Iodine status and associated dietary factors among preschool children in Shanghai.

Children aged 3-6 years undergo a critical stage of growth and development and are irreversibly affected by their iodine status. In order to reveal iodine status in preschool children, we detected iodine concentrations in urine samples from 1382 children aged 3-6 years based on a cross-sectional study. The median urinary iodine concentration (UIC) of children was 193.36 µg/L and was 336.96 µg/g·Cr corrected for creatinine. The study developed a link between dietary habits and iodine status, revealing that regular calcium supplement (OR: 1.79, (95% CI: 1.03, 3.12)) increased deficiency risk, while moderate seafood consumption (OR: 0.60, (95% CI: 0.38, 0.95)) decreased it. Additionally, modest intake of shellfish (OR: 0.58, (95% CI: 0.33, 1.00)), vegetables (OR: 0.61, (95% CI: 0.38, 0.97)), and eggs (OR: 0.53, (95% CI: 0.30, 0.95)) was found to protect against excess iodine. The findings underline the importance of balanced diets and various nutrients' roles in preschoolers' iodine status.

Effects of food-borne docosahexaenoic acid supplementation on bone lead mobilisation, mitochondrial function and serum metabolomics in pre-pregnancy lead-exposed lactating rats.

Large bone lead (Pb) resulting from high environmental exposure during childhood is an important source of endogenous Pb during pregnancy and lactation. Docosahexaenoic acid (DHA) attenuates Pb toxicity, however, the effect of DHA on bone Pb mobilisation during lactation has not been investigated. We aimed to study the effects of DHA supplementation during pregnancy and lactation on bone Pb mobilisation during lactation and its potential mechanisms. Weaning female rats were randomly divided into control (0.05% sodium acetate) and Pb-exposed (0.05% Pb acetate) groups, after a 4-week exposure by ad libitum drinking and a subsequent 4-week washout period, all female rats were mated with healthy males until pregnancy. Then exposed rats were randomly divided into Pb and Pb + DHA groups, and the latter was given a 0.14% DHA diet, while the remaining groups were given normal feed until the end of lactation. Pb and calcium levels, bone microarchitecture, bone turnover markers, mitochondrial function and serum metabolomics were analyzed. The results showed that higher blood and bone Pb levels were observed in the Pb group compared to the control, and there was a significant negative correlation between blood and bone Pb. Also, Pb increased trabecular bone loss along with slightly elevated serum C-telopeptide of type I collagen (CTX-I) levels. However, DHA reduced CTX-I levels and improved trabecular bone microarchitecture. Metabolomics showed that Pb affected mitochondrial function, which was further demonstrated in bone tissue by significant reductions in ATP levels, Na+-K+-ATPase, Ca2+-Mg2+-ATPase and CAT activities, and elevated levels of MDA, IL-1ß and IL-18. However, these alterations were partially mitigated by DHA. In conclusion, DHA supplementation during pregnancy and lactation improved bone Pb mobilisation and mitochondrial dysfunction in lactating rats induced by pre-pregnancy Pb exposure, providing potential means of mitigating bone Pb mobilisation levels during lactation, but the mechanism still needs further study.

Effects of food-borne cholesterol supplementation on lead-induced neurodevelopmental impairments of rats based on BDNF signaling pathway and cholesterol metabolism.

Despite the ubiquity and prevalence of lead (Pb) in the environment and industry, the mechanism of lead-induced neurotoxicity in the brain remains unclear, let alone its prevention and treatment. In this study, we hypothesized that exogenous cholesterol supplementation acts as an effective remedy for lead-induced neurodevelopmental impairments caused by lead. Forty 21-day-old male rats were randomly divided into four groups and administered 0.1 % lead water and/or 2 % cholesterol-containing feed for 30 d. Ultimately, rats in the lead group lost weight, accompanied by spatial learning and memory impairments as verified by the Morris water maze test, in which the escape latency of rats was prolonged, and the number of crossings in the target platform and the residence time in the target quadrant were significantly diminished compared to the control group. Hematoxylin-Eosin (H&E) staining and Nissl staining illustrated that typical pathological morphology occurred in the brain tissue of the lead group, where the tissue structure was loose, the number of hippocampal neurons and granulosa cells decreased significantly and were arranged loosely, along with enlarged intercellular space, light matrix staining, and decline in Nissl bodies. In addition, inflammatory response and oxidative stress were significantly induced by lead. Immunofluorescence experiments showed apparent activation of astrocytes and microglia, followed by the enhancement of TNF-α and IL-ß levels. Moreover, the MDA content in the lead group was elevated dramatically, whereas the activities of SOD and GSH were significantly inhibited. As for the mechanism, western blot and qRT-PCR experiments were performed, where lead could significantly inhibit the BDNF-TrkB signaling pathway, lowering the protein expression of BDNF and TrkB. Cholesterol metabolism was also affected by lead exposure, in which cholesterol metabolism-related protein expression and gene transcription, including SREBP2, HMGCR, and LDLR, were downregulated. However, cholesterol supplementation efficiently detoxified the negative effects of lead-induced neurotoxicity, reversing the inflammatory response, oxidative stress, inactivation of the BDNF signaling pathway, and imbalance of cholesterol metabolism, thus improving the learning and memory ability of rats. In brief, our study demonstrated that cholesterol supplementation could ameliorate the deficiency of learning and memory induced by lead, which is closely associated with the initiation of the BDNF/TrkB signaling pathway and regulation of cholesterol metabolism.