Effect of Pyridoxine on the Growth of Morris Hepatoma No. 7288Ctc and Enzyme Activity

Abstract

The effect(s) of lack of dietary pyridoxine (PX) on the growth of Morris hepatoma no. 7288Ctc was studied. Buffalo strain female rats were fed a diet lacking PX. Pair-fed controls were fed the same diet with PX added. Animals were inoculated with no. 7288Ctc hepatoma cells at 21 days and were sacrificed 16 days later. Host livers and tumors were removed, weights recorded and the activity of tyrosine aminotransferase (TAT; L-tyrosine: 2-oxoglutarate aminotransferase, EC 2.6.1.5) was determined in both host liver and hepatoma. The average weight of 30 hepatomas grown in pair-fed control rats was 11.61 ± 1.5 g while the average weight of the same number of hepatomas grown in animals fed the PX free diet was 4.73 ± 0.7 g (P < 0.001). Further TAT specific activity levels were 39% and 32% higher in host livers and tumors from deficient animals, respectively. The results show that availability of dietary pyridoxine stimulates the growth of this hepatoma and, in addition, exercises a type of control over the expression of TAT activity.

Effects of vitamin B6 metabolism on oncogenesis, tumor progression and therapeutic responses

“…The vast majority of such early studies, most of which were performed in immunodeficient rodents, concluded that systemic vitamin B6 deficiency exerts consistent antineoplastic effects, [25][26][27][28][29] most likely as highly proliferating malignant cells are characterized by an intense metabolic activity that requires adequate levels of bioactive PLP. [30][31][32][33][34][35] These observations ignited an intense experimental effort aimed at the identification and characterization of vitamin B6 antagonists with potential antineoplastic applications. [36][37][38][39][40][41] Unfortunately, none of these agents has ever exhibited a preclinical activity profile compatible with clinical development.…”

Expression of Hormonally Induced Tyrosine Aminotransferase in Host Liver and Morris Hepatoma No. 7777 During Cofactor Depletion

“…Biochemicals Corp., Cleveland. O H ) diet lacking pyridoxine [2,8,10]. A fter 21 days, cells from Morris hepatom a No.…”

“…A fter 21 days, cells from Morris hepatom a No. 7777 (gen. 101) were inoculated into the hinds legs of the animals [2,8,10]. The animals were maintained on a strict lighting schedule.…”

“…The response of the enzyme to hydrocortisone varies in different Morris hepatom a lines from com plete unresponsiveness to significant increases [1,2], The pattern of its horm onal induction is drastically altered in host liver and this hepatom a [3], In animals without tum ors, cofac tor depletion, i. e. pyridoxine depletion, alters the am inotrans ferase horm onal induction pattern and effects further resolu tion of the enzyme on electrophoresis in polyacrylamide gel [4,5,6], Further, lack of dietary pyridoxine significantly inhibits the growth of several M orris hepatom a lines, including that of hepatom a No. 7777 [3,[7][8][9][10], R at liver cytoplasmic tyrosine am inotransferase consists of multiple forms which may be affected by horm onal adm inistration [11][12][13][14][15][16][17][18][19]. W hether cofactor depletion affects the expression of the enzyme in hepatom a-bearing animals has not been investigated.…”