RESUMO
To examine the relationship between heavy metal accumulation in mitochondria and their respiration function in fish during in vivo exposure, juvenile Spinibarbus sinensis were exposed to different waterborne cadmium (Cd) concentrations for up to 28 days. We measured the state III respiration rate and cytochrome c oxidase (CCO) activity of mitochondria in hepatopancreas and kidney and the accumulated Cd concentrations in mitochondria and heat-stable protein (HSP) fractions. Dose- and time-dependent Cd accumulation occurred at different levels in both organs, but was lower in hepatopancreas. When hepatopancreas mitochondrial Cd concentrations in Cd-exposed groups were > 5.5 µg/g dwt, their state III respiration rates were significantly lower than the control. CCO activity of hepatopancreas mitochondria exhibited decreasing dose- and time-dependent trends. However, kidney mitochondria respiratory activities were not affected significantly by Cd exposure. Cd concentrations in kidney HSP fraction were 2-5 times higher than in hepatopancreas under all exposure conditions, and were mainly present as non-deleterious metallothionein (MT)-Cd complexes. These results suggest that Cd accumulation occurred in hepatopancreas and kidney mitochondria of S. sinensis following waterborne Cd exposure, which significantly inhibited the respiration function of hepatopancreas mitochondria but did not have a deleterious effect on kidney mitochondria. The inhibitory pattern of hepatopancreas mitochondrial Cd concentrations related to function exhibited threshold and saturation effects, suggesting the capacity of S. sinensis to manage Cd toxicity. The difference in the relative proportion of Cd occurring as MT-Cd complexes in organs likely causes the organ-specific effects of Cd on hepatopancreas and kidney mitochondrial function.