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母体暴露于硝酸钇对 BALB/c 仔鼠的发育免疫毒性。

Developmental immunotoxicity of maternal exposure to yttrium nitrate on BALB/c offspring mice.

机构信息

Department of Toxicology, School of Public Health, Peking University, Beijing, People's Republic of China.

Beijing Key Laboratory of Toxicological Research and Risk Assessment for Food Safety, School of Public Health, Peking University, Beijing, People's Republic of China.

出版信息

Environ Toxicol. 2023 Aug;38(8):1939-1950. doi: 10.1002/tox.23820. Epub 2023 Apr 27.

DOI:10.1002/tox.23820
PMID:37102272
Abstract

Yttrium is a typical heavy rare earth element with widespread use in numerous sectors. Only one previous study has indicated that yttrium has the potential to cause developmental immunotoxicity (DIT). Therefore, there remains a paucity of evidence on the DIT of yttrium. This study aimed to explore the DIT of yttrium nitrate (YN) and the self-recovery of YN-induced DIT. Dams were treated with 0, 0.2, 2, and 20 mg/kg bw/day YN by gavage during gestation and lactation. No significant changes were found in innate immunity between the control and YN-treated groups in offspring. In female offspring at postnatal day 21 (PND21), YN markedly inhibited humoral and cellular immune responses, the proliferative capacity of splenic T lymphocytes, and the expression of costimulatory molecules in splenic lymphocytes. Moreover, the inhibitory effect on cellular immunity in female offspring persisted to PND42. Unlike females, YN exposure did not change the adaptive immune responses in male offspring. Overall, maternal exposure to YN showed a strong DIT to offspring, with the lowest effective dose of 0.2 mg/kg in the current study. The toxicity of cellular immunity could persist throughout development into adulthood. There were sex-specific differences in YN-induced DIT, with females being more vulnerable.

摘要

钇是一种典型的重稀土元素,在众多领域都有广泛应用。仅有一项先前的研究表明,钇具有引发发育免疫毒性(DIT)的潜力。因此,关于钇的 DIT 证据仍然不足。本研究旨在探究硝酸钇(YN)的 DIT 及其诱导的 DIT 的自我恢复。通过灌胃,在妊娠和哺乳期将 0、0.2、2 和 20mg/kg bw/day 的 YN 分别施用于母体。在后代中,未发现对照组与 YN 处理组之间的固有免疫有显著变化。在产后第 21 天(PND21)的雌性后代中,YN 明显抑制体液和细胞免疫反应、脾 T 淋巴细胞的增殖能力以及脾淋巴细胞中协同刺激分子的表达。此外,细胞免疫的抑制作用在雌性后代中持续到 PND42。与雌性不同,YN 暴露并未改变雄性后代的适应性免疫反应。总体而言,母体暴露于 YN 对后代表现出强烈的 DIT,本研究中最低有效剂量为 0.2mg/kg。细胞免疫的毒性可能会持续整个发育过程直至成年。YN 诱导的 DIT 存在性别特异性差异,雌性更为脆弱。

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