INSULIN SIGNALLING AND OXIDATIVE STRESS IN THE MECHANISM UNDERLYING STREPTOZOTOCIN AGGRAVATED DENTAL FLUOROSIS.

Jingchun Sun; Yan Wang; Hui Xu; Xiuhua Yu

The aim of this study was to elucidate whether insulin status affected the severity of dental fluorosis by characterizing changes in incisor morphology and oxidative stress status in vivo and analyzing the insulin receptor expression in osteoblasts exposed to the fluoride ion (F) in vitro. The development of drinking water-type dental fluorosis, with or without streptozotocin (STZ), was studied in 60 Wistar rats. The F-treated rats received F in low or high doses, 10 and 20 mg F/kg body weight per day by gavage for 2 months, respectively, and STZ in a single dose of 52 mg/kg bw by intraperitoneal injection. The results indicated that the F-treatment induced dental fluorosis which was significant aggravated by the deficiency of insulin activity mediated by the STZ administration. The low dose F-treatment, with 10 mg F/kg body weight per day significantly reduced the activity of glutathione peroxidase (GPX) and the combination of 20 mg F/kg body weight per day and STZ inhibited the activity of superoxide dismutase (SOD). No significant change occurred in the malondialdehyde (MDA) levels with the F or STZ treatments. In the in vitro experiment, a low dose of 2 mg F/L stimulated the protein expression of the insulin receptor, while at a high dose of 16 mg F/L inhibition occurred. The results indicate that insulin and its intracellular signaling are involved in the development of dental fluorosis and that the process may also involve the occurrence of oxidative stress.

FLUOROSIS; GLUTATHIONE peroxidase; INSULIN receptors

Fluoride, 2016, Vol 49, Issue 3, Part 2, p327

0015-4725

Academic Journal