Polycyclic aromatic hydrocarbons as inducers of cytochrome P4501A enzyme activity in the rainbow trout liver cell line, RTL-W1, and in primary cultures of rainbow trout hepatocytes
A. Behrens et al., Polycyclic aromatic hydrocarbons as inducers of cytochrome P4501A enzyme activity in the rainbow trout liver cell line, RTL-W1, and in primary cultures of rainbow trout hepatocytes, ENV TOX CH, 20(3), 2001, pp. 632-643
In order to investigate cell-specific differences in the response of in vit
ro models to environmental toxicants, we compared the capacity of nine poly
cyclic aromatic hydrocarbons (PAHs) to induce cytochrome P4501A (CYP1A) in
primary rainbow trout (Oncorhynchus mykiss) hepatocytes and a rainbow trout
liver cell line, RTL-W1. Induction of CYP1A was estimated from the catalyt
ic activity of 7-ethoxyresorufin-O-deethylase (EROD) and compared by median
effective concentration (EC50) values, induction spans, and benzo[a]pyrene
induction equivalency factors for inducing PAHs. The influence of culture
conditions was investigated with respect to the presence or absence of seru
m and varying exposure times. Both in vitro systems lead to an identical cl
assification of the PAHs in noninducing (anthracene, fluoranthene, phenanth
rene, and pyrene) and inducing compounds with a similar ranking of inducing
PAHs. Mean EC50 values in RTL-W1 cells were, respectively, 343 and 266 nM
far benzo[a]anthracene, 57 and 92 nM for BaP, 134 and 283 nM for benzo[b]fl
uoranthene, 455 and 270 nM for chrysene, and 98 and 116 nM for 3-methylchol
anthrene. Compared to primary hepatocytes, the RTL-W1 cell line was more se
nsitive in its EROD response to the presence or absence of serum and to the
increase in exposure time, which led to higher EC50 values.