Lr. Curtis et al., TEMPERATURE-MODULATED INCIDENCE OF AFLATOXIN B1-INITIATED LIVER-CANCER IN RAINBOW-TROUT, Fundamental and applied toxicology, 25(1), 1995, pp. 146-153
Rainbow trout (initial weight of 4 or 5 g) were acclimated at a cool,
11.0 degrees C (C), a warm, 18.0 degrees C (W), or an intermediate tem
perature 14.5 degrees C (I) for 1 month. There was a slight difference
in hepatic microsomal content of one of six cytochrome P450 isozymes
between acclimation groups. Monounsaturated fatty acids in hepatic pho
sphotidylethanolamine but not phosphotidylcholine increased at lower a
cclimation temperatures. Saturated fatty acid content decreased with t
emperature for both phospholipid classes. Fish were exposed to 0.08-0.
12 ppm waterborne aflatoxin B1 (AFB1) for 30 min at respective acclima
tion temperatures or after acute temperature shifts (24 hr) and reared
for 9 months at C, I, or W. With exposure concentrations which delive
red equivalent target organ doses, trout acclimated, exposed, and rear
ed at C, I, or W had liver tumor incidences of 4, 35, and 61%, respect
ively. The average number of tumors per liver increased from 1.25-1.34
at C to 2.46-2.66 at W. There were no temperature-dependent differenc
es in tumor diameter. When C- and W-acclimated fish were AFB1 exposed
and reared at I, tumor incidence was 12.5% for W-I-shifted fish and 26
.5% for C-I-shifted fish. This was consistent with previous work which
demonstrated acute downward temperature shift reduced [H-3]AFB1 adduc
tion to hepatic DNA. Tumor incidence and multiplicity data suggested m
anipulation of temperature permitted selective modulation of cancer in
itiation and promotion in rainbow trout. (C) 1995 Society of Toxicolog
y.