Little is known of the effects of nutritional deficiencies on lymphopo
ietic processes. Nevertheless, deficiencies in zinc adversely affect i
mmune function causing thymic atrophy and lymphopenia in both humans a
nd animals. Previous studies of the effects of zinc deficiency (ZD) on
lymphopoiesis in adult mice indicated that a suboptimal intake of zin
c caused a 50% or more depletion of the marrow of developing B cells.
Thus, interference in the production of lymphocytes by ZD appeared to
be a significant factor in the loss of host defence capacity. In the c
urrent study three-colour immunofluorescence phenotyping of early bone
marrow B lymphocytes (B220(+) immunoglobulin(-)) using flow cytometry
demonstrated that a 27-day period of ZD caused a 50-70% decline in pr
e-B cells (B220(+) CD43(-) immunoglobulin M (IgM)(-)) for moderate and
severely zinc-deficient mice, respectively. Conversely, early pro-B c
ells (B220(+) CD43(+) 6C3(-)) and late pro-B cells (B220(+) CD43(+) 6C
3(+)) exhibited little or no change in their distribution within the m
arrow. Indeed, the greater resistance of pro-B cells resulted in a 50%
increase in the proportion of this subset within the B-cell compartme
nt of the marrow as the deficiency in zinc advanced. Collectively, the
data indicate that the B-cell compartment of the marrow is substantia
lly altered by ZD and the stage specific sensitivity noted among early
B cells may be related to chronically elevated levels of glucocortico
ids present during ZD or other parameters that affect their survival a
nd resistance to apoptosis.