Effect of dietary restriction on DNA synthesis in vitamin E-deficient rats.
To assess the effect of dietary restriction on increased oxidative stress conditions, we measured the proliferative response of spleen lymphocytes from the following groups of adult rats: (1) control fed ad libitum (14 months of age); (2) vitamin E-deficient (12 months of age); and (3) vitamin E-deficient maintained on dietary restricted paradigm, that is, every other day schedule (12 months of age) animals. No significant change was observed among the three groups investigated at 24 h. At 48 h, [(3)H]thymidine incorporation was significantly lower in vitamin E-deficient rats vs. the other groups at Con A concentrations of 1 and 5 mug/mL, while at Con A concentration of 10 mug/mL the incorporation of the labeled compound in lymphocytes was significantly lower than only the vitamin E-deficient rats vs. controls. At 72 h: nonstimulated lymphocytes from ad libitum fed control rats showed significant higher values of [(3)H]thymidine incorporation vs. the other groups; no significant difference was found among the three groups investigated at 1 and 10 mug/mL Con A concentrations, while at 5 mug/mL Con A concentration, the lymphocytes from vitamin E-deficient rats showed a significant lower value of [(3)H]thymidine incorporation vs. the other groups. These data support that vitamin E-deficiency impairs the proliferative response of spleen lymphocytes from adult rats, while dietary restriction appears to be able to reverse this alteration. Although the mechanism(s) of action of dietary restriction in prolonging the life span and ameliorating health conditions are not know, it is currently supported that a reduced food intake results in a better control of free radical attacks to biological molecules as well as to several cellular and system functions. With specific reference to the present findings, dietary restriction may help the mitotic process dynamics to be accomplished in a condition of low rate of free radical damage, thus representing a physiological intervention capable of modulating positively the proliferative capacity of spleen lymphocytes and, in turn, the immune system, even in adverse conditions such as increased oxidative stress.