jest powszechnym sposobem terapii osób z rozpoznanym zatruciem metalami ciężkimi, ale jest to sposób skuteczny tylko częściowo. Obiecującym sposobem leczenia jest terapia złożona z zastosowaniem chelatorów o różnej budowie lub działających długoterminowo. U pacjentów z objawami przewlekłego zatrucia metalami ciężkimi korzystne jest stosowanie terapii złożonej chelatorem i antyoksydantem. Ekspozycja na działanie ołowiu powinna być czynnikiem uwzględnianym w szacowaniu całkowitego ryzyka sercowo naczyniowego.


Background:
Exposure to heavy metals leads to functional and metabolic disturbances and many of them are included in pathogenesis of common diseases (arterial hypertension, atherosclerosis, neurodegenerative processes). In this context new therapeutic and prophylactic strategies are necessary. Patients diagnosed with chronic heavy metals intoxication usually require chelation to increase mobilisation of metals from tissues and elimination of them via urine. Acute poisoning with toxic metal may be difficult to diagnosis, especially in case of accidental intoxication or suicidal intention. Patients also require chelation after causative factor is identified.

Objectives:
To describe some problems connected with toxicity of metals poisoning and to review pharmacologic therapies that could have a role in poisoning with metals.

Methods:
A review of the literature was carried out and expert opinion expressed.

Results/conclusion:
Chelation is a common therapy in case of poisoning with toxic metals but it is satisfied only partially. A combined therapy with structurally different chelators or long-term acting chelators could become viable alternatives in the future. A combined therapy with an antioxidant plus chelator may be a good choice in patients chronically poisoned with metals. Exposure to lead should be taken into account during estimation of global cardiovascular risk.

 
REFERENCJE (35)
1.
Fischbein A. Occupational and environmental exposure to lead. In: Rom WN, editor. Environmental and occupational medicine. 3rd ed. Philadelphia: Lippincott-Raven; 1998:973- 96.
 
2.
Adult blood lead epidemiology and surveillance — United States, 2002. MMWR Morb Mortal Wkly Rep 2004;53:578- 82.
 
3.
Dunbabin DW, Tallis GA, Popplewell PY, at al. Lead poisoning from Indian herbal medicine (Ayurveda) Med J Aust 1992;157:835-6.
 
4.
Roche A, Florkowski C, Walmsley T. Lead poisoning due to ingestion of Indian herbal remedies. N Z Med J 2005;118:U1587.
 
5.
Product recalls. Recalls: a bad summer for toys from China but risks should be kept in perspective. Child Health Alert 2007;25:5-6.
 
6.
US Centers for Disease Control and Prevention (CDC). Third national report on human exposure to environmental chemicals. Atlanta: CDC; 2005.
 
7.
Schroeder HA, Balassa JJ. Influence of chromium, cadmium, and lead on rat aortic lipids and circulating cholesterol. Am J Physiol 1965;209:433-437.
 
8.
Victery W. Evidence for effects of chronic lead exposure on blood pressure in experimental animals: an overview. Environ Health Perspect 1988;78:71-76.
 
9.
Chai S, Webb RC. Effects of lead on vascular reactivity. Environ Health Perspect 1988;78:85-89.
 
10.
Carmignani M, Volpe AR, Boscolo P, at al. Catcholamine and nitric oxide systems as targets of chronic lead exposure in inducing selective functional impairment.Life Sci 2000;68:401-15.
 
11.
Skoczynska A, Stojek E. The impact of subchronic lead poisoning on the vascular effect of nitric oxide in rats. Environ Toxicol Pharmacol 2005;19:99-106.
 
12.
Chang HR, Tsao DA, Yu HS, at al. The change of betaadrenergic system after cessation of lead exposure. Toxicology 2005;207:73-80.
 
13.
Skoczynska A, Andrzejak R, Turczyn B. Urinary activity of tubular enzymes in rats poisoned simultaneously with lead and cadmium. Metal Ions Biol Med 1998;5:661-665.
 
14.
Skoczynska A, Martynowicz H, Por´ba R, at al. Urinary trehalase as marker of renal dysfunction in workers occupationally exposed to lead. Med Pracy 2001;52:247-252.
 
15.
Sakai T. Biomarkers of lead exposure. Ind Health 2000;38:127-42.
 
16.
Suzen HS, Duydu Y, Avdin A, at al. Influence of the deltaaminolewulinic acid dehydratase (ALAD) polymorphism on biomarkers of lead exposure in Turkish storage battery manufacturing workers. Am J Ind Med 2003;43:165-71.
 
