Ascorbate exacerbates iron toxicity on intestinal barrier function against Salmonella infection.

IF 1.2 4区 环境科学与生态学 Q4 ENVIRONMENTAL SCIENCES Journal of Environmental Science and Health Part C-Toxicology and Carcinogenesis Pub Date : 2020-01-01 Epub Date: 2020-04-27 DOI:10.1080/26896583.2020.1729632
Tengjiao Guo, Yisheng Yang, Jiayou Zhang, Yu Miao, Feifei Lin, Suqin Zhu, Caili Zhang, Haohao Wu
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引用次数: 2

Abstract

Ascorbic acid is often used to enhance iron absorption in nutritional interventions, but it produces pro-oxidant effects in the presence of iron. This study aimed to evaluate ascorbate's role in iron toxicity on intestinal resistance against foodborne pathogens during iron supplementation/fortification. In polarized Caco-2 cell monolayers, compared to the iron-alone treatment, the iron-ascorbate co-treatment caused more than 2-fold increase in adhesion, invasion and translocation of Salmonella enterica serovar Typhimurium. According to 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, lactate dehydrogenase release and transepithelial electrical resistance, the iron-ascorbate co-treatment resulted in reduced cell viability and increased impairment of cell membrane and paracellular permeability compared to the iron-alone treatment. Butylated hydroxytoluene protected cells against these prooxidant toxicities of ascorbate. Ascorbate completely restored iron-induced intracellular oxidant burst and depletion of cytosolic antioxidant reserve, according to dichlorodihydrofluorescein fluorescence and intracellular reduced glutathione levels. In Salmonella-infected C57BL/6 mice, iron-ascorbate co-supplementation resulted in greater loss of body weight and appetite, lower survival rate, shorter colon length, heavier intestinal microvilli damage, and more intestinal pathogen colonization and translocation than the iron-alone supplementation. Overall, ascorbate would exacerbate iron toxicity on intestinal resistance against Salmonella infection through pro-oxidant impairment of intestinal epithelial barrier from extracellular side and/or by facilitating intestinal pathogen colonization.

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抗坏血酸加剧铁毒性对肠道屏障功能对沙门氏菌感染。
在营养干预中,抗坏血酸常用于促进铁的吸收,但在铁存在的情况下,它会产生促氧化作用。本研究旨在评估在补铁/强化过程中抗坏血酸在铁毒性和肠道对食源性病原体耐药性中的作用。在极化Caco-2细胞单层中,与单独铁处理相比,铁-抗坏血酸盐共处理导致肠炎沙门氏菌血清型鼠伤寒杆菌的粘附、侵袭和易位增加2倍以上。根据3-(4,5-二甲基噻唑-2-酰基)-2,5-二苯基溴化四唑测定、乳酸脱氢酶释放和经上皮电阻,与铁单独处理相比,铁-抗坏血酸共处理导致细胞活力降低,细胞膜和细胞旁通透性损伤增加。丁基羟基甲苯保护细胞免受抗坏血酸的这些促氧化毒性。根据二氯二氢荧光素和细胞内还原性谷胱甘肽水平,抗坏血酸完全恢复铁诱导的细胞内氧化爆发和细胞内抗氧化储备的消耗。在沙门氏菌感染的C57BL/6小鼠中,与单独补充铁相比,铁-抗坏血酸联合补充导致体重和食欲下降更大,存活率更低,结肠长度更短,肠道微绒毛损伤更严重,肠道病原体定植和易位更多。总的来说,抗坏血酸会通过从细胞外侧和/或通过促进肠道病原体定植来促进肠道上皮屏障的氧化损伤,从而加剧肠道对沙门氏菌感染的铁毒性。
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4.60
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