Glutathione protects heavy metal-induced inhibition of hepatic microsomal ethoxyresorufin O-deethylase activity in Dicentrarchus labrax L.

The in vitro effects of chromium (Cr(VI)), copper (Cu2+), iron (Fe2+), mercury (Hg2+), and zinc (Zn2+) were assessed on liver microsomal ethoxyresorufin O-deethylase (EROD) activity from a sea bass (Dicentrarchus labrax L.) preexposed under laboratory conditions to 2.7 μM β-naphthoflavone. The reduced glutathione (GSH) protection potential against heavy metal effects was also studied. The heavy metal concentration ranges used for this study were as follows: 10 pM–5 mM Cr(VI), 10 pM–100 μM Cu2+, 10 pM–1 mM Fe2+, 10 pM–10 μM Hg2+, and 10 pM–100 μM Zn2+. Liver microsomal EROD activity was significantly inhibited after in vitro exposure to Cr(VI) (500 μM), Cu2+ (1 μM), Fe2+ (100 μM), Hg2+ (100 pM), and Zn2+ (10 μM). Heavy metals inhibitory effect on liver EROD activity was ordered as follows: Hg2+>Cu2+>Zn2+>Fe2+>Cr(VI). Protective effects against Hg2+ (1 and 10 μM), Cu2+ (1, 10, and 100 μM), and Zn2+ (10, 50, and 100 μM) were observed in the presence of 0.5 mM GSH by a decrease in liver microsomal EROD activity inhibition. However, 0.5 mM GSH did not protect liver microsomal EROD activity from Cr(VI), and Fe2+-induced inhibition. The effect of metal mixtures (Cu2++Zn2+, Zn2++Fe2+, Zn2++Cr(VI), and Cr(VI)+Fe2+) (100 μM) on liver microsomal EROD activity was also assessed, revealing a synergistic interaction.