NUCLEAR LESIONS DURING RAT HEPATOCARCINOGENESIS .1. MEASURING THE SISTER-CHROMATID EXCHANGES DURING INITIATION, PROMOTION AND PROGRESSION OF RAT HEPATOCARCINOGENESIS INDUCED WITH DIETHYLNITROSAMINE
C. Herens et al., NUCLEAR LESIONS DURING RAT HEPATOCARCINOGENESIS .1. MEASURING THE SISTER-CHROMATID EXCHANGES DURING INITIATION, PROMOTION AND PROGRESSION OF RAT HEPATOCARCINOGENESIS INDUCED WITH DIETHYLNITROSAMINE, Mutation research, 329(2), 1995, pp. 153-159
Cytogenetic endpoints such as sister-chromatid exchanges (SCEs), chrom
osomal aberrations and micronuclei (MNs) have been widely used as indi
cators of genetic damage. However, no systematic attempts have been ma
de to correlate the levels of these cytogenetic endpoints with the dif
ferent steps of carcinogenesis. In the present report, the induction,
accumulation and persistence of SCEs and high frequency cells (HFCs) w
ere measured in liver cells during the initiation, promotion and progr
ession steps of rat hepatocarcinogenesis induced by diethylnitrosamine
(DEN). The results indicate that lesions leading to SCEs accumulate d
uring initiation only. When DEN administration is longer than the dura
tion of this first step, SCE values stabilize. After stopping the carc
inogenic treatment, the SCE levels decrease to control values whether
or not promotion and progression occur.