Molecular basis of vanadium-mediated inhibition of hepatocellular preneoplasia during experimental hepatocarcinogenesis in rats

Chakraborty, T; Swamy, A; Chatterjee, A; Rana, B; Shyamsundar, A; Chatterjee, M

HERO ID

459018

Reference Type

Journal Article

Year

2007

Language

English

PMID

17243116

HERO ID 459018
In Press No
Year 2007
Title Molecular basis of vanadium-mediated inhibition of hepatocellular preneoplasia during experimental hepatocarcinogenesis in rats
Authors Chakraborty, T; Swamy, A; Chatterjee, A; Rana, B; Shyamsundar, A; Chatterjee, M
Journal Journal of Cellular Biochemistry
Volume 101
Issue 1
Page Numbers 244-258
Abstract Carcinogen-induced early DNA lesions and metallothionein (MT) over-expression have been implicated in cell proliferation and thereby subsequent expression of premalignant phenotype of the cell. We have therefore investigated the chemopreventive potential of vanadium in a multi-biomarker approach, viz. 8-hydroxy-2' -deoxyguanosines (8-OHdGs), DNA single-strand breaks (SSBs), DNA-protein crosslinks (DPCs), chromosomal aberrations (CAs), in situ MT expression, and cell proliferation in rat liver preneoplasia. Hepatocarcinogenesis was induced in male Sprague-Dawley rats with a single, necrogenic, intraperitoneal (i.p.) injection of diethylnitrosamine (DEN) (200 mg/Kg body weight) at week 4 of the experimental protocol followed by promotion with phenobarbital (PB) (0.05% in basal diet), on and from week 8 and continued till 32 weeks in a long-term regimen. There was a significant and steady elevation of modified DNA bases 8-OHdGs (P < 0.0001; 90.69%) along with substantial increments of the extent of SSBs (P < 0.001) and CAs (P < 0.001) following DEN exposure. Supplementation of vanadium at a dose of 0.5 ppm abated the formations of 8-OHdGs (80.63%; P < 0.0001), SS-DNAs (P < 0.001) and SSBs/DNA unit (P < 0.01; 56.39%), DPCs (59.26%; P < 0.0001) and CAs (71.52%; P < 0.001) in preneoplastic rat liver studied at various time points. Low dose of vanadium treatment further reduced liver-MT immunoreactivity (P < 0.05) and BrdU-labeling index (P < 0.02) and a significant positive correlation (r=0.92; r(2) =0.85; P=0.0001) was noted between them. Continuous vanadium administration also decreased nodular incidence (66.67%) and nodule multiplicity (62.12%; P < 0.001) along with substantial improvement in the altered hepatocellular phenotype when compared to DEN+PB treatment alone. The study indicates that vanadium-mediated suppression of cell proliferation and resulting premalignant expression might be due to the observed reductions in hepatic 8-OHdGs, SSBs, DPCs, CAs, and MT immunoreactivity. Vanadium is chemopreventive for DEN-induced hepatocellular preneoplasia in rats.
Doi 10.1002/jcb.21169
Pmid 17243116
Wosid WOS:000245909200021
Is Certified Translation No
Dupe Override No
Is Public Yes
Language Text English