Effect of superoxide dismutase, allopurinol and glucocorticoids on liver and lung metallothionein induction by endotoxin in the rat

Abstract

Liver and lung metallothionein (MT) levels were increased by endotoxin. The administration of superoxide dismutase (SOD) or allopurinol (ALLO) before (30-60 min) or after (24-32 h) the endotoxin treatment either increased or did not affect the effect of endotoxin on MT levels, depending on the particular treatment and tissue. SOD and ALLO also increased liver and lung MT levels in control rats. In contrast, liver MT levels tended to be decreased by the glucocorticoid prednisolone (PRED) when administered before the endotoxin and were significantly decreased when it was administered after endotoxin. The effect of PRED on lung MT levels was completely different, since it decreased the effect of endotoxin when injected before the lipopolysaccharide, but increased it when injected after the endotoxin. Liver lipid peroxidation, as measured by thiobarbituric acid reactants (TBARs), increased after endotoxin in the liver but not in the lung, an effect even potentiated in some cases by the antioxidants studied. As expected, tissue MT and TBARs could not be correlated.

Involvement of PI3K/Akt and p38 MAPK in the induction of COX-2 expression by bacterial lipopolysaccharide in murine adrenocortical cells

“…LPS is known to enhance the formation of reactive oxygen species and lipid peroxidation products in different tissues and cell types (Giralt et al, 1993;Nowak et al, 1993) mainly by promoting mitochondrial dysfunction (Noble et al, 2007) and/or the activation of NADPH oxidase (Lee et al, 2012). In turn, increase formation of free radicals has been linked to the activation of the stress-sensitive p38 MAPK (McCubrey et al, 2006;Torres and Forman, 2003).…”