Chronic oral exposure to bunker C fuel oil causes adrenal insufficiency in ranch mink (Mustela vison).
Animals living in the near-shore marine environment are predisposed to contact with chemical contaminants through land- and ocean-based activities. The release of petroleum hydrocarbons into the marine environment is a stressor to this environment and its resident wildlife. The stress response to chemical threats is dependent on an intact hypothalamic-pituitary-adrenal axis, which also may be a target to the effects of these chemicals. Ranch mink (Mustela vison) were used as surrogates for sea otters (Enhydra lutris) to examine the development of adrenal hypertrophy after chronic, oral exposure to low concentrations of bunker C fuel oil. Animals were fed three different concentrations of fuel oil (48, 520, and 908 ppm) or mineral oil (control) for 60-62 days. At the end of the exposure, blood and fecal samples were collected and organs were weighed and examined microscopically. In all fuel oil groups, exposure resulted in adrenal hypertrophy, an adaptation suggestive of adrenal activation. However, concentrations of serum and fecal glucocorticoids and serum progesterone were not elevated over control values. Hematologic parameters and serum chemistries showed no changes consistent with increased adrenal activity. In addition, adrenal glands from animals fed the higher concentrations of fuel oil contained large numbers of heavily vacuolated cells. We conclude that petroleum hydrocarbons are inducing an adrenal insufficiency that leads to the adaptive enlargement of the gland. This would increase the susceptibility of fuel oil-exposed animals to the deleterious effects of other environmental stressors.
Mohr
F C
FC
Department of Veterinary Pathology, Microbiology and Immunology, School of Veterinary Medicine, University of California, Davis, CA 95616, USA. fcmohr@ucdavis.edu
Lasley
B
B
Bursian
S
S
D000284:Administration, Oral; D000311:Adrenal Glands / Q000187:drug effects* / Q000473:pathology; D000309:Adrenal Insufficiency / Q000139:chemically induced* / Q000378:metabolism / Q000473:pathology / Q000662:veterinary; D000410:Alanine Transaminase / Q000097:blood; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000473:pathology; D005243:Feces / Q000737:chemistry; D005648:Fuel Oils / Q000633:toxicity*; D005938:Glucocorticoids / Q000097:blood; D006403:Hematologic Tests; D006854:Hydrocortisone / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000473:pathology; D008297:Male; D008907:Mink / Q000097:blood / Q000378:metabolism; D009929:Organ Size / Q000187:drug effects; D011374:Progesterone / Q000097:blood; D036401:Toxicity Tests, Chronic
D005648:Fuel Oils; D005938:Glucocorticoids; D011374:Progesterone; D000410:Alanine Transaminase; D006854:Hydrocortisone