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Published in final edited form as: Biochim Biophys Acta. 2013 Sep 21;1840(1):10.1016/j.bbagen.2013.09.018. doi: 10.1016/j.bbagen.2013.09.018

Fig. 3 — Sulforaphane treatment blunts binge-ethanol-induced oxidative stress. Mice were treated with ethanol in the absence or presence of sulforaphane as described in the legend to Fig. 1. A; Hepatic levels of TBARs as a reflection of lipid peroxidation. B; Hepatic levels of GSH. C: Immunohistochemical staining for 3-NT protein adducts in liver. Results for A and B are from 3 experiments. * P< 0.05 for the ethanol –induced increase in TBARs or decrease in GSH compared to saline. ¥ P<0.05 for the effect of sulforaphane on the ethanol-induced changes. Arrows in C point to the pericentral zone of the liver acinus.

Fig. 3 — Sulforaphane treatment blunts binge-ethanol-induced oxidative stress. Mice were treated with ethanol in the absence or presence of sulforaphane as described in the legend to Fig. 1. A; Hepatic levels of TBARs as a reflection of lipid peroxidation. B; Hepatic levels of GSH. C: Immunohistochemical staining for 3-NT protein adducts in liver. Results for A and B are from 3 experiments. * P< 0.05 for the ethanol –induced increase in TBARs or decrease in GSH compared to saline. ¥ P<0.05 for the effect of sulforaphane on the ethanol-induced changes. Arrows in C point to the pericentral zone of the liver acinus.