PARENT SESSION
Molecular & Cellular Toxicology Poster Session.
Tuesday, November 14, 2000
8:00 AM to 12:00 PM
CC West/Center Exhibit Hall
(PTA006) Tissue-specific apoptosis and biochemical indicators of chemical exposure in lake trout experiencing early mortality syndrome.
Whyte, Jeffrey J.1, Allert, J. Alan2, Edsall, Carol C.3, Honeyfield, Dale C.4, Tillitt, Donald E.2, 1 2 3 4
ABSTRACT- The symptoms of early mortality syndrome (EMS) in Great Lakes salmonids with low thiamine concentrations in their eggs resemble those seen in fish embryos exposed to planar halogenated hydrocarbons (PHHs). Previous studies have observed programmed cell death (apoptosis) in the embryonic vasculature, neural and digestive tissues during development of fish with low egg thiamine concentrations and in embryos exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). These results indicate that apoptosis in specific embryonic tissues may result from disruption of a pathway common to both thiamine utilization and PHH metabolism. The present study examines the temporal and tissue-specific nature of apoptosis, cytochrome P4501A induction (an indicator of PHH exposure), and antioxidant vitamin levels during development in lake trout (Salvelinus namaycush) exhibiting low egg thiamine levels, elevated PHH concentrations, and a high incidence of EMS. Lake trout eggs from both feral (Lake Michigan) and laboratory sources were spawned and reared in laboratory culture conditions. Some hatchery eggs were obtained from females with modified thiamine levels or were injected with TCDD. Developing embryos were monitored for expression of clinical signs of EMS. At several critical stages of development, embryos were collected and preserved for histological analysis of apoptosis and CYP1A induction. Our preliminary results reveal that apoptotic cells are readily apparent in gill and neural tissue of developing lake trout from Lake Michigan, supporting the previous laboratory and field investigations. CYP1A protein is elevated in gill tissue of TCDD injected embryos. Thiamine concentrations did not appear to be the sole predictor of EMS in developing lake trout from Lake Michigan. By examining the temporal relationship between the onset of EMS and cellular or biochemical changes, our studies will isolate the early stages of toxicity that occur prior to gross pathological effects and will contribute greatly to an understanding the cellular etiology of this disorder.
Key words: Early mortality syndrome, Apoptosis, Thiamine, CYP1A