Histological and lipid peroxidation changes after administration of 2-acetylaminofluorene in a rat liver injury model following selective periportal and pericentral damage.

摘要

Administration of 2-acetylaminofluorene (2-AAF) suppresses mature hepatocyte proliferation following selective periportal or pericentral damage induced by allyl-alcohol (AA) or carbon tetrachloride (CCl(4)) administration, respectively. The aim of the present study was to investigate the histological and the lipid peroxidation changes after 2-AAF administration following CCl(4) and AA treatment. The study comprised 108 male Wistar rats that were assigned in four groups: Group A: a placebo pellet was implanted in their neck and on 7th day single dosages of AA and CCl(4) were administrated. Group B: 28-day release 2-AAF pellets (7 0mg-2.5mg per day) were implanted on the neck and on 7th day received a single dose of CCl(4). Group C: 28-day release 2-AAF pellets (70-2.5mg per day) were implanted on the neck and on 7th day a single dose of AA and CCl(4) were administrated. Group D: Sham-operated. Rats of each group were sacrificed on the 9th, 11th, 13th and 21st day. Liver tissue was obtained for histological examination and blood was collected for lipid peroxidation evaluation by measuring malondialdehyde (MDA) and for liver enzymes. On the 9th and 21st day the histological score of liver necrosis was statistically higher on Groups B and C compared to Group A. Concentration of MDA in Group A was significantly higher than in Groups B and C on 9th and 11th days. Transaminase levels, however, were significantly higher in Group A on 9th day compare to the Groups B and C. In conclusion, it appears that oxidative stress was correlated with liver necrosis and with liver regeneration. Suppression of liver regeneration after 2-AAF administration leads to lower malondialdehyde concentrations.