Lower level of vitamin D could increase the risk of precocious puberty.

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Context Gallic acid (GA) and lecithin showed important roles in antioxidant and drug delivery, respectively. A complex synthesized from GA and soybean lecithin (SL-GAC), significantly improved bioavailability of GA and pharmacological activities. However, the antioxidant activity of SL-GAC and its effect on iron-overload-induced liver injury remains unexplored. Objective This study investigates the antioxidant properties of SL-GAC in vitro and in mice, and its remediating effects against liver injury by iron-overloaded. Materials and methods In vitro , free radical scavenging activity, lipid peroxidation inhibition, and ferric reducing power of SL-GAC were measured by absorbance photometry. In vivo , C57BL/6J mice were randomized into 4 groups: control, iron-overloaded, iron-overloaded + deferoxamine, and iron-overloaded + SL-GAC. Treatments with deferoxamine (150 mg/kg/intraperitioneally) and SL-GAC (200 mg/kg/orally) were given to the desired groups for 12 weeks, daily. Iron levels, oxidative stress, and biochemical parameters were determined by histopathological examination and molecular biological techniques. Results In vitro , SL-GAC showed DPPH and ABTS free radicals scavenging activity with IC 50 values equal to 24.92 and 128.36 μg/mL, respectively. In C57BL/6J mice, SL-GAC significantly reduced the levels of serum iron (22.82%), liver iron (50.29%), aspartate transaminase (25.97%), alanine transaminase (38.07%), gamma glutamyl transferase (42.11%), malondialdehyde (19.82%), total cholesterol (45.96%), triglyceride (34.90%), ferritin light chain (18.51%) and transferrin receptor (27.39%), while up-regulated the levels of superoxide dismutase (24.69%), and glutathione (11.91%). Conclusions These findings encourage the use of SL-GAC to treat liver injury induced by iron-overloaded. Further in vivo and in vitro studies are needed to validate its potential in clinical medicine.

Approximately, 40% of ingested dietary aluminium accumulates in the intestine, which has been considered a target organ for dietary aluminium exposure. The gut microbiota may be the first protective barrier against the toxic metal aluminium and a crucial mediator of the bioavailability of metal aluminium. We previously evaluated dietary aluminium intake and its health risks in a population from Jilin Province, China, and found that the average daily intake of aluminium in the diet of residents in Jilin Province was 0.163 mg/kg after the total diet survey. In the present study, the equivalent concentration of aluminium in rats was extrapolated by the average dietary aluminium intake in the population of Jilin Province based on body surface area. Furthermore, healthy adult Wistar rats were randomly divided into four groups (n = 15 for each group): a control group and three groups treated with aluminium solution (1, 10, and 100 mg/kg/day, intragastrically) for 28 days. Following treatment, necrosis of renal tubular epithelial cells, hyperplasia of bile ducts and hyperplasia of heart tissue, as well as fiber in the liver, kidney, and heart tissues of aluminium‐treated rats were observed, although there were no significant changes in the spleen and brain. Subsequently, fecal samples were withdrawn for 16S rRNA gene sequence analysis. It was found that aluminium decreased the microbiota diversity and changed the overall community structure of the gut microbiota, including three phyla and four genera, together with the regulation of 12 signaling pathways. Collectively, treatment with aluminium markedly altered the structure of the gut microbiota, suggesting that the disorders of intestinal flora induced by aluminium may be an important mechanism for aluminium toxicity.

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