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Titolo:
MECHANISMS OF KIDNEY-CELL INJURY FROM METALS
Autore:
FOWLER BA;
Indirizzi:
UNIV MARYLAND,PROGRAM TOXICOL,660 W REDWOOD ST BALTIMORE MD 21201
Titolo Testata:
Environmental health perspectives
, volume: 100, anno: 1993,
pagine: 57 - 63
SICI:
0091-6765(1993)100:<57:MOKIFM>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
AMINOLEVULINIC-ACID DEHYDRATASE; LEAD-BINDING PROTEIN; INTRANUCLEAR INCLUSION-BODIES; METHYL MERCURY EXPOSURE; LOW-MOLECULAR WEIGHT; RAT-KIDNEY; CADMIUM-METALLOTHIONEIN; PROXIMAL TUBULES; NEPHROPATHY; INHIBITION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
90
Recensione:
Indirizzi per estratti:
Citazione:
B.A. Fowler, "MECHANISMS OF KIDNEY-CELL INJURY FROM METALS", Environmental health perspectives, 100, 1993, pp. 57-63

Abstract

The most environmentally abundant toxic metals/metalloids (arsenic, cadmium, lead, and mercury) are each known to produce cell injury in the kidney but the molecular mechanisms underlying these events are now being elucidated. It is clear that the nephrotoxicity of these agents is due, in part, to the fact th at urinary elimination is a major route of excretion from the body. The role(s) of molecular factors such asmetal-binding proteins, inclusion bodies, and cell-specific receptorlike proteins that appear to influence renal tubule cell expression, have attracted increased interest as determinants that modulate cell populations as special risk for toxicity and renal cancer. The future of mechanistic toxicology studies with regard to how and why only certainrenal cell populations become targets for toxicity from these metals/metalloids and other less common inorganic nephrotoxicants must focus on the molecular handling of these agents by target cell populations.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/12/20 alle ore 14:24:55