Chronic fuel oil toxicity in American mink (Mustela vison): systemic and hematological effects of ingestion of a low-concentration of bunker C fuel oil.
Petroleum oil enters the coastal marine environment through various sources; marine mammals such as sea otters that inhabit this environment may be exposed to low concentrations of petroleum hydrocarbons through ingestion of contaminated prey. The inability to perform controlled studies in free-ranging animals hinders investigations of the effects of chronic petroleum oil exposure on sea otter morbidity and mortality, necessitating the development of a reliable laboratory model. We examined the effects of oral exposure to 500 ppm bunker C fuel oil over 113-118 days on American mink, a species phylogenetically related to the sea otter. Hematological parameters and organs were examined for fuel oil-associated changes. Hepatic cytochrome P4501A1 mRNA expression and fecal cortisol concentrations were also measured. Ingestion of fuel oil was associated with a decrease in erythrocyte count, hemoglobin concentration (Hgb), hematocrit (HCT), and an increase in mean corpuscular volume (MCV). Total leukocytes were elevated in the fuel oil group from increases in neutrophils, lymphocytes, and monocytes. Significant interactions between fuel oil and antigen challenge were found for erythrocyte parameters, monocyte and lymphocyte counts. Liver and adrenal weights were increased although mesenteric lymph node weights were decreased in the fuel oil group. Hepatic cytochrome P4501A1 mRNA was elevated in the fuel oil group. Fecal cortisol concentration did not vary between the two groups. Our findings show that fuel oil exposure alters circulating leukocyte numbers, erythrocyte homeostasis, hepatic metabolism and adrenal physiology and establish a framework to use mink as a model for sea otters in studying the systemic effects of marine contaminants.
Department of Veterinary Pathology, Microbiology and Immunology School of Veterinary Medicine, University of California, Davis 95616-8739, USA.
Julie A
JA
Schwartz
Brian M
BM
Aldridge
Bill L
BL
Lasley
Paul W
PW
Snyder
Jeff L
JL
Stott
F Charles
FC
Mohr
D000818:Animals; D056486:Chemical and Drug Induced Liver Injury; D019363:Cytochrome P-450 CYP1A1 / Q000096:biosynthesis / Q000235:genetics; D004136:Dinitrobenzenes / Q000378:metabolism; D004906:Erythrocyte Count; D005243:Feces / Q000737:chemistry; D005648:Fuel Oils / Q000633:toxicity*; D006454:Hemoglobins / Q000378:metabolism; D006651:Histocytochemistry; D006854:Hydrocortisone / Q000378:metabolism; D007958:Leukocyte Count; D008107:Liver Diseases / Q000097:blood / Q000378:metabolism; D008297:Male; D008907:Mink / Q000097:blood / Q000378:metabolism*; D023421:Models, Animal; D009929:Organ Size / Q000187:drug effects; D010041:Otters / Q000097:blood / Q000378:metabolism; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D011897:Random Allocation; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014874:Water Pollutants, Chemical / Q000633:toxicity*
D004136:Dinitrobenzenes; D005648:Fuel Oils; D006454:Hemoglobins; D012333:RNA, Messenger; D014874:Water Pollutants, Chemical; D019363:Cytochrome P-450 CYP1A1; D006854:Hydrocortisone