Fluoride induces immunotoxicity by regulating riboflavin transport and metabolism partly through IL-17A in the spleen.

The impairment of the immune system by fluoride is a public health concern worldwide, yet the underlying mechanism is unclear. Both riboflavin and IL-17A are closely related to immune function and regulate the testicular toxicity of fluoride. However, whether riboflavin or IL-17A is involved in fluoride-induced immunotoxicity is unknown.

Relieved Fluoride-Induced Hepatic and Ileal Toxicity via Inflammatory Response and Bile Acid Transporters in Mice.

Fluoride is a pervasive environmental contaminant. Prolonged excessive fluoride intake can inflict severe damage on the liver and intestines. Previous 16S rDNA sequencing revealed a decrease in ileal abundance during fluoride-induced hepatointestinal injury.

KIF2A participates in the progression of hepatocellular carcinoma and angiogenesis by interacting with Notch1.

Kinesin family member 2A (KIF2A) serves a vital role in the development of hepatocellular carcinoma (HCC); however, the biological effect of KIF2A on the malignant progression of HCC remains unclear. Therefore, the present study was conducted to systematically determine the biological role of KIF2A in HCC and to better understand the molecular mechanism. The differences of KIF2A expression in HHL-5 normal human hepatocytes and the HCC cell lines Li-7, Huh7 and MHCC97 were assessed by reverse transcription-quantitative PCR and western blotting analysis.