Fluoride induces hepatointestinal damage and vitamin B mitigation by regulating IL-17A and Bifidobacterium in ileum.

Introduction: Fluorosis is a global public health disease affecting more than 50 countries and 500 million people. Excessive fluoride damages the liver and intestines, yet the mechanisms and therapeutic approaches remain unclear.

Objectives: To explore the mechanisms by which fluoride-induced intestinal-hepatic damage and vitamin B alleviation.

Riboflavin Attenuates Fluoride-Induced Testicular Injury via Interleukin 17A-Mediated Classical Pyroptosis.

Male reproductive toxicity of fluoride is of great concern worldwide, yet the underlying mechanism is unclear. Pyroptosis is a novel mode of inflammatory cell death, and riboflavin with anti-inflammatory properties has the potential to protect against fluoride damage. However, it is unknown whether pyroptosis is involved in fluoride-induced testicular injury and riboflavin intervention.

Chronic arsenic exposure lowered sperm motility via impairing ultra-microstructure and key proteins expressions of sperm acrosome and flagellum formation during spermiogenesis in male mice.

Arsenic (As) poisoning and its potential reproductive functional lesions are a global environmental concern. Recent studies shown that spermiogenesis tends to be a major target process in arsenic-induced male infertility, however, the underlying mechanisms are not fully illuminated. In the present study, 32 fertility related indices including sperm motility, dynamic acrosome formation and sperm flagellum during spermiogenesis in testes were evaluated in adult male mice treated with 0, 0.