[Environmental and geochemical behaviors of fluorine and its impacts on ecological environment]. / æ°Ÿçš„çŽ¯å¢ƒåœ°çƒåŒ–å­¦è¡Œä¸ºåŠå ¶å¯¹ç”Ÿæ€çŽ¯å¢ƒçš„å½±å“.

In past decades, fluorine exposure of plants and human caused by regional geochemical anomalies of fluorine or environmental pollution has received widespread concerns. Many in-depth researches have been conducted on the geochemical behavior of fluorine in different environmental media, but with disputes and uncertainties. We reviewed the research advances on geochemical behaviors of fluorine in the atmosphere, water and soil, including source, quantity, existence form, migration, transformation, and controlling factors. The observation of correlation between geochemical behaviors of fluorine and plant and human fluoride exposure was also reviewed. Moreover, we proposed that the future research on environmental geochemical behaviors of fluorine should give priority to particular directions.

[Biological exposure limits caused by co exposure to fluoride and arsenic based on Wnt signaling pathway]. / 基于Wntä¿¡å·é€šè·¯æŽ¢è®¨æ°Ÿç ·æ··åˆæš´éœ²çš„ç”Ÿç‰©æš´éœ²é™å€¼.

Chronic fluoride-arsenic combined poisoning is a global public health problem. While the cause of the disease is clear, the pathogenesis is unknown. Given that there is no specific treatment, early prevention is particularly important. Biological exposure limits are designed to investigate the maximum allowable concentration of harmful effects from exogenous chemicals. To explore the biological exposure limits for mixed exposures of fluoride and arsenic, we compared the contents of fluorine and arsenic in the environmental media of the control and fluoride-arsenic combined exposure areas and analyzed the dose-effect and dose-response relationship between fluoride, arsenic and the key proteins of Wnt signaling pathways. The benchmark dose method was used to estimate the biological exposure limit for fluoride-arsenic combined exposure. The results showed that the content of fluoride in coal, clay, indoor air, outdoor air, chili and rice, as well as arsenic content in coal, clay, outdoor air, chili and rice was higher than that of the control. With the increase of fluoride and arsenic exposure levels, the glycogen synthase kinase 3β (GSK3β), β-catenincontents and the prevalence of Wnt/β-catenin signaling pathway antagonistic protein Dickkopf-1 (DKK1), GSK3β, Beta-catenin (β-catenin) gradually increased, but the content of DKK1 significantly decreased. Based on the Wnt signaling pathway, the biological exposure limit for fluoride-arsenic combined exposure was urinary fluoride of 0.52 mg·g-1 creatinine and urinary arsenic of 6.59 mg·g-1 creatinine. Our results had important guiding significance for early prevention of body damage caused by fluoride-arsenic combined poisoning.

A possible new mechanism and drug intervention for kidney damage due to arsenic poisoning in rats.

Arsenic poisoning is a worldwide endemic disease that affects thousands of people. Currently, the aetiology of the disease is known, but its pathogenesis is uncharacterized and there is no specific treatment. We established a rat model of coal-burning arsenic poisoning by feeding the animals corn powder baked with high arsenic coal. By observing subsequent changes in kidney and immune function, we found that arsenic induces both kidney and immune damage. Furthermore, there is a significant correlation between kidney and immune damage. Moreover, Ginkgo biloba, a known immune enhancer, was used as an intervention agent in arsenic poisoned rats to validate the relationship between kidney and immune damage. Meanwhile, we also explored the mechanism of Ginkgo biloba treatment of kidney damage in burning-coal arsenic poisoned rats. We found that Ginkgo biloba enhanced immune function in rats with arsenic poisoning and ameliorated arsenic-induced kidney damage. These results suggest that immune suppression may be one of the mechanisms underlying arsenic-induced kidney damage and that Ginkgo biloba might relieve kidney damage by enhancing immune function.

Correction: A possible new mechanism and drug intervention for kidney damage due to arsenic poisoning in rats.

[This corrects the article DOI: 10.1039/C5TX00165J.].

Arsenic may be involved in fluoride-induced bone toxicity through PTH/PKA/AP1 signaling pathway.

Chronic exposure to combined fluoride and arsenic continues to be a major public health problem worldwide, affecting thousands of people. In recent years, more and more researchers began to focus on the interaction between the fluorine and the arsenic. In this study, the selected investigation site was located in China. The study group was selected from people living in fluoride-arsenic polluted areas due to burning coal. The total number of participants was 196; including the fluoride-arsenic anomaly group (130) and the fluoride-arsenic normal group (63). By observing the changes in gene and protein expression of PTH/PKA/AP1 signaling pathway, the results show that fluoride can increase the expression levels of PTH, PKA, and AP1, but arsenic can only affect the expression of AP1; fluoride and arsenic have an interaction on the expression of AP1. Further study found that fluoride and arsenic can affect the mRNA expression level of c-fos gene (AP1 family members), and have an interaction on the expression of c-fos, but not c-jun. The results indicate that PTH/PKA/AP1 signaling pathway may play an important role in bone toxicity of fluoride. Arsenic can affect the expression of c-fos, thereby affecting the expression of transcription factor AP1, indirectly involved in fluoride-induced bone toxicity.