The
trace element vanadium was investigated for its anti-neoplastic role in relation to haematological status, hepatic histopathology and histochemical analysis of
glycogen in liver. Its impact on the survival of male Sprague-Dawley rats subjected to a two-stage hepatocarcinogenesis regimen was also assessed. Initiation was performed using a single
intraperitoneal injection of
diethylnitrosamine (DENA) (200 mg/kg) followed by promotion with
phenobarbital (0.05%) in a basal diet.
Vanadium supplementation as
ammonium monovanadate at 0.5 ppm
vanadium in
drinking water was given ad libitum throughout the experiment (20 weeks), before the initiation (4 weeks), or during the promotional period (14 weeks). At the end of the study, there was a significant decrease in red blood cell count, haemoglobin content, haematocrit value, mean corpuscular haemoglobin, mean corpuscular haemoglobin concentration, plasma volume change and total white cell count, with a concurrent alteration in lymphoid:myeloid ratio in DENA control animals compared with their normal counterparts.
Vanadium supplementation throughout the study or before the initiation significantly reversed the DENA-induced alterations in most of the haematological indices. A single
intraperitoneal injection of DENA also depleted the
plasma albumin concentration, raised the plasma
globulin content, and decreased the ratio of
albumin to
globulin. These altered features began to return to normal following
vanadium supplementation. Supplementary
vanadium also elicited substantial 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-treated animals was considerably increased in the presence of
vanadium. The critical involvement of
vanadium in modulating several factors associated with erythropoiesis under carcinogenic challenge may thus have a possible impact on the eventual increased survival of the host.