Jh. Mitchell et al., SELENIUM AND IODINE DEFICIENCIES - EFFECTS ON BRAIN AND BROWN ADIPOSE-TISSUE SELENOENZYME ACTIVITY AND EXPRESSION, Journal of Endocrinology, 155(2), 1997, pp. 255-263
Adequate dietary iodine supplies and thyroid hormones are needed for t
he development of the central nervous system (CNS) and brown adipose t
issue (BAT) function. Decreases in plasma thyroxine (T-4) concentratio
ns may increase the requirement for the selenoenzymes types I and II i
odothyronine deiodinase (ID-I and ID-II) in the brain and ID-II in BAT
to protect against any fall in intracellular 3,3',5 tri-iodothyronine
(T-3) concentrations in these organs. We have therefore investigated
selenoenzyme activity and expression and some developmental markers in
brain and BAT of second generation selenium- and iodine-deficient rat
s. Despite substantial alterations in plasma thyroid hormone concentra
tions and thyroidal and hepatic selenoprotein expression in selenium a
nd iodine deficiencies, ID-I, cytosolic glutathione peroxidase (cGSHPx
) and phospholipid hydroperoxide glutathione peroxidase (phGSHPx) acti
vities and expression remained relatively constant in most brain regio
ns studied. Additionally, brain and pituitary ID-II activities were in
creased in iodine deficiency regardless of selenium status. This can h
elp maintain tissue Tg concentrations in hypothyroidism. Consistent wi
th this, no significant effects of iodine or selenium deficiency on th
e development of the brain were observed, as assessed by the activitie
s of marker enzymes. In contrast, BAT from selenium- and iodine-defici
ent rats had impaired thyroid hormone metabolism and less uncoupling p
rotein than in tissue from selenium-and iodine-supplemented animals. T
hus, the effects of selenium and iodine deficiency on the brain are li
mited due to the activation of the compensatory mechanisms but these m
echanisms are less effective in BAT.