Data indicate that
methylselenol is a critical
selenium (Se) metabolite for anticancer activity in vivo. We tested the hypothesis that oral dosing
methylseleninic acid (MSeA), a
methylselenol precursor, inhibits the growth of
colon cancer xenografts in C57BL/6 mice fed a Se adequate diet. In this study, MSeA supplementation was given by an oral dose (0, 1, or 3 mg/kg
body weight) regimen. MSeA increased Se content of liver, kidney, muscle, stomach (w/intestine) and plasma, and elevated blood
glutathione peroxidase (GPx) activities. However, MSeA did not change lean/fat body composition, food consumption, levels of plasma
leptin/
adiponectin, and
body weight gain. MSeA (3 mg/kg
body weight) inhibited
tumor growth up to 61% when compared to the control group, and this inhibition was associated with a reduction of plasma
tumor necrosis factor (TNFα)/
interleukin 6 (
IL6) level but elevated blood GPx activities. In addition, MSeA (1 mg/kg
body weight) increased the activation of
caspase-3, a major apoptotic
enzyme, in
tumor tissues. Taken together, our MSeA oral dosing regimen was at safe levels; and high blood GPx activities,
caspase-3 activities in
tumor tissue and a reduction of plasma TNFα/
IL6 level, play critical roles in inhibiting colon
tumor growth in an immune-competent C57BL/6 mouse model.