Abstract
It is experimentally known that antioxidants such as vitamin E (VE), selenium or ascorbic acid prevent chemical carcinogenesis in animals. Inhibitory effect of tumor growth was also reported by administration of VE into mouse whose serum level was maintained 2 to 3 times higher than normal value. The present study aimed to demonstrate the effect of VE at sufficient or deficient on tumor growth and host immune response, since host immunity is an important factor on tumor development.
CDF1 mice were fed with VE deficient (d-α-tocopherol 0.16 mg/100 g diet, VE-D group) or normal diet (dl-α-tocopheryl acetate 20 mg/100 g diet) for their life-span since the animal was 4-week-old. VE sufficient diet (dl-α-tocopheryl nicotinate 585 mg/100 g diet, VE-S group) was also given for the same period. Serum VE level measured by HPLC was maintained 1.5 to 2.4 times higher than that of normal level in VE-S group. However those in VE-D group was found to be lower than 0.1 μg/ml. Low responses of in vitro lymphocyte proliferation to PHA and LPS were found in VE-D group. After 1×105 cells/head of Meth A fibrosarcoma were s. c. transplanted in 12-week-old mice, tumor size was measured every week. Rapid growth of tumor was observed in both VE-D and VE-S groups, and there was no significant difference between the two groups. Their survival time was shorter in VE-D group. Based on these data, it was concluded that supplement of VE in this system had no tumor inhibitory effect, but VE deficient state was rather disadvantageous in tumor bearing host.
