Vitamin E, which has its advocates in the treatment of diabetes mellitus. autoimmune disease, cancer and peripheral vascular and thromboemboiic disease, has now been alleged to have a powerful antioxident effect and to affect various biological activities such as fertility factor, inhibition of human platelet aggregation and stabilization of biological membranes. The present study was designed to test whether vitamin E( alpha-tocopherol) can: (1)enhance the hemagglutinin response to sheep red blood cells (SRBC), (2)modulate Arthus and delayed type hypersensitivity(DTH) to SRBC and contact hypersensitivity to dinitrofluorobenzene (DNFB). (3)enhance the mitogenic response of murine splenocyte, (4)decrease the recovery of Cryptococcus neoformans from brain, lung, liver, spleen and kidney of infected mice and (5)have an inhibitory or enhancing effect on the induction of active systemic anaphylaxis(ASA) induced by chicken-gamma globulin (CGG) in mice. Mice were given either intramuscular injections of 0.3ml (300mg) of vitamin E before immunization or were infection for 10 consecutive days or were given by vitamin E esophageal intubation, 0.lml(l00mg), for 20 days before sacrifice for the mitogenic response experiments. It was found that vitamin E treated mice showed a significant enhancement in hemagglutinin response, Arthus reaction and DTH to SRBC and contact hypersensitivity to DNFB. There was no significant difference in the mitogenic response to phytohemagglutinin(PHA), but the response to concanavalin A(ConA) or pokeweed mitogem(PWM) was increased in vitamin E-treated mice. Interestingly, the vitamin E administration before C. neoformans infection decreased significantly the recovery of C. neoformans from brain, lung, liver, spleen and kidney of the infected mice as compared with that of the control mice, strongly suggesting that vitamin E pretreatment may increase the resistance of mice to the fungal infection. Unexpectedly, vitamin E administration enhanced the production of CGG-induced ASA. Taken together, it can be concluded that vitamin E administration may increase the humoral and cellular immune response and resistance to C. neoformans infection, but enhance the induction of ASA to CGG. Further studies are necessary to clarify the underlying mechanism accounting for these effects.

This study was undertaken to assess the effect of sound stress on humoral and cellular immune responses to thymus-dependent and independent antigens in mice. After mice were exposed to 4 hr daily sound stessors(83dB) for 4 days before or after immunization, the primary and / or secondary immune response to sheep red blood cells (SRBC), polyvinylpyrroridone( PVP) or picryl chloride(TNCB) were assayed. When mice were exposed to sound stressor before or after immunization, delayed-type hypersensitivity reaction and contact sensitivity to TNCB was remarkably depressed compared with those of the unstressed control mice. However, the primary and secondary hemagglutinin response of the stresed mice to SRBC showed a pronounced increase compared with that of the unstressed mice, In contrast to antibody response to SRBC, the primary antibody response of the stressed mic to PVP was almost not detected. surprisingly, the secondary antibody response to PVP of the mice receiving the secondary sound stress was markedly increased when the immune-depressed mice received the secondary immunization with PVP at 46 days after the primary immunization. The susceptibility of mice to intravenoulsy infected Candida albicans was not changed by the sound stress.