Cellular Proliferation, Cell Death, and Liver Histology in Gambusia affinis After Dietary Exposure to Benzidine and 2-Aminofluorene

Abstract

Chronic exposure to arylamines through diet and/or smoking has been associated with genetic changes and tumorigenesis. Cellular proliferation, apoptosis, and histological changes in liver tissue were investigated in Gambusia affinis ( G affinis) after chronic dietary exposure to 6.9 mM and 0.069 mM concentrations of benzidine (BZ), 2-aminofluorene (2AF), and their combination for 4, 8, and 12 weeks, respectively. The proliferation assay indicated non–dose-dependent increases in cellular proliferation over the controls for all treatment groups at 4 and 12 weeks but not at 8 weeks except for the low dose of 2AF. The apoptosis assay showed effects in the low-dose group of 2AF and BZ at 4 weeks only. Hematoxylin/eosin staining of liver tissue revealed an increase in oval/spindle cell proliferation and altered foci formation in the treated groups compared with controls. These results demonstrate a mammalian-like response to 2AF and BZ in G affinis liver.

Exposure to benzidine caused apoptosis and malformation of telencephalon region in zebrafish

“…In a similar manner, chromosome aberration increased in the lymphocytes of mice exposed to benzidine compared with those of mice of the control groups (Das et al, ). Apoptosis was observed in Gambusia affinis in response to chronic exposure to 0.069 mM benzidine for 4 weeks (Lentz et al, ).…”

Overview of biological mechanisms of human carcinogens

“…In benzidine-induced hepatomas from B6C3F1 mice, the Ha-Ras and Ki-Ras oncogenes were hypo-methylated in tumor as compared to adjacent non-tumor tissue, and elevated oncogene expression was detected (Vorce and Goodman 1989). In vivo studies showed that benzidine induces apoptosis, cell proliferation and differentiation (Chen et al 2014a;Lentz et al 2010).…”