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Cancer chemopreventive effect of oral feeding á-tocopherol on UVB induced photocarcinogenesis of hairless mouse
Masashi Kuchide, Harukuni Tokuda, Junko Takayasu, Fumio Enjo, Wataru Aoi, Takeshi Ishikawa, Toshikazu Yoshikawa, Hoyoku Nishino.
Kyoto Prefectural University of Medicine, KYOTO, Japan.
Ultraviolet (UV) light is the most common cause of skin cancers in humans. Several effects of UVB (290-320 nm) are thought to contribute to skin carcinogenesis.
The generation of free radicals and related oxidants produced by UVB exposure, cause to carcinogenesis by directly damaging DNA and activating several cytokines.
Vitamin E (á-tocopherol) has been reported to be a potent antioxidant. We examined the inhibitory effect on UVB-induced skin carcinogenesis in hairless mice model. Hairless mice were divided into three groups of 21 mice each as follows: group 1:
Vitamin E oral feeding group (including 500 IU á-tocopherol);
group 2: normal diet group (including 20 IU), and
group 3: Vitamin E defficient group (including 0 IU).
After initiation by DMBA, al l groups were irradiated twice a week at a dose of 3.43 kJ/m2 for 20 weeks. The number of diameter more than 1 mm tumors was counted once a week during the repeated UVB irradiations. Both tumor incidence and multiplicity were remarkably inhibited in Vitamin E diet group.
These mouse skin samples were analyzed by immunohistochemical staining of 8-OHdG and PCNA at the end of the study protocol. Both 8-OHdG and PCNA expressions significantly reduced in Vitamin E diet group, and showed the sign ificant inhibitory effect on UVB-induced mouse skin carcinogenesis.
By scavenging effect of free radical generation, we supposed that Vitamin E inhibited both initiating and promoting activity, and caused the activation of various signaling pathways, contribute to the tumor cell suppression.
AACR Abstract 3389, 2003
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