Since the mid-1980s, a 'mysterious' wasting disease has been afflicting the moose (Alces alces L.) population of south-western Sweden. In 1994, molybdenosis combined with copper deficiency was suggested as the cause of this complex syndrome of clinical signs, diversity of necropsy findings and changes in trace element concentrations. These findings were corroborated by scientists in many countries by similar observations in other ruminants, particularly cattle and sheep, and also by changes in trace element concentrations and clinical chemical findings in our model experiments with goats. The biochemistry of copper is dependent on a number of copper-dependent enzymes in the animal organism. An important example is cytochrome c oxidase (COX), responsible for oxidative phosphorylation and energy production within the cell. In the present study, COX activity and trace element concentrations were determined in myocardium from affected and healthy moose. Citrate synthase (CS) activity was also measured for use as a mitochondrial marker. COX activity had decreased by 45% and the COX/CS ratio by 37%, while Mo and Na were found to have increased by 140% and 25%, respectively. The increase in Na was indicative of the frequently reported oedematous changes in 'flabby' moose heart. The concentrations of the elements Cu, Mg, Mn, P and Zn had decreased by 20%, 20%, 35%, 7% and 19%, respectively. The simultaneous decrease in COX activity and Cu concentration and the increase in Mo further support the hypothesis that molybdenosis is the cause of the moose disease.