Oxidative stress responses in longnose sucker (Catostomus catostomus) exposed to pulp and paper mill and municipal sewage effluents.
While recent evidence indicates that the generation of reactive oxygen species (ROS) and associated oxidative damage are frequently observed in fish populations with exposure to pulp and paper mill effluents, the potential for ROS generation from municipal sewage effluents has not been addressed. This study investigates the utility of measures of oxidative stress in delineating the effects of both pulp and paper mill and municipal sewage discharges. Longnose sucker (Catostomus catostomus) were collected below three pulp and paper mill and two municipal sewage effluent discharges over a 3-year period within the Wapiti and Athabasca River systems in northern Alberta. Biochemical responses in longnose sucker varied between the two rivers systems, with more pronounced changes occurring within the Wapiti River. Of the suite of biochemical parameters examined, fatty acyl-CoA oxidase (FAO) activity was the most sensitive indicator of pulp and paper mill exposure, but was only infrequently induced with exposure to municipal sewage effluent. Hepatic and gonadal 2-thiobarbituric acid reactive substances, lipid hydroperoxides, and hepatic free iron were less consistently elevated with exposure to pulp and paper mill effluent than FAO activity, and were also only infrequently altered with sewage effluent exposure. Hepatic ascorbic acid, liver somatic index, and condition factor were consistently altered with exposure to both sewage and pulp and paper mill effluents. While specific biochemical and organismal responses varied with effluents and time, the collective suite of oxidative stress endpoints proved to be useful tools in identifying relative influences of municipal sewage and pulp and paper mill effluent on fish populations in adjacent receiving waters.
Oakes
Ken D
KD
Department of Zoology, University of Guelph, Guelph, Ont., Canada N1G 2W1.
McMaster
Mark E
ME
Van Der Kraak
Glen J
GJ
D042962:Acyl-CoA Oxidase / Q000378:metabolism; D000416:Alberta; D000818:Animals; D001205:Ascorbic Acid / Q000378:metabolism; D003531:Cypriniformes / Q000378:metabolism*; D006066:Gonads / Q000378:metabolism; D007501:Iron / Q000378:metabolism; D008099:Liver / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D010209:Paper; D017382:Reactive Oxygen Species / Q000378:metabolism*; D045483:Rivers; D012722:Sewage / Q000032:analysis*; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014866:Waste Products / Q000032:analysis*; D014874:Water Pollutants, Chemical / Q000032:analysis / Q000633:toxicity*
D017382:Reactive Oxygen Species; D012722:Sewage; D017392:Thiobarbituric Acid Reactive Substances; D014866:Waste Products; D014874:Water Pollutants, Chemical; D007501:Iron; D042962:Acyl-CoA Oxidase; D001205:Ascorbic Acid