RESUMO
We have used a new sensitive and non-invasive method, measuring exhaled pentane production, to evaluate in vivo lipid peroxidation (LP) in rats treated i.p. with CdCl2. Pentane, a by-product of LP, was measured 2, 6, 12, 24, 72 h and 8, 15, 22 days after treatment. No increase in pentane production was detected at these time periods for cadmium (Cd) doses reported to increase malondialdehyde (MDA) in major organs such as liver and lungs. This suggests that Cd cannot induce LP in vivo, but a prooxidant state which fragilized the tissues. Cd could also cause changes either in the production or in the metabolism of LP by-products (e.g. pentane).
Assuntos
Cádmio/toxicidade , Cloretos/toxicidade , Peroxidação de Lipídeos/efeitos dos fármacos , Pentanos/metabolismo , Animais , Testes Respiratórios , Cádmio/administração & dosagem , Cloreto de Cádmio , Cloretos/administração & dosagem , Injeções Intraperitoneais , Fígado/efeitos dos fármacos , Pulmão/efeitos dos fármacos , Masculino , Ratos , Testículo/efeitos dos fármacosRESUMO
Lipid peroxidation (LPO), measured as thiobarbituric acid reactive substances (TBARS), was evaluated in lungs of rats 24 h after intraperitoneal injection of 50, 250, and 1000 micrograms Cd/kg body weight as CdCl2. In order to gain some insight into possible causative factors responsible for these oxidative phenomena, the redox-active elements iron (Fe) and copper (Cu), and total lung protein content (an indication of pulmonary inflammatory processes) were also measured. Results obtained demonstrate a similar dose-related, non-linear evolution of total lung TBARS and total lung protein as a function of increasing lung Cd concentrations. Standardization of total lung TBARS to lung protein content further resulted in a linear relationship with lung Cd concentrations, thus suggesting a possible cause-effect relationship between these parameters. No statistically significant association was observed between the dose-related evolution of lung TBARS, and iron (Fe) and copper (Cu) after Cd exposure. The results obtained provide support for the possible involvement of inflammatory phenomena as the most likely events responsible for the generation of LPO in lung tissue following acute exposure to Cd salts.