Zn(II)–curcumin protects against hemorheological alterations, oxidative stress and liver injury in a rat model of acute alcoholism

• Heavy alcohol consumption can lead to oxidative stress and zinc deficiency.
• Curcumin can chelate metal ions, forming metallocomplexes.
• We investigated the effects of Zn(II)–curcumin in a rat model of acute alcoholism.
• Zn(II)–curcumin prevented oxidative stress, hemorheological abnormalities and liver injury.
• Zn(II)–curcumin exerted a more potent, synergistic protective effect than curcumin.

Curcumin can chelate metal ions, forming metallocomplexes. We compared the effects of Zn(II)–curcumin with curcumin against hemorheological alterations, oxidative stress and liver injury in a rat model of acute alcoholism. Oral administration of Zn(II)–curcumin dose-dependently prevented the ethanol-induced elevation of serum malondialdehyde (MDA) content and reductions in glutathione level and superoxide dismutase (SOD) activity. Zn(II)–curcumin also inhibited ethanol-induced liver injury. Additionally, Zn(II)–curcumin dose-dependently inhibited hemorheological abnormalities, including the ethanol-induced elevation of whole blood viscosity, plasma viscosity, blood viscosity at corrected hematocrit (45%), erythrocyte aggregation index, erythrocyte rigidity index and hematocrit. Compared to curcumin at the same dose, Zn(II)–curcumin more effectively elevated SOD activity, ameliorated liver injury and improved hemorheological variables. These results suggest that Zn(II)–curcumin protected the rats from ethanol-induced liver injury and hemorheological abnormalities via the synergistic effect of curcumin and zinc.

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