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Protective role of ascorbic acid on lead-induced damage to the thyroid gland in the rat

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Abstract Lead exposure is known to affect the pituitary-thyroid axis. Likewise, ascorbic acid (AA) has a protective action against lead poisoning. We examine the protective role of AA in lead-induced damage to the thyroid gland. The Wistar rats were divided into three groups: control that received 0.2% AA in drinking water throughout the experiment (15 days), intoxicated with lead acetate (20 mg/kg) intraperitoneally every 48 h for 15 days, and the experimental group treated with lead acetate and 0.2% AA in drinking water throughout the experiment. Plasma thyroid-stimulating hormone, triiodothyronine, thyroxine, and lead were determined. The thyroid gland was weighed, then epithelial cell height and nuclear volume were measured on histological slides. The results show that AA reduced the thyroid atrophy caused by lead acetate, as well as the loss of weight of the gland. In addition, it prevented the decrease of the hormone triiodothyronine, although the thyroxine hormone remained lower than the control values ​​and the thyroid-stimulating hormone remains high. Our results indicated that AA could play a protective role in lead poisoning in the thyroid gland.
Title: Protective role of ascorbic acid on lead-induced damage to the thyroid gland in the rat
Description:
Abstract Lead exposure is known to affect the pituitary-thyroid axis.
Likewise, ascorbic acid (AA) has a protective action against lead poisoning.
We examine the protective role of AA in lead-induced damage to the thyroid gland.
The Wistar rats were divided into three groups: control that received 0.
2% AA in drinking water throughout the experiment (15 days), intoxicated with lead acetate (20 mg/kg) intraperitoneally every 48 h for 15 days, and the experimental group treated with lead acetate and 0.
2% AA in drinking water throughout the experiment.
Plasma thyroid-stimulating hormone, triiodothyronine, thyroxine, and lead were determined.
The thyroid gland was weighed, then epithelial cell height and nuclear volume were measured on histological slides.
The results show that AA reduced the thyroid atrophy caused by lead acetate, as well as the loss of weight of the gland.
In addition, it prevented the decrease of the hormone triiodothyronine, although the thyroxine hormone remained lower than the control values ​​and the thyroid-stimulating hormone remains high.
Our results indicated that AA could play a protective role in lead poisoning in the thyroid gland.

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