Effects of combined exposure to low levels of aerosolised nickel, copper and arsenic on myocardial injury in rats.

IF 2.1 4区 医学 Q3 TOXICOLOGY
Toxicology Research Pub Date : 2025-07-27 eCollection Date: 2025-08-01 DOI:10.1093/toxres/tfaf101
Xinyue Mu, Shuxia Yu, Yiwen Zhang, Junpu Yu, Tingting Gao, Xin Wang, Li Ma, Ye Ruan, Tian Tian, Rentong Chen
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Abstract

Chronic low-level exposure to nickel (Ni), copper (Cu), and arsenic (As) may contribute to myocardial injury via oxidative stress. This study investigated the effects of these metals in male Sprague-Dawley rats exposed to aerosols of Ni (0.106 mg/m3), Cu (0.048 mg/m3), and As (0.025 mg/m3) at environmental and 10-fold concentrations for 3 mo. Blood metal levels were analyzed using inductively coupled plasma-mass spectrometry (ICP-MS), and oxidative stress and myocardial injury biomarkers were measured with enzyme-linked immunosorbent assay (ELISA). Blood As levels showed a dose-dependent increase in both exposure groups. Myocardial ultrastructural damage, including mitochondrial swelling, disorganized myofibrils, and increased autolysosomes, was observed. Biomarkers of oxidative stress, including catalase (CAT), superoxide dismutase (SOD), and glutathione (GSH), were significantly elevated in both exposure groups, while malondialdehyde (MDA) levels were notably higher in the 10-fold group. Myocardial injury markers (TNNI3, LDHA, and α-HBDH) were elevated in both exposure groups. Significant correlations were found between Cu and As levels and oxidative stress and myocardial injury biomarkers. These findings demonstrate that prolonged low-level exposure to Ni, Cu, and As induces oxidative stress and myocardial injury in rats. The results highlight the potential cardiovascular risks associated with environmental exposure to mixed heavy metals and emphasize the importance of stricter regulatory measures to limit such pollutants.

同时暴露于低水平雾化镍、铜和砷对大鼠心肌损伤的影响。
长期低水平暴露于镍(Ni)、铜(Cu)和砷(As)可能通过氧化应激导致心肌损伤。本研究研究了雄性Sprague-Dawley大鼠在环境浓度和10倍浓度下暴露于Ni (0.106 mg/m3)、Cu (0.048 mg/m3)和As (0.025 mg/m3)气溶胶3个月后对这些金属的影响。采用电感耦合等离子体质谱(ICP-MS)分析血液金属水平,并采用酶联免疫吸附试验(ELISA)测量氧化应激和心肌损伤生物标志物。两个暴露组的血砷水平均呈剂量依赖性增加。观察到心肌超微结构损伤,包括线粒体肿胀、肌原纤维紊乱和自溶酶体增加。氧化应激的生物标志物,包括过氧化氢酶(CAT)、超氧化物歧化酶(SOD)和谷胱甘肽(GSH),在两个暴露组中都显著升高,而丙二醛(MDA)水平在10倍暴露组中显著升高。两组心肌损伤标志物TNNI3、LDHA、α-HBDH均升高。Cu和As水平与氧化应激和心肌损伤生物标志物之间存在显著相关性。这些发现表明,长期低水平暴露于Ni、Cu和As可诱导大鼠氧化应激和心肌损伤。研究结果强调了与环境暴露于混合重金属有关的潜在心血管风险,并强调了采取更严格的监管措施限制此类污染物的重要性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Toxicology Research
Toxicology Research TOXICOLOGY-
CiteScore
3.60
自引率
0.00%
发文量
82
期刊介绍: A multi-disciplinary journal covering the best research in both fundamental and applied aspects of toxicology
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