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锌通过抑制雄性 Wistar 大鼠镉摄取来调节脾脏免疫抑制吲哚胺 2,3-双加氧酶活性、血液学指标和 CD4 T 细胞,从而改善镉诱导的免疫毒性。

Zinc Ameliorates Cadmium-Induced Immunotoxicity by Modulating Splenic Immunosuppressive Indoleamine 2,3-Dioxygenase Activity, Hematological Indices, and CD4 T Cells via Inhibition of Cadmium Uptake in Male Wistar Rats.

机构信息

Toxicology and Immunotherapy Research Unit, Department of Biochemistry, Alex Ekwueme Federal University Ndufu Alike, PMB 1010, Abakaliki, Ebonyi State, Nigeria.

Department of Biochemistry, University of Benin, Benin City, Nigeria.

出版信息

Biol Trace Elem Res. 2024 Mar;202(3):1140-1149. doi: 10.1007/s12011-023-03752-7. Epub 2023 Jul 1.

Abstract

Cadmium (Cd)-induced immunotoxicity has become a matter of public health concern owing to its prevalence in the environment consequently, great potential for human exposure. Zinc (Zn) has been known to possess antioxidant, anti-inflammatory, and immune-boosting properties. However, the ameliorating influence of Zn against Cd-induced immunotoxicity connecting the IDO pathway is lacking. Adult male Wistar rats were exposed to normal drinking water with no metal contaminants (group 1), group 2 received drinking water containing 200 μg/L of Cd, group 3 received drinking water containing 200 μg/L of Zn, and group 4 received Cd and Zn as above in drinking water for 42 days. Cd exposure alone significantly triggered the splenic oxidative-inflammatory stress, increased activities of immunosuppressive tryptophan 2,3-dioxygenase (TDO), indoleamine 2,3-dioxygenases (IDO) activities/protein expression, and decreased CD4 T cell count, and a corresponding increase in the serum kynurenine concentration, as well as alterations in the hematological parameters and histologic structure when compared with the control (p < 0.05). Zn alone did not have any effect relative to the control group while co-exposure significantly (p < 0.05) assuaged the Cd-induced alterations in the studied parameters relative to the control. Cd-induced modifications in IDO 1 protein expression, IDO/TDO activities, oxidative-inflammatory stress, hematological parameters/CD4 T cell, and histological structure in the spleen of rats within the time course of the investigation were prevented by Zn co-exposure via inhibition of Cd uptake.

摘要

镉(Cd)诱发的免疫毒性由于其在环境中的普遍性而成为公共卫生关注的问题,因此人类暴露的潜在风险很大。锌(Zn)具有抗氧化、抗炎和增强免疫的特性。然而,Zn 对 Cd 诱导的免疫毒性通过 IDO 途径的缓解作用尚不清楚。雄性 Wistar 大鼠暴露于不含金属污染物的正常饮用水中(第 1 组),第 2 组给予含 200μg/L Cd 的饮用水,第 3 组给予含 200μg/L Zn 的饮用水,第 4 组给予 Cd 和 Zn 如上所述在饮用水中 42 天。单独暴露于 Cd 会显著引发脾脏氧化应激和炎症,增加免疫抑制色氨酸 2,3-双加氧酶(TDO)和吲哚胺 2,3-双加氧酶(IDO)的活性/蛋白表达,并降低 CD4 T 细胞计数,同时血清犬尿氨酸浓度相应增加,以及与对照组相比,血液学参数和组织学结构发生改变(p<0.05)。Zn 单独使用与对照组相比没有任何影响,而共同暴露时,与对照组相比,显著(p<0.05)缓解了 Cd 诱导的研究参数变化。Zn 共同暴露通过抑制 Cd 摄取,防止了 Cd 诱导的 IDO1 蛋白表达、IDO/TDO 活性、氧化应激、血液学参数/CD4 T 细胞和脾脏组织学结构的改变。

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