IntroductionGarlic (Allium sativum L.) is renowned for its health-promoting properties, largely due to its sulfur-rich compounds. While copper is essential for plant growth and metabolism, excessive levels can disrupt cellular processes and lead to oxidative stress.ObjectivesThis study aims to investigate the impact of copper supplementation on the metabolic profile of garlic, with a particular focus on changes in sulfur metabolism.MethodsIto garlic cloves were harvested in 2020 on Red-Yellow Latosol soil. Copper chelate fertilizer was applied foliarly at 300 mL/ha, 30, 20, and 10 days before harvest. After harvesting, cloves were refrigerated and analyzed. Using LC-MS metabolomics, the metabolic profile of garlic was analyzed after copper supplementation to assess changes, specifically in sulfur-containing compounds.ResultsCopper supplementation led to a significant reduction in key sulfur-containing metabolites critical for the health-promoting properties of garlic, including allicin (FC = 0.0947), alliin (FC = 0.0147), and gamma-glutamyl-S-allylcysteine (FC = 0.0076). Enrichment analysis identified alterations in pathways related to glutamine, glutamate, alanine, and aspartate metabolism. Additionally, precursors of glutathione (GSH) were depleted, likely as a result of GSH sparing efforts to counteract copper-induced oxidative stress. This redirection may increase susceptibility to ferroptosis, a form of cell death linked to oxidative damage.ConclusionThe metabolomic analysis of copper-supplemented Ito garlic cloves showed a significant reduction in sulfur compounds allicin, alliin, and gamma-glutamyl-S-allylcysteine, important for organoleptic and medicinal properties. This decrease indicates a metabolic shift towards antioxidant defenses, with glutathione being redirected to defense pathways rather than secondary metabolites. Future studies should explore oxidative stress and ferroptosis markers, and lipidomics for a deeper understanding of garlic response to copper exposure.

Although selenium (Se) and cadmium (Cd) often coexist naturally in the soil of China, the health risks to local residents consuming Se-Cd co -enriched foods are unknown. In the present study, we investigated the effects of chemical -based selenocystine (SeCys2) on cadmium chloride -induced human hepatocarcinoma (HepG2) cell injury and plant (Cardamine hupingshanensis)-derived SeCys2 against Cd-induced liver injury in mice. We found that chemical- and plant -based SeCys2 showed protective effects against Cd-induced HepG2 cell injury and liver damage in mice, respectively. Compared with Cd intervention group, co -treatment with chemical- or plant -based SeCys2 both alleviated liver toxicity and ferroptosis by decreasing ferrous iron, acyl-CoA synthetase long -chain (ACSL) family member 4, lysophosphatidylcholine acyltransferase 3, reactive oxygen species and lipid peroxide levels, and increasing ACSL3, peroxisome proliferator-activated receptor alpha, solute carrier family 7 member 11 (SLC7A11) and glutathione and glutathione peroxidase 4 (GPX4) levels. In conclusion, chemical- and plant -based SeCys2 alleviated Cd-induced hepatotoxicity and ferroptosis by regulating SLC7A11/GPX4 signaling and lipid peroxidation. Our findings indicate that potential Cd toxicity from consuming foods grown in Se- and Cd-rich soils should be re-evaluated. This study offers a new perspective for the development of SeCys2-enriched agricultural products.

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.