Oxidative stress and bioindicators of reproductive function in pulp and paper mill effluent exposed white sucker.
This study investigates oxidative stress and bioindicators of reproductive function in wild white sucker (Catostomus commersoni) collected from environments receiving pulp and paper mill effluent discharges in northern Ontario. Samples were collected over an eight-year period adjacent to three pulp and paper mills using a variety of processing and bleaching techniques. Fish collected downstream of pulp and paper mills within the Moose River basin exhibited elevated hepatic and gonadal 2-thiobarbituric acid reactive substances (TBARS), the presence of which is indicative of oxidative stress in these tissues. Within the Jackfish Bay system, exposure to pulp and paper mill effluent did not elevate hepatic or gonadal TBARS. Hepatic cytochrome P4501A activity (CYP1A) and fatty acyl-CoA oxidase (FAO) activities were frequently increased in livers of Moose River basin fish exposed to pulp and paper mill effluent, while lower activities of both enzymes were found within fish from the Jackfish Bay system. This suggests that oxidative stress may be related to CYP1A and FAO activities. Within the Moose River system, increases in measures of oxidative stress (TBARS, FAO) were generally coincident with decreased levels of 17 beta-estradiol; however, testosterone was often lower in Jackfish Bay system fish without any commensurate changes in oxidative stress. The suite of reproductive and oxidative stress parameters measured in this study varied between seasons and mills suggesting responses to effluent are dynamic and effects are complicated by different receiving environments. The relationship between gonad size, gonadal oxidative stress, and circulating plasma steroids remains unclear.
Department of Zoology, University of Guelph, Guelph, Ontario, Canada N1G 2W1.
Ken D
KD
Oakes
Mark E
ME
McMaster
Andrea C
AC
Pryce
Kelly R
KR
Munkittrick
Cam B
CB
Portt
L Mark
LM
Hewitt
Dan D
DD
MacLean
Glen J
GJ
Van Der Kraak
D000726:Androgen Antagonists / Q000494:pharmacology; D059002:Androgen Receptor Antagonists; D000728:Androgens; D001943:Breast Neoplasms / Q000473:pathology; D002460:Cell Line; D003907:Dexamethasone / Q000494:pharmacology; D003633:Dichlorodiphenyl Dichloroethylene / Q000494:pharmacology; D013196:Dihydrotestosterone / Q000494:pharmacology; D005260:Female; D005938:Glucocorticoids / Q000494:pharmacology; D006801:Humans; D007306:Insecticides / Q000494:pharmacology; D008044:Linuron / Q000494:pharmacology; D008156:Luciferases / Q000235:genetics; D018384:Oxidative Stress; D010957:Plasmids / Q000235:genetics; D011401:Promoter Regions, Genetic / Q000235:genetics; D011965:Receptors, Glucocorticoid / Q000819:agonists / Q000037:antagonists & inhibitors; D013473:Sunscreening Agents / Q000494:pharmacology*; D045165:Testosterone Congeners / Q000494:pharmacology; D013778:Tetrazolium Salts; D013844:Thiazoles; D015533:Transcriptional Activation / Q000187:drug effects*; D014466:Ultraviolet Rays
D000726:Androgen Antagonists; D059002:Androgen Receptor Antagonists; D000728:Androgens; D005938:Glucocorticoids; D007306:Insecticides; D011965:Receptors, Glucocorticoid; D013473:Sunscreening Agents; D045165:Testosterone Congeners; D013778:Tetrazolium Salts; D013844:Thiazoles; D008044:Linuron; D013196:Dihydrotestosterone; D003633:Dichlorodiphenyl Dichloroethylene; D003907:Dexamethasone; D008156:Luciferases; C022616:thiazolyl blue