Herein, we report for the first time the incorporation of riboflavin as a bioactive additive in soy protein isolate films, along with investigating the impact of UV light treatment, thereby creating functional packaging material. Our investigation involves a comprehensive characterization of the films, including morphological, physicochemical, and mechanical properties, as well as their effectiveness as light barriers, antimicrobial potential, and biodegradation properties. The UV treatment of riboflavin/soy protein dispersions leads to the formation of films exhibiting minor water swelling and total soluble matter compared to those untreated with UV light, suggesting the development of a cross-linked network. Moreover, increased riboflavin content enhances the cross-linked network's robustness. The mechanical properties of the films exhibit a notable improvement with UV treatment and with increasing riboflavin content until a limit value, showcasing increased tensile strength and Young's modulus. Films showed homogeneous surfaces with an absence of pores and cracks and the ability to act as a barrier for oil passage. Films were assayed as a coating material for chia oil samples exposed to highintensity UV light, showing great protection capacity. It has been demonstrated that an increase in riboflavin concentration enhances the UV light-blocking properties, making these films promising candidates for storing light-sensitive food products while preserving their nutritional quality. In addition, antibacterial action against S. aureus was determined by disk diffusion assay. Furthermore, the films exhibited relatively short disintegration times under soil burial conditions, even after chemical modification. This research contributes valuable insights to the innovative field of sustainable food packaging materials.

Fluoride is widely found in groundwater, soil, animal and plant organisms. Excessive fluoride exposure can cause reproductive dysfunction by activating IL -17A signaling pathway. However, the adverse effects of fluoride on male reproductive system and the mechanisms remain elusive. In this study, the wild type and IL -17A knockout C57BL/6J mouse were treated with 24 mg/kg & sdot;bw & sdot;d sodium fluoride and/or 5 mg/kg & sdot;bw & sdot;d riboflavin-5 '-phos- phate sodium for 91 days. Results showed that fluoride caused dental fluorosis, increased the levels of ROS in testicular Leydig cells and GSSG in testicular tissue, and did not affect the iron and serum hepcidin levels in testicular tissue. Riboflavin alleviated above adverse changes, whereas IL -17A does not participate in the oxidative stress -mediated reproductive toxicity of fluoride. Based on this, TM3 cells were used to verify the injury of fluoride on Leydig cells. Results showed that fluoride increased mRNA levels of ferroptosis marker SLC3A2, VDAC3, TFRC, and SLC40A1 and decreased Nrf2 mRNA levels in TM3 cells. The ferroptosis inhibitor Lip -1 and DFO were used to further investigate the relationship between male reproductive toxicity and ferroptosis induced by fluoride. We found that the fluoride -induced decrease in cell viability, increase in xCT, TFRC, and FTH protein expression, and decrease in GPX4 protein expression, can all be rescued by Lip -1 and DFO. Similar results were also observed in the riboflavin treatment group. Moreover, riboflavin mitigated fluoride -induced increases in ROS levels and SLC3A2 protein levels. In all, our work revealed that riboflavin inhibited ferroptosis in testicular Leydig cells and improved the declined male reproductive function caused by fluoride. This study provides new perspectives for revealing new male reproductive toxicity mechanisms and mitigating fluoride toxicity damage.