17.
Alexander BH, Checkoway H, Costa-Mallen P, at al. Interaction of blood lead and delta-aminolevulinic acid dehydratase genotype on markers of heme synthesis and sperm production in lead smelter workers. Environ Health Perspect 1998;106:213-6.
 
18.
Duydu Y, Dur A, Suzen HS. Evaluation of increased proportion of cells with unusually high sister chromatid exchange counts as a cytogenetic biomarker for lead exposure. Biol Trace Elem Res 2005;104:121-9.
 
19.
Weaver VM, Schwartz BS, Ahn KD, at al. Associations of renal function with polymorphisms in the delta-aminolevulinic acid dehydratase, vitamin D receptor, and nitric oxide synthase genes in Korean lead workers. Environ Health Perspect 2003;111:1613-19.
 
20.
Lee BK, Lee GS, Stewart WF, at al. Associations of blood pressure and hypertension with lead dose measures and polymorphisms in the vitamin D receptor and delta-aminolevulinic acid dehydratase genes.Environ Health Perspect 2001;109:383-9.
 
21.
Schwartz J. Lead, blood pressure, and cardiovascular disease in men and women. Environ Health Perspect 1991;91:71-75.
 
22.
Micciolo R, Canal L, Maranelli G, at al. Non-occupational lead exposure and hypertension in northern Italy. Int J Epidemiol 1994;23:312-320.
 
23.
Ding Y., Vaziri N.D., Gonick H.C. Lead – induced hypertension. II. Response to sequential infusions of L-arginine, superoxide dismutase, and nitroprusside. Environ Res 1998;76:107-113.
 
24.
Malvezzi C.K., Moreira E.G., Vassilieff I, at al. Effect of Larginine, DMSA and the association of L-arginine and DMSA on tissue lead mobilization and blood pressure level in plumbism. Braz J Med Biol Res 2001; 34:1341-1346.
 
25.
Tsao D., Yu H.S., Cheng J.T., at al. The change of beta-adrenergic system in lead-induced hypertension. Toxicol Appl Pharmacol 2000;164:127-133.
 
26.
Morisi G, Menditto A, Spagnolo A, at al. Association of selected social, environmental and constitutional factors to blood lead levels in men aged 55-75 years. Sci Total Environ 1992;126:209-229.
 
27.
Vaziri ND, Ding Y, Ni Z. Compensatory up-regulation of nitric oxide synthase isoforms in lead-induced hypertension; reversal by a superoxide dismutase-mimetic drug. J Pharm Exp Ther 2001;298:679-685.
 
28.
Ding Y, Vaziri ND, Gonick HC. Lead – induced hypertension. II. Response to sequential infusions of L-arginine, superoxide dismutase, and nitroprusside. Environ Res1998;76:107-113.
 
29.
Skoczynska A, Por´ba R, Derkacz A. Endothelial dysfunction in workers exposed to lead. In: Atherosclerosis: risk factors, diagnosis and treatment. Monduzzi Editore, International Proceedings Division, Salzburg, July 7-10, 2002;77-81.
 
30.
Skoczynska A, Martynowicz H, Rupnik A, at al. Glycosaminoglycans content in the organs of rats chronically treated with lead. Metal Ions Biol Med 2004;8:364-367.
 
31.
Brodkin E, Copes R., Mattman A., at al. Lead and mercury exposures: interpretation and action. CMAJ. 2007;176:59-63.
 
32.
Kalia K, Narula GD, Kannan GM, at al. Effects of combined administration of captopril and DMSA on arsenite induced oxidative stress and blood and tissue arsenic concentration in rats. Comp Biochem Physiol C Toxicol Pharmacol 2007;144:372-9.
 
33.
Skoczynska A, Kwiecinska D, Kielbinski M, at al. Acute iron poisoning in adult female. Hum Exp Toxicol 2007;26:663- 666.
 
34.
Flora SJ, Pande M, Bhadauria S, at al. Combined administration of taurine and meso 2, 3-dimercaptosuccinic acid in the treatment of chronic lead intoxication in rats. Hum Exp Toxicol 2004;23:157-66.
 
35.
Flora SJ, Pande M, Kannan GM, at al. Lead induced oxidative stress and its recovery following co-administration of melatonin or N-acetylcysteine during chelation with succimer in male rats. Cell Mol Biol (Noisy-le-grand) 2004; 50.
 
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