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Hepatic and renal oxidative stress in acute toxicity of N-nitrosodiethylamine in rats.
Indian J Exp Biol ; 2000 Sep; 38(9): 916-20
Artigo em Inglês | IMSEAR | ID: sea-58700
ABSTRACT
Nitrosoamines such as N-nitrosodiethylamine (NDEA) produce oxidative stress due to generation of reactive oxygen species and may alter antioxidant defence system in the tissues. NDEA was administered ip as a single dose to rats in LD50 or in lower amounts and the animals were sacrificed after 0-48 hr of treatment. The results showed that lipid peroxidation in liver increased, however no significant increase in kidney LPO was observed after NDEA administration. Superoxide dismutase (SOD) and glutathione reductase (GSH-R) activity increased in liver, however, catalase (CAT) activity in liver was inhibited in NDEA treated rats. Kidney showed an increase in SOD activity after an initial decrease along with increase in GSH-R activity in NDEA treated rats. However, kidney CAT activity was not significantly altered in NDEA intoxicated rats. Serum transaminases, serum alkaline phosphatase blood urea nitrogen, serum creatinine and scrum proteins were elevated in NDEA treated rats. The results indicate NDEA-induced oxidative stress and alteration in antioxidant enzymes in liver and kidney to neutralise oxidative stress.
Assuntos
Texto completo: DisponíveL Índice: IMSEAR (Sudeste Asiático) Assunto principal: Tamanho do Órgão / Ratos / Baço / Superóxido Dismutase / Nitrogênio da Ureia Sanguínea / Masculino / Proteínas Sanguíneas / Peroxidação de Lipídeos / Catalase / Substâncias Reativas com Ácido Tiobarbitúrico Idioma: Inglês Revista: Indian J Exp Biol Ano de publicação: 2000 Tipo de documento: Artigo

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Texto completo: DisponíveL Índice: IMSEAR (Sudeste Asiático) Assunto principal: Tamanho do Órgão / Ratos / Baço / Superóxido Dismutase / Nitrogênio da Ureia Sanguínea / Masculino / Proteínas Sanguíneas / Peroxidação de Lipídeos / Catalase / Substâncias Reativas com Ácido Tiobarbitúrico Idioma: Inglês Revista: Indian J Exp Biol Ano de publicação: 2000 Tipo de documento: Artigo