Effects of salinity on aldicarb toxicity in juvenile rainbow trout (Oncorhynchus mykiss) and striped bass (Morone saxatilis x chrysops).
Fluctuations in several environmental variables, such as salinity, can influence the interactions between organisms and pollutants in aquatic organisms, and, therefore, affect the toxicity of xenobiotics. In this study, after 2 species of fish, rainbow trout (Oncorhynchus mykiss) and hybrid striped bass (Morone saxatilis x chrysops) were acclimated to 4 salinity regimens of 1.5, 7, 14, and 21 ppt for 1 week and then exposed to 0.5 mg/l aldicarb. Mortality, brain, and muscle cholinesterase levels were measured after 96 h. Rates of (14)C-aldicarb sulfoxide formation were determined in kidney (trout only), liver, and gill microsomes from each species acclimated to the 4 salinity regimens. Salinity significantly enhanced aldicarb toxicity, cholinesterase inhibition, and (14)C-aldicarb sulfoxide formation in rainbow trout but not in striped bass. In vitro incubations with (14)C-aldicarb and the cytochrome P450 (CYP) inhibitor, N-benzylimidazole, did not significantly alter aldicarb sulfoxide formation in tissue microsomes from either species of fish, indicating CYP did not contribute to aldicarb sulfoxidation. Salinity increased flavin-containing monooxygenase (FMO) mRNA expression and catalytic activities in microsomes of liver, gill, and kidney of rainbow trout, which was consistent with the salinity-induced enhancement of aldicarb toxicity. Salinity did not alter FMO mRNA expression and catalytic activities in striped bass, which was also consistent with the lack of an effect of salinity on aldicarb toxicity in this species. These results suggest that salinity-mediated enhancement of aldicarb toxicity is species-dependent, and at least partially due to the salinity-related upregulation of FMOs, which, in turn, increases the bioactivation of aldicarb to aldicarb sulfoxide, which is a more potent inhibitor of cholinesterase than aldicarb.
Wang
J
J
Environmental Toxicology Research Program, Research Institute of Pharmaceutical Sciences, University of Mississippi, University, MS 38677, USA.
Grisle
S
S
Schlenk
D
D
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000448:Aldicarb / Q000031:analogs & derivatives / Q000378:metabolism / Q000633:toxicity*; D000818:Animals; D001492:Bass / Q000378:metabolism*; D001921:Brain / Q000187:drug effects; D002802:Cholinesterases / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005880:Gills / Q000187:drug effects; D007093:Imidazoles / Q000494:pharmacology; D007306:Insecticides / Q000378:metabolism / Q000633:toxicity*; D007668:Kidney / Q000187:drug effects; D008862:Microsomes, Liver / Q000187:drug effects / Q000201:enzymology; D009132:Muscles / Q000187:drug effects; D017686:Oncorhynchus mykiss / Q000378:metabolism*; D010105:Oxygenases / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000187:drug effects / Q000235:genetics / Q000378:metabolism; D012965:Sodium Chloride / Q000494:pharmacology*; D013860:Thiocholine / Q000378:metabolism; D014874:Water Pollutants, Chemical / Q000378:metabolism / Q000633:toxicity
D000317:Adrenergic alpha-Antagonists; D007093:Imidazoles; D007306:Insecticides; D012333:RNA, Messenger; D014874:Water Pollutants, Chemical; C017062:1-benzylimidazole; D012965:Sodium Chloride; D013860:Thiocholine; D000448:Aldicarb; D010105:Oxygenases; C020066:dimethylaniline monooxygenase (N-oxide forming); D002802:Cholinesterases