VANADIUM-MEDIATED CHEMOPROTECTION AGAINST CHEMICAL HEPATOCARCINOGENESIS IN RATS - HEMATOLOGICAL AND HISTOLOGICAL CHARACTERISTICS

Citation
A. Bishayee et al., VANADIUM-MEDIATED CHEMOPROTECTION AGAINST CHEMICAL HEPATOCARCINOGENESIS IN RATS - HEMATOLOGICAL AND HISTOLOGICAL CHARACTERISTICS, European journal of cancer prevention, 6(1), 1997, pp. 58-70
Citations number
56
Categorie Soggetti
Oncology
ISSN journal
09598278
Volume
6
Issue
1
Year of publication
1997
Pages
58 - 70
Database
ISI
SICI code
0959-8278(1997)6:1<58:VCACH>2.0.ZU;2-3
Abstract
The trace element vanadium was investigated for its anti-neoplastic ro le in relation to haematological status, hepatic histopathology and hi stochemical analysis of glycogen in liver. Its impact on the survival of male Sprague-Dawley rats subjected to a two-stage hepatocarcinogene sis regimen was also assessed. Initiation was performed using a single intraperitoneal injection of diethylnitrosamine (DENA) (200 mg/kg) fo llowed by promotion with phenobarbital (0.05%) in a basal diet. Vanadi um supplementation as ammonium mono-vanadate at 0.5 ppm vanadium in dr inking water was given ad libitum throughout the experiment (20 weeks) , before the initiation (4 weeks), or during the promotional period (1 4 weeks). At the end of the study, there was a significant decrease in red blood cell count, haemoglobin content, haematocrit value, mean co rpuscular haemoglobin, mean corpuscular haemoglobin concentration, pla sma volume change and total white cell count, with a concurrent altera tion in lymphoid:myeloid ratio in DENA control animals compared with t heir normal counterparts. Vanadium supplementation throughout the stud y or before the initiation significantly reversed the DENA-induced alt erations in most of the haematological indices. A single intraperitone al injection of DENA also depleted the plasma albumin concentration, r aised the plasma globulin content, and decreased the ratio of albumin to globulin. These altered features began to return to normal followin g vanadium supplementation. Supplementary vanadium also elicited subst antial protection against DENA-mediated rat liver carcinogenesis. This was fairly evident from hepatic histology and evaluation of glycogen accumulation by periodic acid-Schiff reaction. The survival of DENA-tr eated animals was considerably increased in the presence of vanadium. The critical involvement of vanadium in modulating several factors ass ociated with erythropoiesis under carcinogenic challenge may thus have a possible impact on the eventual increased survival of the host.