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After 1 h of CCl<jats:sub>4<\/jats:sub> treatment, rats were in glucose and pancreatic hormone balance but plasma levels of T<jats:sub>3<\/jats:sub> and T<jats:sub>4<\/jats:sub> were decreased 29 and 22%, respectively. After 24 hours of CCl<jats:sub>4<\/jats:sub> treatment, rats were: hypoglycaemic and insulin and glucagon levels were increased 33\u2010 and 35\u2010fold, respectively; total T<jats:sub>4<\/jats:sub> levels were decreased 62%; while total T<jats:sub>3<\/jats:sub> levels were normalized. In liver fractions from CCI<jats:sub>4<\/jats:sub>\u2010treated rats, 1 h after CCl<jats:sub>4<\/jats:sub> administration: (i) calcium binding was decreased 65% in the mitochondrial fraction, 66% in the endoplasmic reticular fraction and 46% in the plasma membrane fraction; (ii) calcium uptake was decreased 59% in the mitochondrial fraction, 46% in the endoplasmic reticular fraction and 37% in the plasma membrane fraction. After 24 h of CCl<jats:sub>4<\/jats:sub> administration: (i) calcium binding was decreased 57% in the mitochondrial fraction, 50% in the endoplasmic reticular fraction and 71% in the plasma membrane fraction; (ii). calcium uptake was decreased 55% in the mitochondrial fraction, 17% in the endoplasmic reticular fraction and 53% in the plasma membrane fraction. <jats:italic>In vitro<\/jats:italic> studies indicated the plasma membrane calcium transport system to be rapidly (within a minute) and strongly (&gt;90%) inhibited by CCl<jats:sub>4<\/jats:sub>. We conclude that CCl<jats:sub>4<\/jats:sub> produces a differential inhibitory effect on the hepatoctye calcium pumps that are implicated with hepatocellular damage. 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