Liver microsomal parameters related to oxidative stress and antioxidant systems in hyperthyroid rats subjected to acute lindane treatment

Liver microsomal parameters related to oxidative stress and antioxidant systems in hyperthyroid rats subjected to acute lindane treatment

Autor Giavarotti, KAS Google Scholar
Rodrigues, L. Google Scholar
Rodrigues, T. Google Scholar
Junqueira, VBC Google Scholar
Videla, L. A. Google Scholar
Instituição Univ Chile
Universidade de São Paulo (USP)
Universidade Federal de São Paulo (UNIFESP)
Resumo Liver microsomal functions related to xenobiotic biotransformation and free radical production were studied in control rats and in animals subjected to L-3,3',5-triiodothyronine (T-3) and/or lindane administration as possible mechanisms contributing to oxidative stress, in relation to the activity of enzymes (superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glucose-6-phosphate dehydrogenase (G-6PDH) and content of lipid-soluble vitamins (alpha-tocopherol, beta-carotene, and lycopene) affording antioxidant protection. Lindane treatment in euthyroid rats at a dosage of 20 mg/kg did not modify the content of liver microsomal cytochromes P450 and b(5), the activity of NADPH-cytochrome P450 reductase and NADH-cytochrome b(5) reductase, and the production of superoxide radical (O-2(.-)), as well as antioxidant systems, except for the reduction in lycopene levels. Hyperthyroidism elicited a calorigenic response and increased specific and molecular activities of NADPH-cytochrome P450 reductase, O-2(.-) generation, and G-6PDH activity, concomitantly with diminution in liver SOD and catalase activities and in alpha-tocopherol, beta-carotene, and lycopene levels. the administration of Lindane to hyperthyroid animals led to a further increase in the molecular activity of NADPH-cytochrome P450 reductase and in the O-2(.-) production/SOD activity ratio, and decrease of hepatic alpha-tocopherol content, in a magnitude exceeding the sum of effects elicited by the separate treatments, as previously reported for reduced glutathione depletion. Collectively, these data support the contention that the increased susceptibility of the liver to the toxic effects of acute lindane treatment in hyperthyroid state is conditioned by potentiation of the hepatic oxidative stress status.
Palavra-chave hyperthyroidism
lindane
oxidative stress
microsomal functions
antioxidant enzymes
antioxidant vitamins
Idioma Inglês
Data de publicação 1998-01-01
Publicado em Free Radical Research. Reading: Harwood Acad Publ Gmbh, v. 29, n. 1, p. 35-42, 1998.
ISSN 1071-5762 (Sherpa/Romeo, fator de impacto)
Publicador Harwood Acad Publ Gmbh
Extensão 35-42
Fonte http://dx.doi.org/10.1080/10715769800300051
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000075637800005
Endereço permanente http://repositorio.unifesp.br/handle/11600/25847

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