Evaluation of kidney and liver subacute toxicity induced by Bezalip-Pravastatin-Lopid antihyperlipidaemic compounds in rats.
Biochem Mol Biol Int
; 47(3): 519-28, 1999 Mar.
Article
en En
| MEDLINE
| ID: mdl-10204089
ABSTRACT
Renal and hepatic subacute toxicity induced by the antihyperlipidaemic drugs Bezalip-Pravastatin and Lopid was investigated in rats using serum biochemical parameters. Toxicological evaluation was performed in serum samples following the administration of the therapeutic dose regimens of the compounds that were previously shown to be effective in inhibition of 3-hydroxy-methylglutaryl coenzyme A (HMG CoA) reductase, the enzyme controlling the rate-limiting step in the synthesis of cholesterol, and acyl-CoA cholesterol acyl transferase (ACAT) which converts intracellular free cholesterol to cholesterol ester. Renal and hepatic subacute toxicity was evaluated by measuring enzyme activity or concentrations of alanine aminotransferace, alkaline phosphatase, aspartate aminotransferase, gamma-glutamyltransferase, glucose, potassium, sodium, blood urea nitrogen, uric acid and creatinine. The use of the above serum biochemical parameters indicated that the overall toxicity impact of antihyperlipidaemic drugs was Bezalip = Pravastatin < Lopid. We have found that the Pravastatin--in contrast to the above antihyperlipidaemic drugs--only transiently affects the biochemical parameters associated with toxicity, but, it affects some of the biochemical parameters associated with hepatic and renal toxicity, up to a significantly lower extent than the antihyperlipidaemic drugs.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Bezafibrato
/
Gemfibrozilo
/
Pravastatina
/
Riñón
/
Hígado
/
Antihipertensivos
Límite:
Animals
Idioma:
En
Revista:
Biochem Mol Biol Int
Asunto de la revista:
BIOLOGIA MOLECULAR
/
BIOQUIMICA
Año:
1999
Tipo del documento:
Article
País de afiliación:
Grecia
Pais de publicación:
ENGLAND
/
ESCOCIA
/
GB
/
GREAT BRITAIN
/
INGLATERRA
/
REINO UNIDO
/
SCOTLAND
/
UK
/
UNITED KINGDOM