BIOTIN DEFICIENCY INDUCES CHANGES IN SUBPOPULATIONS OF SPLEEN LYMPHOCYTES IN MICE

Citation
A. Baezsaldana et al., BIOTIN DEFICIENCY INDUCES CHANGES IN SUBPOPULATIONS OF SPLEEN LYMPHOCYTES IN MICE, The American journal of clinical nutrition, 67(3), 1998, pp. 431-437
Citations number
21
Categorie Soggetti
Nutrition & Dietetics
ISSN journal
00029165
Volume
67
Issue
3
Year of publication
1998
Pages
431 - 437
Database
ISI
SICI code
0002-9165(1998)67:3<431:BDICIS>2.0.ZU;2-W
Abstract
Biotin deficiency is known to affect immune function in both humans an d experimental animals. In this study, we determined the effect of bio tin deficiency on 4-wk-old Balb/cAnN mice during 20 wk of experimentat ion. The growth rate of mice slowed significantly during the first 6 w k of consumption of a diet designed to induce biotin deficiency; there after, from weeks 7 to 20 there was progressive weight loss in the mic e receiving the biotin-deficient diet. In the livers of biotin-deficie nt mice, the specific activities of two biotin-dependent enzymes-pyruv ate carboxylase and propionyl-CoA carboxylase-decreased by as much as 75% and 80%, respectively, and in spleen lymphocytes the specific acti vities of these two enzymes decreased by 63% and 75%, respectively. Wi th respect to the effects of biotin deficiency on the immune system, w e observed statistically significant changes in both the absolute numb er of spleen cells and in the proportions of spleen cells carrying dif ferent phenotypic markers: after 16 wk the percentage of cells express ing surface immunoglobulin (sIg) decreased from 47% (control and suppl emented) to 27% (deficient) and CD3(+) cells increased from 42% (contr ol and supplemented) to 54% (deficient). The mitogen-induced prolifera tion of spleen cells from deficient mice was lower than that of spleen cells from the control mice. These findings suggest that biotin could have an important role in lymphocyte maturation and responsiveness to stimulation, and consequently in the capacity of the immune system to respond to an antigenic challenge.