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Mutaku, Many
Cell necrosis and apoptosis are differentially regulated during goitre development and iodine-induced involution.Mutaku JF, Poma JF, Many MC, Denef JF, van Den Hove MF. J Endocrinol. 2002 Feb;172(2):375-86.
"Necrosis and
apoptosis coexist in the thyroid during goitre development and
involution, but little is known about their respective causes. To
test the possible role of free radicals, we analysed separately
necrosis and apoptosis in male Wistar rats with depressed or
normal antioxidant protection. Vitamin E-deficient and
-sufficient rats were made goitrous with perchlorate in drinking
water; involution was induced by repeated injection of NaI,
without or with methimazole. Increase of thyroid malondialdehyde
concentration and decrease of glutathione peroxidase activity
confirmed the depressed antioxidant protection in vitamin
E-deficient rats. Plasma thyroxine and TSH levels were not
modified. Necrosis (swollen cells) and apoptosis (pyknotic cells)
were quantified on histological sections. In vitamin E-sufficient
rats, dead cells were very rare in control thyroids, increased
3-fold in goitre and still further during involution. Necrotic
epithelial cells predominated in the goitre and their number
declined after iodide supplementation, without or with
methimazole. In contrast, the number of apoptotic cells and the
caspase-3 activity were increased in goitre and further increased
after involution, with two-thirds of pyknotic cells being
observed in the interstitium. Apoptosis was prevented by
methimazole. Vitamin E deficiency significantly increased total
cell death and epithelial cell necrosis and induced the
occurrence of much cell debris in the follicular lumen during
involution, with no modification of the apoptotic reaction. These
results show that the type of cell death is differentially
regulated during goitre development and involution: necrosis is
related to the oxidative status of the cells, while apoptosis
comes with iodine-induced involution." |
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