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Et Zucc fruit extract (MCE) against carbon tetrachloride (CCl<jats:sub>4<\/jats:sub>)\u2010induced liver damage was investigated. Pretreatment with 50\u2009mg\u2009kg<jats:sup>\u22121<\/jats:sup>, 150\u2009mg\u2009kg<jats:sup>\u22121<\/jats:sup> or 450\u2009mg\u2009kg<jats:sup>\u22121<\/jats:sup> MCE significantly blocked the CCl<jats:sub>4<\/jats:sub>\u2010induced increase in both serum aspartate aminotransferase (sAST) and serum alanine aminotransferase (sALT) levels in mice (<jats:italic>P<\/jats:italic> &lt; .05 or .01 versus CCl<jats:sub>4<\/jats:sub> group). Ultrastructural observations of decreased nuclear condensation, ameliorated mitochondrial fragmentation of the cristae and less lipid deposition by an electron microscope confirmed the hepatoprotection. The mitochondrial membrane potential dropped from \u2212191.94 \u00b1 8.84\u2009mV to \u2212132.06 \u00b1 12.26\u2009mV (<jats:italic>P<\/jats:italic> &lt; .01) after the mice had been treated with CCl<jats:sub>4<\/jats:sub>. MCE attenuated CCl<jats:sub>4<\/jats:sub>\u2010induced mitochondrial membrane potential dissipation in a dose\u2010dependent manner. At a dose of 150 or 450\u2009mg\u2009kg<jats:sup>\u22121<\/jats:sup> of MCE, the mitochondrial membrane potentials were restored (<jats:italic>P<\/jats:italic> &lt; .05). Pretreatment with MCE also prevented the elevation of intra\u2010mitochondrial free calcium as observed in the liver of the CCl<jats:sub>4<\/jats:sub>\u2010insulted mice (<jats:italic>P<\/jats:italic> &lt; .01 versus CCl<jats:sub>4<\/jats:sub> group). In addition, MCE treatment (50\u2013450\u2009mg\u2009kg<jats:sup>\u22121<\/jats:sup>) significantly increased both transcription and translation of VDAC inhibited by CCl<jats:sub>4<\/jats:sub>. 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