Vanadium-mediated chemoprotection against chemical hepatocarcinogenesis in rats: haematological and histological characteristics.
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.
Bishayee
A
A
Department of Pharmaceutical Technology, Jadavpur University, Calcutta, India.
Karmakar
R
R
Mandal
A
A
Kundu
S N
SN
Chatterjee
M
M
D000284:Administration, Oral; D000818:Animals; D001772:Blood Cell Count; D001798:Blood Proteins / Q000032:analysis; D006528:Carcinoma, Hepatocellular / Q000097:blood / Q000473:pathology / Q000517:prevention & control*; D002467:Cell Nucleus / Q000473:pathology; D003593:Cytoplasm / Q000473:pathology; D004032:Diet; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005527:Food, Fortified; D006003:Glycogen / Q000032:analysis; D008099:Liver / Q000187:drug effects / Q000473:pathology; D008114:Liver Neoplasms, Experimental / Q000097:blood / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012709:Serum Albumin / Q000032:analysis; D012712:Serum Globulins / Q000032:analysis; D015996:Survival Rate; D014639:Vanadium / Q000008:administration & dosage*
D001798:Blood Proteins; D012709:Serum Albumin; D012712:Serum Globulins; D014639:Vanadium; D006003:Glycogen