TY - JOUR
T1 - Heavy metals and glutathione metabolism in mussel tissues
AU - Canesi, L.
AU - Viarengo, A.
AU - Leonzio, C.
AU - Filippelli, M.
AU - Gallo, G.
PY - 1999/6
Y1 - 1999/6
N2 - Data are presented on the tissue glutathione content and on the activity of two of the main enzymes involved in GSH metabolism (γ-glutamyl-cysteine synthetase (GCS), GSH transferase (GST)) in the gills and digestive gland of mussels (Mytilus galloprovincialis Lam.) exposed for 1, 4 and 7 days to sublethal concentrations of copper and of mercury, both in the inorganic form of HgCl2 and in the organic form of CH3HgCl. The results indicate that Cu2+ (0.6 μM) and CH3Hg+ (0.2 μM) can affect, although to a different extent, glutathione metabolism in mussel tissues; common traits were a decrease in tissue glutathione content, stimulation of GST activity and inhibition of GSH synthesis rate; on the other hand, inorganic Hg2+ (0.2 μM) did not significantly affect glutathione content and metabolism in mussel tissues. Exposure to copper (0.6 μM) resulted in a decrease in total glutathione content in both gills and the digestive gland that was maximal after the first day, followed by a tendency to recover at longer exposure times. Such a decrease seemed to be mainly related to a stimulation of GST activity, which was transient in gills and persistent in the digestive gland. The tissue glutathione content was also decreased in mussel exposed to methylmercury (0.2 μM); however, such a decrease seemed to be mainly due to inhibition of the GSH synthesis rate and, to a lesser extent, to an increased GST activity. On the contrary, inorganic Hg2+ (0.2 μM) did not significantly affect glutathione metabolism, although mussel exposure to the same concentration of organic and inorganic Hg2+ resulted in similar total metal tissue load in mussel tissues. The role of glutathione as a potential defense against heavy metals is discussed in relation to different routes of metal toxicity and homeostasis in mussel tissues. Copyright (C) 1999 Elsevier Science B.V.
AB - Data are presented on the tissue glutathione content and on the activity of two of the main enzymes involved in GSH metabolism (γ-glutamyl-cysteine synthetase (GCS), GSH transferase (GST)) in the gills and digestive gland of mussels (Mytilus galloprovincialis Lam.) exposed for 1, 4 and 7 days to sublethal concentrations of copper and of mercury, both in the inorganic form of HgCl2 and in the organic form of CH3HgCl. The results indicate that Cu2+ (0.6 μM) and CH3Hg+ (0.2 μM) can affect, although to a different extent, glutathione metabolism in mussel tissues; common traits were a decrease in tissue glutathione content, stimulation of GST activity and inhibition of GSH synthesis rate; on the other hand, inorganic Hg2+ (0.2 μM) did not significantly affect glutathione content and metabolism in mussel tissues. Exposure to copper (0.6 μM) resulted in a decrease in total glutathione content in both gills and the digestive gland that was maximal after the first day, followed by a tendency to recover at longer exposure times. Such a decrease seemed to be mainly related to a stimulation of GST activity, which was transient in gills and persistent in the digestive gland. The tissue glutathione content was also decreased in mussel exposed to methylmercury (0.2 μM); however, such a decrease seemed to be mainly due to inhibition of the GSH synthesis rate and, to a lesser extent, to an increased GST activity. On the contrary, inorganic Hg2+ (0.2 μM) did not significantly affect glutathione metabolism, although mussel exposure to the same concentration of organic and inorganic Hg2+ resulted in similar total metal tissue load in mussel tissues. The role of glutathione as a potential defense against heavy metals is discussed in relation to different routes of metal toxicity and homeostasis in mussel tissues. Copyright (C) 1999 Elsevier Science B.V.
KW - GSH transferase
KW - Glutathione
KW - Heavy metals
KW - Mussel
KW - γ-Glutamyl-cysteine synthetase
UR - https://www.scopus.com/pages/publications/0032955780
U2 - 10.1016/S0166-445X(98)00116-7
DO - 10.1016/S0166-445X(98)00116-7
M3 - Article
SN - 0166-445X
VL - 46
SP - 67
EP - 76
JO - Aquatic Toxicology
JF - Aquatic Toxicology
IS - 1
ER -