Inhibition of goldfish mitochondrial metabolism by in vitro exposure to Cd, Cu and Ni.
Although impairment of aerobic capacities has been reported in metal-contaminated wild fish, little is known about the direct toxicity of the metals themselves at the low concentrations found in the field compared to indirect consequences mediated by metal effects on ecological variables such as prey type and abundance, predation and competition. This study examined the in vitro effects of Cd, Cu and Ni on mitochondrial enzyme activity and maximal (State 3) mitochondrial oxygen consumption rate in goldfish (Carassius auratus) tissues at concentrations representative of values reported in wild metal-contaminated fish. There was little effect of adding metals to liver or muscle homogenates on the activity of citrate synthase (CS), although a slight inhibition of liver CS was observed at the highest Cd concentration tested. In contrast, adding high concentrations of Ni to muscle homogenates increased muscle CS activity. Unlike CS, the metalloenzyme cytochrome C oxidase (CCO) was quite sensitive to metal additions; its activity was consistently enhanced by all three metals tested. When added to liver mitochondrial preparations, both Cd and Cu strongly inhibited State 3 respiration. In contrast, Ni did not affect mitochondrial respiration even at the highest concentration tested. Taken together, these results demonstrate that low concentrations of Cd, Cu and Ni have toxic effects on mitochondrial metabolism and enzyme activities and suggest that the inhibition of aerobic capacities frequently reported for wild metal-contaminated fish is at least partly due to metal effects on mitochondrial function, although the mechanisms probably do not involve direct enzyme inhibition.
Garceau
Nicolas
N
Institut National de la Recherche Scientifique, Centre - Eau Terre Environnement, 490 rue de la Couronne, Québec, QC, Canada G1K 9A9.
Pichaud
Nicolas
N
Couture
Patrice
P
D000818:Animals; D002104:Cadmium / Q000633:toxicity*; D002950:Citrate (si)-Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D003300:Copper / Q000633:toxicity*; D004305:Dose-Response Relationship, Drug; D003576:Electron Transport Complex IV / Q000037:antagonists & inhibitors / Q000378:metabolism; D004781:Environmental Exposure / Q000009:adverse effects*; D004791:Enzyme Inhibitors / Q000633:toxicity; D006054:Goldfish / Q000378:metabolism*; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008928:Mitochondria / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D009532:Nickel / Q000633:toxicity*; D014874:Water Pollutants, Chemical / Q000633:toxicity*
D004791:Enzyme Inhibitors; D014874:Water Pollutants, Chemical; D002104:Cadmium; D003300:Copper; D009532:Nickel; C117108:cytochrome C oxidase subunit II; D003576:Electron Transport Complex IV; D002950:Citrate (si)-Synthase