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The effect of vitamin B-6 deficiency on antitumor cytotoxic immune reactivity in mice

The effect of vitamin B-6 (VB6) deficiency in mice on host
susceptibility to primary and secondary Moloney-sarcoma virus
(MSV)-induced tumor growth, cytotoxic activities of T cells,
antibodies and natural killer (NK) cells, and phagocytosis by
macrophages was examined. Five- to six-week old female C57B1/6 mice
were fed 20% casein diets with pyridoxine (PN) added at 7 (PN-7), 1
(PN-1), 0.5 (PN-0.5), 0.1 (PN-0.1), or 0 (PN-0) mg per kg diet, which
represent 700, 100, 50, 10, and 0% of the VB6 requirement of mice
adequate for both growth and reproduction, for 4-5 weeks prior to MSV
challenge and throughout the period of tumor development or
immunologic testing. Animals fed PN-0.1 and -0 diets developed
deficiency signs including significantly lower body weight, denuding
of the snout, skin irritation and elevated excretion of xanthurenic acid before as well as after tryptophan loading. VB6 deficiency resulted in significant enhancement of tumor susceptibility.
Following MSV/MSB challenge, total incidence of MSV/MSB/splenic tumors
was 2/11, 1/11, 4/10, and 8/11 in mice fed PN-1, -0.5, -0.1, and -0
diets, respectively. In response to challenge with P815 mastocytoma
cells, primary splenic and peritoneal T cell-mediated cytotoxicity
(CMC) was significantly reduced in animals fed PN-0 or -0.1 diet.
Mice fed PN-0 diet also showed significantly suppressed secondary T
CMC of splenic and peritoneal lymphocytes against P815 tumor cells.
Complement-dependent antibody-mediated cytotoxicity against P815 tumor
cells, phagocytosis of sheep red blood cells by macrophages, and
native and interferon-induced NK cell cytotoxicity against YAC tumor
cells were not affected by lack of VB6. The percentage of macrophages
present in the peritoneal exudate cells was increased in animals fed
PN-0 diet. Immune responses were not enhanced or altered by the
excess intake of VB6 (PN-7).
The present studies which showed compromised host resistance
to MSV oncogenesis and altered T cell cytotoxicity in VB6 deficiency
provided practical information on the impaired host defense mechanism
by inadequacy resulting from VB6. / Graduation date: 1984

Identiferoai:union.ndltd.org:ORGSU/oai:ir.library.oregonstate.edu:1957/27268
Date25 October 1983
CreatorsHa, Choonja
ContributorsMiller, Lorraine T.
Source SetsOregon State University
Languageen_US
Detected LanguageEnglish
TypeThesis/Dissertation

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