RESUMO
Cardiac subacute toxicity induced by ciprofloxacin (1-cyclopropyl-6-fluoro-1,4-dihydro-4-oxo-7-(1-piperazinyl)-3-quinoline carboxylic acid, CAS 86393-32-0) a relatively new quinolone carboxylic acid derivative with an extensive antibacterial spectrum was investigated in healthy rats using serum biochemical parameters. Toxicological evaluation was performed in serum samples following the administration of the therapeutic dose regimens of the compound. Cardiac subacute toxicity was evaluated by measuring serum enzyme activity of creatine kinase, creatine kinase isoenzyme-MB (muscular-brain), lactate dehydrogenase and aspartate aminotransferase. The serum biochemical parameters indicated that the cardiac subactue toxicity of ciprofloxacin was: Cipro 1.2 (250 mg) = Cipro 2.4 (500 mg) < Cipro 4.3 (750 mg).
Assuntos
Anti-Infecciosos/toxicidade , Ciprofloxacina/toxicidade , Cardiopatias/sangue , Cardiopatias/induzido quimicamente , Animais , Área Sob a Curva , Aspartato Aminotransferases/sangue , Biomarcadores , Peso Corporal/efeitos dos fármacos , Creatina Quinase/sangue , Creatina Quinase Forma MB , Cardiopatias/patologia , Isoenzimas/sangue , L-Lactato Desidrogenase/sangue , Miocárdio/patologia , RatosRESUMO
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.
Assuntos
Anti-Hipertensivos/toxicidade , Bezafibrato/toxicidade , Genfibrozila/toxicidade , Rim/efeitos dos fármacos , Fígado/efeitos dos fármacos , Pravastatina/toxicidade , Alanina Transaminase/sangue , Fosfatase Alcalina/sangue , Animais , Aspartato Aminotransferases/sangue , Inibidores Enzimáticos/toxicidade , Hidroximetilglutaril-CoA Redutases/sangue , Hidroximetilglutaril-CoA Redutases/metabolismo , Masculino , Ratos , Ratos Wistar , gama-Glutamiltransferase/sangueRESUMO
Cardiac subacute toxicity induced by the antineoplastic drugs epirubicin (CAS 56390-09-1), chlorambucil (CAS 305-03-3), cisplatin (CAS 15663-27-1) and methotrexate (CAS 59-05-2) and the steroid alkylating agent 3 beta-hydroxy-13 alpha-amino-13,17-seco-5 alpha-androstan-17-oic-13, 17-lactam ¿p-[bis(2-chloroethyl)amino] phenyl¿ acetate was investigated in rats using serum biochemical parameters. Toxicology evaluation was performed in serum samples following the administration of dose regimens of the agents that were previously shown to be effective in suppressing malignant tumor growth or to prolong survival in tumor-bearing animals. Cardiac subacute toxicity was evaluated by measuring serum enzyme activity of creatine kinase, creatine kinase isoenzyme-MB, lactate dehydrogenase and aspartate aminotransferase. The use of the above serum biochemical parameters indicated that the cardiac subacute toxicity impact of the antitumor drugs was epirubicin "methotrexate = chlorambucil = cisplatin > homo-aza-steroid ester.
Assuntos
Antineoplásicos/toxicidade , Cardiopatias/induzido quimicamente , Cardiopatias/metabolismo , Animais , Antibióticos Antineoplásicos/toxicidade , Antimetabólitos Antineoplásicos/toxicidade , Antineoplásicos Alquilantes/toxicidade , Antineoplásicos Hormonais/toxicidade , Aspartato Aminotransferases/sangue , Peso Corporal/efeitos dos fármacos , Clorambucila/toxicidade , Cisplatino/toxicidade , Creatina Quinase/sangue , Epirubicina/toxicidade , Cardiopatias/enzimologia , Isoenzimas , L-Lactato Desidrogenase/sangue , Metotrexato/toxicidade , RatosRESUMO
Hepatic and renal subacute toxicity induced by the antineoplastic drugs chlorambucil, cisplatin, epirubicin and methotrexate and the steroid alkylating agent 3 beta-hydroxy-13 alpha-amino-13,17-seco-5 alpha-androstan-17-oic-13, 17-lactam (p-[bis(2-chloroethyl) amino] phenyl) acetate was investigated in rats using serum biochemical parameters. Toxicological evaluation was performed in serum samples following the administration of dose regimens of the agents that were previously shown to be effective in suppressing malignant tumor growth or to prolong survival in tumor bearing animals. Hepatic and renal subacute toxicity was evaluated by measuring enzyme activity or concentrations of: alanine aminotransferase, alkaline phosphatase, aspartate aminotransferase, total cholesterol, gamma-glutamyltransferase, glucose, potassium, sodium, blood urea nitrogen and uric acid. The use of the above serum biochemical parameters indicated that the overall toxicity impact of the antitumor drugs was methotrexate < cisplatin < epirubicin < chlorambucil. The homo-azasteroid ester only transiently affected the biochemical parameters associated with renal toxicity, while it affected some of the biochemical parameters associated with hepatic toxicity, though to a significantly lower extent than the antitumor drugs.
