RESUMEN
The effect of Li(I) on the metabolism of mitochondria isolated from Carassius auratus liver tissue was investigated by microcalorimetric method to provide evidence for mitochondria hypothesis of bipolar disorder (BPD) and to explore therapeutic mechanism of drug for treatment of BPD. Obvious stimulation induced by Li(I) on mitochondria metabolism was reflected by power-time (P-t) curves. The power-time curves of hepatic mitochondria metabolism without Li(I) could be divided into four parts: lag phase, active recovery phase, stationary phase, and decline phase. When Li(I) was added, the second heat peak occurred in a concentration-dependent sequence. Considering the first heat peak on the P-t curves, Li(I) in the range of therapeutic and lower concentration induced slight alterations in comparison with the characteristic heat peak observed in the control. However, Li(I) above the therapeutic concentration resulted in significant changes. Heat output increased with the concentration of Li(I), but the rate constant (k2) and the maximum heat power (Pmax2) for the second heat peak reached maximum value in the range of therapeutic concentration. Mechanism of activation of mitoKatp was suggested and discussed.