Objective This study aims to investigate the impact of lead on neutrophil degranulation and its implications for myocardial injury in mice.

Methods Male C57BL/6 mice were given lead acetate by intraperitoneal injection at 1 and 5 mg/kg for 28 days; enzyme-linked immunosorbent assay(ELISA) was used to detect myeloperoxidase (MPO), neutrophil elastase(NE), and troponin Ⅰ(CTnⅠ) in serum; and an automatic biochemical analyzer was employed to measure other myocardial enzyme indicators. Inductively coupled plasma mass spectrometry(ICP-MS) was used to detect lead concentration in mouse blood cells, and Spearman correlation analysis was performed to examine their associations. The cytotoxicity of lead was detected by MTT assay to select the intoxication concentration for subsequent experiments. Neutrophils were extracted from the bone marrow of untreated mice and cultured with normal saline and 0.5 and 5.0 mg/L lead acetate solution for 1 hour, respectively. The changes in the expression levels of MPO and NE proteins were detected.

Results After 28 days of lead exposure of mice, the serum levels of NE, CTnⅠ, and AST in the 5 mg/kg lead-exposed group were all significantly increased (P < 0.05). The blood lead concentration of mice was positively correlated with the serum levels of NE, CTnⅠ, and AST proteins, and the CTnⅠ level was positively correlated with the NE protein level (both P < 0.05). In vitro experiments, after 1 hour of culture with 0.5 mg/L and 5.0 mg/L lead acetate solutions, the levels of MPO and NE in the supernatant of neutrophils were higher than those in the control group (P < 0.05).

Conclusions Lead exposure could increase the levels of neutrophil degranulation markers in mice, which may be associated with myocardial injury.