It has been confirmed that exposure to various metal pollutants can induce neurotoxicity, which is closely associated with the occurrence and development of neurological disorders. Ferroptosis is a form of cell death in response to metal pollutant exposure and it is closely related to oxidative stress, iron metabolism and lipid peroxidation. Recent studies have revealed that ferroptosis plays a significant role in the neurotoxicity induced by metals such as lead, cadmium, manganese, nickel, and antimony. Lead exposure triggers ferroptosis through oxidative stress, iron metabolism disorder and inflammation. Cadmium can induce ferroptosis through iron metabolism, oxidative stress and ferroptosis related signaling pathways. Manganese can promote ferroptosis through mitochondrial dysfunction, iron metabolism disorder and oxidative stress. Nickel can promote ferroptosis by influencing mitochondrial function, disrupting iron homeostasis and facilitating lipid peroxidation in the central nervous system. Antimony exposure can induce glutathione depletion by activating iron autophagy, resulting in excessive intracellular iron deposition and ultimately causing ferroptosis. This article reviews the effects of metal pollutants on ferroptosis-related indicators and discusses the specific mechanisms by which each metal triggers ferroptosis. It provides a reference for identifying targets for preventing neurotoxicity and for developing treatment strategies for neurological disorders.
Ferroptosis/drug effects* ; Humans ; Iron/metabolism* ; Oxidative Stress/drug effects* ; Neurotoxicity Syndromes/metabolism* ; Cadmium/adverse effects* ; Animals ; Lipid Peroxidation/drug effects* ; Metals/metabolism* ; Lead/adverse effects* ; Environmental Pollutants/toxicity* ; Manganese/adverse effects* ; Nickel/adverse effects* ; Mitochondria/drug effects* ; Signal Transduction/drug effects*

Objective: To observe the preventive effect of alkaline drinking water on hyperuricemia in mice. Methods: Sixty male SPF Kunming mice were randomly divided into six groups: pH 7.3, pH 8.0, pH 9.3 intervention groups, in which the mice were given water with pH values of 7.3±0.5, 8.0±0.5 and 9.3±0.6, respectively; the control group, model group and positive drug group ( with 2 g/L allopurinol ) were given double distilled water. Except for the control group, the mice in each group were given yeast by gavage (1.5 g/mL) for 13 days. On the 14th day, the mice were injected with 300 mg/kg potassium oxyzinate by intraperitoneal injection, and then fasted for 1 day. On the 16th day, serum uric acid, creatinine and urea nitrogen were detected, and renal tissues were stained to observe the morphology.The expression levels of neutrophil gelatinase-associated lipocalin ( NGAL ), tissue inhibitor of metalloproteinase 1( TIMP1 ), organic anion transporter 1 ( OAT1 ) and urate transporter 1 ( URAL-1 ) in renal tissues were determined bywestern blotting. The mRNA expression levels of URAL-1 and OAT1 were detected by real-time fluorescent quantita⁃tive polymerase chain reaction. Results: The level of serum uric acid was higher in the model group than in the control group and in the pH 9.3 intervention group (both P<0.05). The number and area of renal tubular lesions were less in the pH 9.3 intervention group than in the model group (all P<0.05). The relative expression levels of NGAL and URAT-1 proteins were lower in the pH 9.3 intervention group than in the model group, and the relative expression level of OAT1 protein was higher in the pH 9.3 intervention group than in the model group ( all P<0.05). The relativeexpression level of URAT-1 mRNA was lower in the pH 9.3 intervention group than in the model group, and the rela⁃tive expression level of OAT1 mRNA was higher in the pH 9.3 intervention group than in the model group ( all P<0.05 ). Conclusion Alkaline drinking water with pH value of 9.3±0.6 can effectively prevent hyperuricemia and acute kidney injury in mice.

Objective To explore the effect of stromal cell-derived factor-1 α (SDF-1 α) on inducing recruitment of bone marrow-derived cells (BMDCs) to wound area. Methods BMDCs were isolated from bone marrow, cultured with routine method and identified by CXCR4 antibody. Cells cultured with CXCR4 antibody (100 ng,/mL) for 6 hours were labeled with CM-DiI and injected into the tail vein of full-thickness incisional wound model (set as anti-CXCR4 group). BMDCs labeled with CM-DiI without antibody treatment were injected to the rats in BMDCs group, and rats were injected with DMEM/F12 serum-free medium in the control group. The quantity of labeled BMDCs at the wound site and the percentage of wound closure were measured. Results (1) All BMDCs expressed CXCR4. (2) The percentages of wound closure at days 7 and 14 in BMDCs group (7 d: 41.3% ±4.6%; 14 d:92.3% ±2. 1%) were significantly higher than those of control group (7 d: 29.3% ±2. 3%; 14 d: 77.3% ±2.5%) and anti-CXCR4 group (7 d: 30.7% ±4.6% ;14 d: 85.7% ±1.5%) (P＜0.05). The percentage of wound closure of anti-CXCR4 group was significantly higher than that of control group at day 14(P ＜ 0.05). (3) The number of CM-DiI labeled BMDCs at wound site at days 7 and 14 in BMDCs group [7 d: (535 ±84) cells/hpf; 14 d: (769 ±124) cells/hpf) were greater than those of anti-CXCR4 group [7 d: (335 ±97) cells/hpf; 14 d: (521 ± 127) cells/hpf] (P＜0.05). Conclusions BMDCs participate in the cutaneous wound healing. SDF-1α plays an important role in recruiting BMDCs to wound area.