We have reported that selenium (Se) as sodium selenite and/or cadmium (Cd) as cadmium chloride administered intratracheally resulted in increased protein, lactate dehydrogenase and beta-glucuronidase activities in guinea pig lung (Bell et al., 1991). Increase in beta- glucuronidase activity was found to be of a greater magnitude consequent to intratracheal administration of a higher dose of Se (0.9 mg per animal) than Cd of a similar dose (See preliminary report). Measurement of the biochemical parameters mentioned above indicated that acute administration of Se did not offer protection against deleterious effects of Cd; rather, Se itself induced pulmonary cellular damage. Increased peroxidation due to selenite indicated by an increase in organic solvent- soluble lipofuscin pigments has been reported (Csallany and Menken, 1986). However, selenite has been recognized in total parenteral nutrition and is proven to be stable in solutions with pH > 5 (Ganther and Kraus, 1989). Lungs of Se-deficient rats are found to be susceptible to oxidant-induced damage (Cross, et al. 1977). Pulmonary edema, dyspnea and respiratory failure are often the consequences of Se toxicity. In this investigation we propose to study the effects of various Se compounds and Cd on lung enzyme activities, peroxidation, induction of metallothionein, pulmonary mechanics, and significance of dietary Se against damaging effects of acute Se and/or Cd treatment.
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