Enhanced resistance of adriamycin-treated MCR-5 lung fibroblasts by increased intracellular glutathione peroxidase and extracellular antioxidants.
Considerable evidence indicates that reactive oxygen species play an etiological role in both cardiotoxicity and the skin necrosis induced by adriamycin (ADM). An increase in glutathione peroxidase activity on addition of selenium to cultured MCR-5 lung fibroblasts was observed; this increase was accompanied by enhanced cellular resistance to ADM toxicity. Moreover, the presence of exogenous antioxidant systems, such as superoxide dismutase, catalase, vitamin E, dimethylsulfoxide, and desferroxamine, an iron chelating agent, resulted in significant protection from ADM-mediated damage.
Vanella
A
A
Faculty of Pharmacy, University of Catania, V.le A. Doria, 6, Catania, 95125, Italy. CHIMBIO@ICTUNIV.UNICT.IT
Campisi
A
A
di Giacomo
C
C
Sorrenti
V
V
Vanella
G
G
Acquaviva
R
R
D000903:Antibiotics, Antineoplastic / Q000633:toxicity*; D000975:Antioxidants / Q000494:pharmacology*; D002478:Cells, Cultured; D003676:Deferoxamine / Q000494:pharmacology; D004317:Doxorubicin / Q000633:toxicity*; D005347:Fibroblasts / Q000187:drug effects; D005979:Glutathione Peroxidase / Q000096:biosynthesis*; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008168:Lung / Q000187:drug effects; D012643:Selenium / Q000494:pharmacology
D000903:Antibiotics, Antineoplastic; D000975:Antioxidants; D004317:Doxorubicin; D007770:L-Lactate Dehydrogenase; D005979:Glutathione Peroxidase; D012643:Selenium; D003676:Deferoxamine