Effects of pharmaceutical products and municipal wastewaters on temperature-dependent mitochondrial electron transport activity in Elliptio complanata mussels.
The advent of global warming has given rise to the issue on how temperature impacts the susceptibility of ectothermic organisms to pollution. The purpose of this study was to examine the effects of pharmaceutical products and domestic wastewaters on temperature-dependent mitochondrial electron transport activity in the freshwater mussel Elliptio complanata. Mitochondria from mussels were freshly prepared and exposed to increasing concentrations of various pharmaceutical products known to be found in municipal effluents for 30 min at 4, 12 and 20 degrees C. Electron transport activity as well as lipid peroxidation and DNA strand breaks were determined in the mitochondria. Next, mussels were placed in the aeration lagoons of two municipal wastewater treatment plants for 30 days. Mitochondrial electron transport (MET), temperature-dependent MET (MET(T)) and lipid peroxidation in gonad were then determined. The results show that all products were able to increase MET activity, but at two different ranges of threshold concentration. Certain pharmaceutical products (i.e., ibuprofen, cotinine, fluoxetine, coprostanol and trimethoprim) increased MET(T) at a lower threshold concentration than observed at 20 degrees C. Products of lesser potency in reducing lipid peroxidation were those that produced more DNA strand breaks in mitochondria. Both MET and MET(T) were significantly increased in mussels exposed to aeration lagoon effluents. Lipid peroxidation was also increased in the gonad and was significantly correlated with MET and MET(T) activities. The data indicate that pharmaceutical products and municipal effluents increase respiration rates in isolated mitochondria, such that interaction with temperature could enhance the susceptibility of mitochondrial energy production and oxidative stress in environments contaminated by domestic wastewater.
Gagné
F
F
St. Lawrence Centre, Environment Canada, 105 McGill St., Montreal, QC, Canada H2Y 2E7. francois.gagne@ec.gc.ca
Blaise
C
C
André
C
C
Salazar
M
M
D049872:Bivalvia / Q000187:drug effects* / Q000378:metabolism; D002110:Caffeine / Q000494:pharmacology; D002220:Carbamazepine / Q000494:pharmacology; D004083:Cholestanol / Q000494:pharmacology; D003367:Cotinine / Q000494:pharmacology; D004579:Electron Transport / Q000187:drug effects*; D005473:Fluoxetine / Q000494:pharmacology; D007052:Ibuprofen / Q000494:pharmacology; D015227:Lipid Peroxidation / Q000187:drug effects; D008928:Mitochondria / Q000187:drug effects / Q000378:metabolism*; D009675:Novobiocin / Q000494:pharmacology; D004364:Pharmaceutical Preparations; D012722:Sewage; D013696:Temperature; D014295:Trimethoprim / Q000494:pharmacology; D015262:Xenobiotics / Q000494:pharmacology*
D004364:Pharmaceutical Preparations; D012722:Sewage; D015262:Xenobiotics; D005473:Fluoxetine; D009675:Novobiocin; D002220:Carbamazepine; D002110:Caffeine; D004083:Cholestanol; D014295:Trimethoprim; D003367:Cotinine; D007052:Ibuprofen