Yang Liu1, Jun Ji2, Wei Zhang3, Yao Suo4, Jiating Zhao5, Xiaoying Lin5, Liwei Cui5, Bai Li5, Huaiqiang Hu6, Chunying Chen7, Yu-Feng Li8. 1. Baotou Medical College, Inner Mongolia University of Science & Technology, Baotou, 014060, Inner Mongolia, China; CAS Key Laboratory for Biological Effects of Nanomaterials and Nanosafety, and HKU-IHEP Joint Laboratory on Metallomics, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing, 100049, China. 2. Baotou Medical College, Inner Mongolia University of Science & Technology, Baotou, 014060, Inner Mongolia, China. 3. CAS Key Laboratory for Biological Effects of Nanomaterials and Nanosafety, and HKU-IHEP Joint Laboratory on Metallomics, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing, 100049, China; University of Jinan, No. 336, Nanxinzhuang West Road, Jinan, 250022, Shandong, China. 4. Food Science and Engineering College, Northwest A&F University, Yangling, 712100, Shaanxi, China. 5. CAS Key Laboratory for Biological Effects of Nanomaterials and Nanosafety, and HKU-IHEP Joint Laboratory on Metallomics, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing, 100049, China. 6. Department of Neurology, No. 960 Hospital of Chinese PLA, Jinan, 250031, Shandong, China. Electronic address: huhuaiqiang@126.com. 7. CAS Key Laboratory for Biological Effects of Nanomaterials and Nanosafety, National Centre for Nanoscience and Technology, Beijing, 100191, China. 8. CAS Key Laboratory for Biological Effects of Nanomaterials and Nanosafety, and HKU-IHEP Joint Laboratory on Metallomics, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing, 100049, China. Electronic address: liyf@ihep.ac.cn.
Abstract
INTRODUCTION: Selenium plays important roles in antagonizing the toxicity of methylmercury. The underlying mechanism for the antagonism between Se and MeHg is still not fully understood. OBJECTIVE: The role of gut flora against the toxicity of environmental contaminants is receiving more and more attention. The objective of this study was to investigate the role of Se against MeHg-poisoning in the modulation of gut flora and the decomposition of MeHg. METHODS: MeHg-poisoned rats were treated with sodium selenite every other day for 90 days. Fecal samples were collected on Day 8, 30, 60 and 90. Gut flora in feces was determined using 16S rRNA gene profiling, and the concentrations of Se and total mercury (THg) were measured by ICP-MS, and the concentration of MeHg was measured by CVAFS. RESULTS: Gut flora at both the ranks of phylum and genus in the MeHg-poisoned rats after Se treatment was modulated towards that in the control group, suggesting the restoration of the profile of gut flora. Increased THg was found in fecal samples after Se treatment on day 30. The percentage of MeHg (of total mercury) in the MeHg-poisoned group was in the range of 81-105% while it was 65-84% in the Se treatment group on different days, suggesting the increased decomposition of MeHg in MeHg-poisoned rats after Se treatment. CONCLUSIONS: This study suggests that MeHg poisoning damaged the abundance of gut flora and decreased their capacity for the decomposition of MeHg. After Se treatment, the abundance of gut flora was partially restored and the decomposition and excretion of MeHg was enhanced. These findings suggest that the modulation of gut flora may be one way to promote the health status in MeHg-poisoned rats and possibly in human beings.
INTRODUCTION:Selenium plays important roles in antagonizing the toxicity of methylmercury. The underlying mechanism for the antagonism between Se and MeHg is still not fully understood. OBJECTIVE: The role of gut flora against the toxicity of environmental contaminants is receiving more and more attention. The objective of this study was to investigate the role of Se against MeHg-poisoning in the modulation of gut flora and the decomposition of MeHg. METHODS:MeHg-poisoned rats were treated with sodium selenite every other day for 90 days. Fecal samples were collected on Day 8, 30, 60 and 90. Gut flora in feces was determined using 16S rRNA gene profiling, and the concentrations of Se and total mercury (THg) were measured by ICP-MS, and the concentration of MeHg was measured by CVAFS. RESULTS: Gut flora at both the ranks of phylum and genus in the MeHg-poisoned rats after Se treatment was modulated towards that in the control group, suggesting the restoration of the profile of gut flora. Increased THg was found in fecal samples after Se treatment on day 30. The percentage of MeHg (of total mercury) in the MeHg-poisoned group was in the range of 81-105% while it was 65-84% in the Se treatment group on different days, suggesting the increased decomposition of MeHg in MeHg-poisoned rats after Se treatment. CONCLUSIONS: This study suggests that MeHgpoisoning damaged the abundance of gut flora and decreased their capacity for the decomposition of MeHg. After Se treatment, the abundance of gut flora was partially restored and the decomposition and excretion of MeHg was enhanced. These findings suggest that the modulation of gut flora may be one way to promote the health status in MeHg-poisoned rats and possibly in human beings.
Authors: Mara Cristina P Santos Ruybal; Monica Gallego; Thais Bazoti B Sottani; Emiliano H Medei; Oscar Casis; Jose Hamilton M Nascimento Journal: Int J Mol Sci Date: 2020-05-15 Impact factor: 5.923
Authors: João P Novo; Beatriz Martins; Ramon S Raposo; Frederico C Pereira; Reinaldo B Oriá; João O Malva; Carlos Fontes-Ribeiro Journal: Int J Mol Sci Date: 2021-03-18 Impact factor: 5.923