Article,

Molecular defense systems are expressed in the king bolete (Boletus edulis) growing near metal smelters

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Mycologia, 97 (5): 973-983 (September 2005)

Abstract

The induction of defense systems against metal exposure was investigated in 48 wild-growing fruiting bodies of the king bolete (Boletus edulis) from two areas polluted with several transition metals from smelters, as well as five reference areas. To determine the degree of metal exposure, cadmium (Cd), zinc (Zn), and copper (Cu) were determined in caps of fruiting bodies by atomic absorption spectrophotometry (AAS), whereas mercury (Hg) was determined by cold vapor atomic fluorescence spectrometry (CVAFS). Caps were analyzed further with respect to relative activities of the antioxidant enzymes, superoxide dismutase (SOD) and catalase (CAT), as well as concentrations of total glutathione (GSHTOT = GSH + GSSG) and relative concentrations of heat shock protein 70 kDa (HSP70). The results showed that concentrations of the four metals, as well as SOD, CAT and HSP70, were significantly elevated in the exposed group (Mann-Whitney, P < or = 0.001). In contrast, GSHTOT was significantly lowered in the exposed group (P < or = 0.05). Significant positive correlations were established between concentrations of Cd, Zn, Hg, or Cu and activities of SOD (Spearman's P < or = 0.01 for the association between SOD and Cd, P < or = 0.001 for all other metal exposure parameters), CAT (P < or = 0.001 for all exposure parameters), or expression of HSP70 (P < or = 0.001 for all exposure parameters). Significant negative correlations were found between total GSH and Cd (P < or = 0.001), Zn (P < or = 0.001), or Hg (P < or = 0.05). We conclude that antioxidant enzymes are induced in wild-growing B. edulis exposed to environmentally relevant concentrations of potentially toxic transition metals; whereas the net consumption of GSH that occurs with increasing metal exposure may reflect GSH consumption by mechanisms of metal detoxification. Finally, the induction of HSP70 suggests that the antioxidant response and the mechanisms in which GSH is consumed are insufficient for protection against the harmful effects of severe metal stress.

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